{"title":"All Products","description":"","products":[{"product_id":"bpc-157","title":"BPC-157","description":"\u003cdiv class=\"wp-block-woocommerce-product-details alignwide is-style-minimal\" data-hide-tab-title=\"true\" data-block-name=\"woocommerce\/product-details\"\u003e\n\u003cdiv class=\"woocommerce-tabs wc-tabs-wrapper\"\u003e\n\u003cdiv aria-labelledby=\"tab-title-description\" role=\"tabpanel\" id=\"tab-description\" class=\"woocommerce-Tabs-panel woocommerce-Tabs-panel--description panel entry-content wc-tab\"\u003e\n\u003cp\u003eBPC-157 (Body Protective Compound-157) is a research peptide composed of 15 amino acids, originally isolated from a protective protein in human gastric juice. It has gained significant attention in scientific studies for its potential role in accelerating the body’s natural healing processes. Research suggests that BPC-157 may promote tissue repair by enhancing angiogenesis (the formation of new blood vessels), supporting collagen production, and modulating growth factors involved in recovery.This peptide has been studied for a wide range of applications, including muscle tears, tendon and ligament injuries, joint damage, and gastrointestinal health. Its potential protective effects on the gut lining have also made it of interest in research on inflammatory bowel conditions. While findings are promising, BPC-157 is intended strictly for laboratory and research purposes, and is not approved for human consumption.\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eBPC-157 has been steadily researched for its potential in wound healing. Presentation of BPC-157 may stimulate the growth hormone (GH) receptors, thereby inducing similar GH potential. BPC-157 peptide appears to bind with growth hormone receptors, possibly stimulating cell proliferation. This may lead to the development of new tissue composed of collagen and the development of a network of blood vessels in a process also called ‘angiogenesis.’ Consequently, the wound is ‘rebuilt’ and healed faster than the usual rate.\u003csup dir=\"ltr\"\u003e(1)\u003c\/sup\u003e\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eBPC-157 has also been studied in correlation to gastrointestinal function. Serotonin, an enteric neurotransmitter, is localized in the GI tract and GI mucosa. Altered serotonin levels may inhibit gastric acid secretion, affecting gut mucosal function and influencing gastric blood flow.\u003csup dir=\"ltr\"\u003e(2)\u003cspan\u003e \u003c\/span\u003e\u003c\/sup\u003eBPC-157 appears to have a particular antidepressant activity, which may counteract serotonin-induced action. The peptide may counteract the 5-HT2A receptors, restricting the serotonin binding with these receptors and thereby inhibiting its action.\u003csup dir=\"ltr\"\u003e(3)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eThe peptide has been researched for its potential action across diverse functions, including tissue repair, pain perception, gastrointestinal regulation, and tendon, ligament, muscle, and bone cell reparations.\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eMultiple studies have since been conducted to understand the full action of the peptide, especially in the area of healing gastrointestinal ulceration, which is elaborated on below. Studies have suggested the peptide may increase the build-up of the blood vessels and induce anti-inflammation potential via improving functional recovery.\u003csup dir=\"ltr\"\u003e(4)\u003c\/sup\u003e\u003c\/p\u003e\n\u003ch3\u003eChemical Makeup\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003e\u003cstrong dir=\"ltr\"\u003eMolecular Formula:\u003c\/strong\u003e\u003cspan\u003e \u003c\/span\u003eC\u003csub dir=\"ltr\"\u003e62\u003c\/sub\u003eH\u003csub dir=\"ltr\"\u003e98\u003c\/sub\u003eN\u003csub dir=\"ltr\"\u003e16\u003c\/sub\u003eO\u003csub dir=\"ltr\"\u003e22\u003c\/sub\u003e\u003cbr dir=\"ltr\"\u003e\u003cstrong dir=\"ltr\"\u003eMolecular Weight:\u003c\/strong\u003e\u003cspan\u003e \u003c\/span\u003e1419.55 g\/mol\u003cbr dir=\"ltr\"\u003e\u003cstrong dir=\"ltr\"\u003eOther Known Titles:\u003c\/strong\u003e\u003cspan\u003e \u003c\/span\u003eBody Protection Compound-157\u003c\/p\u003e\n\u003ch2\u003eResearch and Clinical Studies\u003c\/h2\u003e\n\u003ch3\u003e\u003cem\u003eBPC-157 Peptide and Wound Healing\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eIn a study, three experimental murine models were used – first with skin tissue wounds, second with colon tissue anastomosis, and third with synthetic sponge implantation. A portion of the murine models were presented with a placebo, whereas others were presented with the BPC 157 peptide. After the study, all models were histologically examined. The researchers reported that the BPC-157 murine models appeared to exhibit higher numbers of collagen, reticulin, and blood vessel development than the ones in the control group.\u003csup dir=\"ltr\"\u003e(5)\u003c\/sup\u003e\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eIn a particular study, researchers explored the theory that the peptide BPC-157 might potentially hasten wound healing compared to a control group. This hypothesis was rooted in observing possible improvements in several key areas of wound healing. These included the formation of new granulation tissue, which is critical in the healing process, along with reepithelialization. In this process, new epithelial cells form to replace those damaged by the wound. Additionally, there was an observation of potential improvements in dermal remodeling, a phase where the skin regains strength and elasticity, and collagen deposition, crucial for tissue repair.\u003csup dir=\"ltr\"\u003e(6)\u003c\/sup\u003e\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eThe study also suggested that BPC-157 might have enhanced the expression of vascular endothelial growth factor (VEGF) in the injured skin tissues. VEGF is a significant protein that promotes blood vessel growth, vital to healing damaged tissues. The researchers further speculated that the peptide could have influenced umbilical vein endothelial cell proliferation (HUVECs). These cells line the blood vessels and are considered to be integral to forming new blood vessels during wound healing.\u003csup dir=\"ltr\"\u003e(6)\u003c\/sup\u003e\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eAdditionally, there was a conjecture about a noticeable increase in the migration of HUVECs. This observation was based on results from wound healing assays, tests designed to measure various aspects of wound healing. The presence of BPC-157 might have led to an increased expression of VEGF-a, a variant of VEGF, and consequently accelerated the formation of vascular tubes in a laboratory setting. Moreover, the study hinted at the possibility that BPC-157 might influence the activity of specific proteins and enzymes involved in cellular signaling pathways. Specifically, it seemed that BPC-157 could regulate the phosphorylation level of extracellular signal-regulated kinases 1 and 2 (ERK1\/2). Phosphorylation is a process that activates or deactivates many protein enzymes and is a crucial step in sending signals within cells. The affected enzymes, ERK1\/2, along with their downstream targets, including c-Fos, c-Jun, and Egr-1, are believed to play significant roles in cell growth, migration, and angiogenesis, which is the development of new blood vessels.\u003csup dir=\"ltr\"\u003e(6)\u003c\/sup\u003e\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eBPC-157 Peptide and Tendon Healing\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eAn experiment was conducted in the cultured tendon fibroblasts derived from the tendons of murine models. The cultures were divided into two groups; one was the control, whereas the other was presented with the peptide. Following the study, the following was reported:\u003csup dir=\"ltr\"\u003e(1)\u003c\/sup\u003e\u003c\/p\u003e\n\u003cul\u003e\n\u003cli\u003eThe peptide appeared to promote the outgrowth of tendon fibroblasts and tissue healing;\u003c\/li\u003e\n\u003cli\u003eEven under H2O2 stress, BPC-157 appeared to stimulate apparent cell survival under stress;\u003c\/li\u003e\n\u003cli\u003eThe peptide appeared to promote migration of the tendon fibroblasts;\u003c\/li\u003e\n\u003cli\u003eBPC-157 reportedly induced increased levels of phosphorylation of both PAK and paxillin, while the total protein level remained unchanged.\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003cp dir=\"ltr\"\u003eUpon analysis, it was suggested that the peptide may impact tendon healing, tendon outgrowth, and cell survival via the F-actin formation and activation of the FAK and paxillin pathways.\u003csup dir=\"ltr\"\u003e(1)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eF-actin formation is considered a key component in the cell's cytoskeleton, providing structure and aiding in cell movement. If BPC-157 enhances F-actin formation, this might indicate an improvement in the cytoskeletal organization and cell motility of tendon fibroblasts, which are essential for the repair and regeneration of tendon tissues. Further into the study, researchers utilized Western blotting, a laboratory method to detect specific proteins in a sample. Through this analysis, they suggested that BPC-157 might activate focal adhesion kinase (FAK) and paxillin, two proteins that play a significant role in cellular processes. The tentative finding was that the phosphorylation levels of FAK and paxillin appeared to increase in the presence of BPC-157. Interestingly, the total amounts of these proteins appeared to have remained unchanged, leading to the speculation that BPC-157's role might be more about activating existing molecules rather than increasing their production. This led to a further hypothesis that BPC-157 might activate the FAK-paxillin pathway. This pathway is considered to promote cell migration and adhesion, especially in tendon fibroblasts. The activation of this pathway could imply that BPC-157 plays a role in enhancing the movement and adherence of these cells, which are key processes in tendon healing and regeneration.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eBPC-157 Peptide and Gastrointestinal Healing\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eA study was conducted to scrutinize the action of BPC-157 peptide against similar angiogenic growth factors such as EGF, FGF, and VEGF. The primary assumptions were that BPC-157 is highly stable, biocompatible, and sufficient to exert action when presented by itself. While the study reported improved healing, only BPC-157 appeared to have exhibited consistent results in all wound types (i.e., chronic and acute) on the esophagus, stomach, duodenum, and lower GI tract. This study suggested the extent of the angiogenic potential of the peptide is apparently very high as it appeared to extend not only on local wounds and ligaments but also on GI wounds and bone healing.\u003csup dir=\"ltr\"\u003e(7)\u003c\/sup\u003e\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eBPC-157 Peptide and Tissue Damage\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eA study was conducted to understand the extent of the angiogenic potential of the peptide beyond local wounds, ligaments, and GI tract wounds and to study its action on multiple gastrointestinal lesions on the pancreas, liver injuries, heart damage, endothelium damage, and blood pressure. Following the results, scientists suggested that the BPC-157 peptide may induce a network of activities via peptidergic defense systems. There is also a possibility that BPC-157 may play a role in addressing both acute and chronic inflammation, aiding in wound healing, and assisting in the healing of fractures, including cases of pseudoarthrosis. This broad spectrum of potential suggests that BPC-157 could be part of the organism's unique peptidergic defense system.\u003csup dir=\"ltr\"\u003e(8)\u003c\/sup\u003e\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eThere are several neurotransmitters and functions considered by scientists to be important, such as dopamine, nitrous oxide, prostaglandin, and other neuron systems. Any over-activity or inhibition of these systems may lead to lesions in different organs. BPC-157, through its defense system, appears to counteract these systems and possibly reverse their over-activation and inhibition. The researchers commented that these might include important systems, ”\u003cem dir=\"ltr\"\u003enamely, dopamine-, NO-, prostaglandin-, somatosensory neuron-system,\u003c\/em\u003e” and more.\u003csup dir=\"ltr\"\u003e(\u003c\/sup\u003e\u003csup dir=\"ltr\"\u003e8)\u003c\/sup\u003e\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eBPC-157 Peptide and Muscle Healing\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eA study was conducted on murine models with injured gastrocnemius muscle complex. These murine models were then presented with methylprednisolone (corticosteroid). These corticosteroid murine models were then divided into two groups: one was presented with BPC-157, and the other was presented with a placebo. Both compounds were presented once in 24 hours and examined on days 1, 2, 4, 7, and 14. Upon examination, it was reported that the corticosteroid appeared to significantly worsen the muscle damage in the murine models. However, BPC-157 appeared to exhibit apparent signs of healing and restoration of the damaged gastrocnemius muscle and restoring functioning ability.\u003csup dir=\"ltr\"\u003e(9)\u003c\/sup\u003e\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eAmphetamine-Induced Hypersensitivity\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eLaboratory experiments have suggested that the BPC-157 peptide may have the ability to heal multiple different lesions – in the GI tract, liver, pancreas, and others. This trend in lab findings indicated that the peptide had some interaction with the dopamine system. To investigate further, this study presented the BPC-157 peptide in amphetamine (dopamine agonist) murine models. It was observed that BPC-157 appeared to be able to reverse the amphetamine-induced excitability in the murine models. Furthermore, murine models were presented with another dopamine agonist, haloperidol, and then presented with amphetamine on days 1, 2, 4, and 10. These murine models were then presented with BPC-157 to illustrate its action. Upon examination, it was suggested by the researchers that the peptide appeared to cause an almost complete reversal of the haloperidol action.\u003csup dir=\"ltr\"\u003e(10)\u003c\/sup\u003e\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eBPC-157 Peptide and Central Nervous System\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eIn a particular study using a murine model, researchers explored the potential of BPC-157 in the context of traumatic brain injury (TBI). BPC-157 might have played a role in significantly reducing the damage caused by TBI in experimental models, as indicated by improved early outcomes in the experiments conducted. During the critical 24-hour period following the injury, the observations hinted a minimal mortality rate in the BPC-157 group. Furthermore, the severity of traumatic lesions typically associated with TBI, such as subarachnoid hemorrhage (bleeding in the space between the brain and the tissues that cover it), intraventricular hemorrhage (bleeding inside the brain's ventricular system), brain laceration, and hemorrhagic laceration, appeared to be less pronounced in the murine models of the BPC-157 group. This suggested a protective potential of the peptide against such injuries.\u003csup dir=\"ltr\"\u003e(11)\u003c\/sup\u003e\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eAnother interesting observation was the considerable improvement in brain edema, swelling in the brain tissue often caused by traumatic injuries. The hypothesis extended to the possibility that if BPC-157 were introduced before the occurrence of TBI, it might show an improved ratio of conscious\/unconscious\/death states in the test subjects. In other words, the peptide might potentially prevent or reduce the severity of unconsciousness and lower mortality rates associated with TBI in experimental models. Moreover, there was a suggestion that the immediate exposure of BPC-157 immediately before the injury may have mitigated the damage in the murine models subjected to a force impulse, typically used to simulate TBI in research. This hinted at the possibility of the peptide having preventive or protective potential against the immediate consequences of traumatic brain injury in experimental models.\u003csup dir=\"ltr\"\u003e(11)\u003c\/sup\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cem\u003e\u003cstrong dir=\"ltr\"\u003eBPC 157 peptide is available for research and laboratory purposes only.\u003c\/strong\u003e\u003c\/em\u003e\u003c\/p\u003e\n\u003ch3\u003eReferences:\u003c\/h3\u003e\n\u003col\u003e\n\u003cli\u003eChang, Chung-Hsun et al. “The promoting effect of pentadecapeptide BPC 157 on tendon healing involves tendon outgrowth, cell survival, and cell migration.” Journal of applied physiology (Bethesda, Md. : 1985) vol. 110,3 (2011): 774-80. doi:10.1152\/japplphysiol.00945.2010.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/21030672\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/21030672\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eOrmsbee, H S 3rd, and J D Fondacaro. “Action of serotonin on the gastrointestinal tract.” Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.) vol. 178,3 (1985): 333-8. doi:10.3181\/00379727-178-42016.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/3919396\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/3919396\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eSikiric, Predrag et al. “Brain-gut Axis and Pentadecapeptide BPC 157: Theoretical and Practical Implications.” Current neuropharmacology vol. 14,8 (2016): 857-865. doi:10.2174\/1570159x13666160502153022.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC5333585\/#r1\"\u003ehttps:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC5333585\/#r1\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eKrivic, A., Majerovic, M., Jelic, I. et al. Modulation of early functional recovery of Achilles tendon to bone unit after transection by BPC 157 and methylprednisolone. Inflamm. res. 57, 205–210 (2008).\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/doi.org\/10.1007\/s00011-007-7056-8\"\u003ehttps:\/\/doi.org\/10.1007\/s00011-007-7056-8\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eS Seiwerth, et al. “BPC 157's effect on healing.” Journal of physiology, Paris vol. 91,3-5 (1997): 173-8. doi:10.1016\/s0928-4257(97)89480-6.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/9403790\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/9403790\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eHuang, T., Zhang, K., Sun, L., Xue, X., Zhang, C., Shu, Z., Mu, N., Gu, J., Zhang, W., Wang, Y., Zhang, Y., \u0026amp; Zhang, W. (2015). Body protective compound-157 enhances alkali-burn wound healing in vivo and promotes proliferation, migration, and angiogenesis in vitro.\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003eDrug design, development and therapy\u003c\/em\u003e,\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003e9\u003c\/em\u003e, 2485–2499.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/doi.org\/10.2147\/DDDT.S82030\"\u003ehttps:\/\/doi.org\/10.2147\/DDDT.S82030\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eSeiwerth, Sven et al. “BPC 157 and Standard Angiogenic Growth Factors. Gastrointestinal Tract Healing, Lessons from Tendon, Ligament, Muscle and Bone Healing.” Current pharmaceutical design vol. 24,18 (2018): 1972-1989. doi:10.2174\/1381612824666180712110447.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/29998800\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/29998800\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eSikiric P. (1999). The pharmacological properties of the novel peptide BPC 157 (PL-10).\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003eInflammopharmacology\u003c\/em\u003e,\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003e7\u003c\/em\u003e(1), 1–14.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/doi.org\/10.1007\/s10787-999-0022-z\"\u003ehttps:\/\/doi.org\/10.1007\/s10787-999-0022-z\u003c\/a\u003e\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/17657443\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/17657443\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003ePevec D, Novinscak T, Brcic L, Sipos K, Jukic I, Staresinic M, Mise S, Brcic I, Kolenc D, Klicek R, Banic T, Sever M, Kocijan A, Berkopic L, Radic B, Buljat G, Anic T, Zoricic I, Bojanic I, Seiwerth S, Sikiric P. Impact of pentadecapeptide BPC 157 on muscle healing impaired by systemic corticosteroid application. Med Sci Monit. 2010 Mar;16(3):BR81-88. PMID: 20190676.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/20190676\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/20190676\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eJelovac, N et al. “A novel pentadecapeptide, BPC 157, blocks the stereotypy produced acutely by amphetamine and the development of haloperidol-induced supersensitivity to amphetamine.” Biological psychiatry vol. 43,7 (1998): 511-9. doi:10.1016\/s0006-3223(97)00277-1.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/9547930\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/9547930\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eTudor, M., Jandric, I., Marovic, A., Gjurasin, M., Perovic, D., Radic, B., Blagaic, A. B., Kolenc, D., Brcic, L., Zarkovic, K., Seiwerth, S., \u0026amp; Sikiric, P. (2010). Traumatic brain injury in mice and pentadecapeptide BPC 157 effect.\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003eRegulatory peptides\u003c\/em\u003e,\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003e160\u003c\/em\u003e(1-3), 26–32.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/doi.org\/10.1016\/j.regpep.2009.11.012\"\u003ehttps:\/\/doi.org\/10.1016\/j.regpep.2009.11.012\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eGwyer, D., Wragg, N.M. \u0026amp; Wilson, S.L. Gastric pentadecapeptide body protection compound BPC 157 and its role in accelerating musculoskeletal soft tissue healing. Cell Tissue Res 377, 153–159 (2019).\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/doi.org\/10.1007\/s00441-019-03016-8\"\u003ehttps:\/\/doi.org\/10.1007\/s00441-019-03016-8\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eVeljaca, Marija et al, The development of PL 14736 for treatment of inflammatory bowel disease, Advanced in GI pharmacology, 2002 O-32.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/www.bib.irb.hr\/192824\"\u003ehttps:\/\/www.bib.irb.hr\/192824\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003ePhase I clinical trial in healthy volunteers to study safety and pharmacokinetics of BPC-157, a pentadecapeptide from gastric source.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/clinicaltrials.gov\/ct2\/show\/NCT02637284?\"\u003ehttps:\/\/clinicaltrials.gov\/ct2\/show\/NCT02637284?\u003c\/a\u003e\n\u003c\/li\u003e\n\u003c\/ol\u003e\n\u003cp\u003e\u003ca href=\"https:\/\/purexlabs.io\/pages\/bpc-157-coa\" title=\"BPC-157 COA\"\u003eCOA\u003c\/a\u003e\u003c\/p\u003e\n\u003c\/div\u003e\n\u003c\/div\u003e\n\u003c\/div\u003e","brand":"PureX Labs","offers":[{"title":"5mg","offer_id":48353551319284,"sku":null,"price":20.0,"currency_code":"USD","in_stock":true},{"title":"10mg","offer_id":47487342477556,"sku":null,"price":40.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0804\/5802\/3156\/files\/BPC-157.png?v=1769105831"},{"product_id":"bpc-157-tb500","title":"BPC-157\/TB500","description":"\u003cp\u003eBPC-157 + TB-500 is a regenerative peptide blend designed for advanced research into tissue healing, cellular repair, and recovery processes. By combining two of the most widely studied peptides in regenerative science, this formulation offers researchers a unique opportunity to examine synergistic mechanisms of repair and protection across multiple biological systems.\u003c\/p\u003e\n\u003ch2\u003eResearch and Clinical Studies\u003c\/h2\u003e\n\u003cp\u003eThere are no research or clinical studies currently available where both TB-500 and BPC-157 were used in the same experiment or presented in combination, using the same test model. However, below listed are the studies observing the potential action of the individual peptides.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eBPC-157 \u0026amp; TB-500 Blend and Tissue Repair\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eIn one study with Tβ4 conducted in 1999,\u003csup dir=\"ltr\"\u003e(9)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eexperimentally wounded murine models were used as subjects, where half the number of murine models were presented with saline and the rest were presented with TB-500 peptide. The main aim of this study was to determine the potential tissue repair action of the peptide. Four days after the experiment, it was reported by the researchers that the murine models presented with TB-500 showed an apparent 41% increment in the re-epithelialization process (i.e., formation of new epithelial cells to resurface the wound). After seven days, the wounds presented with TB-500 had reportedly contracted by at least 11% as compared to the saline wounds. The authors commented that “\u003cem dir=\"ltr\"\u003ethese results suggest that Tβ4 is a potent wound healing factor with multiple activities...\u003c\/em\u003e”\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eIn another 2006 clinical trial,\u003csup dir=\"ltr\"\u003e(10)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003e72 test subjects with pressure ulcers were presented with TB-500. The main aim of this randomized, double blind study was to establish the potential of thymosin beta 4 (analogous to TB-500) in ulcer presence. The test subjects were divided into two groups, where one group was presented with placebo for 84 days and the rest were presented daily with various concentrations of the peptide, for up to 84 days. After 84 days, there was an occurrence of wound healing process where the ulcers reportedly exhibited signs of healing.\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eIn a BPC-157 study,\u003csup dir=\"ltr\"\u003e(11)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003ethree experimental murine models were used as subjects where all were experimentally wounded, with either acute or chronic wounds. These murine models were then divided into two groups, where one was presented with a placebo compound and the other was presented with BC-157 peptide. After the experiment, all the murine models were histologically examined, and it was determined that the murine models with BPC-157 exhibited a prominently higher number of collagen and blood vessels formed as compared to the placebo murine models.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eBPC-157 \u0026amp; TB-500 Blend and Ligaments\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eIn one study,\u003csup dir=\"ltr\"\u003e(12)\u003cspan\u003e \u003c\/span\u003e\u003c\/sup\u003ethe medial collateral ligament (MCL) of the murine models was transected (cut across) during surgery. All the murine models were then presented with a fibrin sealing agent, where some murine models were also presented with thymosin beta 4 (TB-500). Four weeks after the surgery, it was reported by the researchers that the healing tissues in the peptide murine models exhibited apparently evenly formed and spaced collagen cells. The collagen cells formed in the peptide murine models were reportedly wider as compared to the control murine models. Furthermore, the mechanical properties of the regenerating tissues, including the femur-medial collateral ligament-tibia complexes, appeared to be improved in the TB-500 group compared to the control.\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eAnother research article indicated that BPC-157 might play a role in aiding the recovery of connective tissues, potentially by promoting the growth of tendon explants. Interestingly, the study suggested that BPC-157 may possibly enhance the resilience of these cells in the face of oxidative stress. This outcome might be linked to the triggering of F-actin formation, as indicated by FITC-phalloidin staining. BPC-157 also appeared to enhance the\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003ein vitro\u003c\/em\u003e\u003cspan\u003e \u003c\/span\u003emovement of tendon fibroblasts as indicated by a transwell filter migration test. Furthermore, BPC-157 appeared to hasten the dispersion of tendon fibroblasts across culture plates. Additionally, the study delved into the possible role of the FAK-paxillin pathway (a pair of focal adhesion-linked proteins that relay signals following integrins) in conveying the action of BPC-157. Western blot tests hinted that the phosphorylation rates of both FAK and paxillin seemed to rise with BPC 157, yet the overall protein quantities stayed constant.\u003csup dir=\"ltr\"\u003e(8)\u003c\/sup\u003e\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eBPC-157 \u0026amp; TB-500 Blend and Muscle\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eA study\u003csup dir=\"ltr\"\u003e(13)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003ewas conducted on murine models with experimentally injured gastrocnemius muscle complex. These murine models were initially presented with corticosteroids, which reportedly contributed to severe muscular damage in these murine models . These murine models were then divided into two groups, where one was presented with placebo and the other with BPC-157 daily for up to 14 days. After the experiment, it was reported that the BPC-157 murine models appeared to exhibit complete restoration of their gastric muscles along with full ability to function. Whereas, the placebo treated group did not exhibit any apparent change to the damaged muscles.\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eTB-500 may also have a potential effect on muscle cell regeneration, more specifically on cardiac muscle cells. One study suggests that TB-500 appears to bolster myocardial resilience in conditions of low oxygen, and seemingly fosters angiogenesis, possibly paving the way for cardiac cell repair. Researchers have hinted at a potential process where cardiac fibroblasts transition into cells resembling cardiomyocytes.\u003csup dir=\"ltr\"\u003e(14)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eIn the end, the scholars observed that TB-500, when combined with cardiac reprogramming techniques, might collaboratively reduce potential harm to cardiac cells and foster its regeneration by activating inherent cells within the cardiac region. An examination using murine models of coronary artery tying appeared to exhibit results which implied that TB-500 might elevate integrin-associated kinase (ILK) and protein kinase B operations in the heart, possibly boosting early cardiomyocyte endurance and seemingly enhancing heart performance.\u003csup dir=\"ltr\"\u003e(15)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eThe experts also suggested that TB-500 might support the movement of myocardial and endothelial cells in the fetal heart and maintains this capability in mature cardiomyocytes.\u003c\/p\u003e\n\u003cp\u003e\u003cem\u003e\u003cstrong dir=\"ltr\"\u003eBPC-157 \u0026amp; TB-500 Peptide Blend is available for research and laboratory purposes only.\u003c\/strong\u003e\u003c\/em\u003e\u003c\/p\u003e\n\u003ch3\u003eReferences:\u003c\/h3\u003e\n\u003col\u003e\n\u003cli\u003eSeiwerth, S., Milavic, M., Vukojevic, J., Gojkovic, S., Krezic, I., Vuletic, L. B., Pavlov, K. H., Petrovic, A., Sikiric, S., Vranes, H., Prtoric, A., Zizek, H., Durasin, T., Dobric, I., Staresinic, M., Strbe, S., Knezevic, M., Sola, M., Kokot, A., Sever, M., … Sikiric, P. (2021). Stable Gastric Pentadecapeptide BPC 157 and Wound Healing.\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003eFrontiers in pharmacology\u003c\/em\u003e,\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003e12\u003c\/em\u003e, 627533.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/doi.org\/10.3389\/fphar.2021.627533\"\u003ehttps:\/\/doi.org\/10.3389\/fphar.2021.627533\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eMaar, K., Hetenyi, R., Maar, S., Faskerti, G., Hanna, D., Lippai, B., Takatsy, A., \u0026amp; Bock-Marquette, I. (2021). Utilizing Developmentally Essential Secreted Peptides Such as Thymosin Beta-4 to Remind the Adult Organs of Their Embryonic State-New Directions in Anti-Aging Regenerative Therapies.\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003eCells\u003c\/em\u003e,\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003e10\u003c\/em\u003e(6), 1343.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/doi.org\/10.3390\/cells10061343\"\u003ehttps:\/\/doi.org\/10.3390\/cells10061343\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eNational Center for Biotechnology Information. “PubChem Compound Summary for CID 132558700, CID 132558700” PubChem,\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubchem.ncbi.nlm.nih.gov\/compound\/132558700\"\u003ehttps:\/\/pubchem.ncbi.nlm.nih.gov\/compound\/132558700\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eNational Center for Biotechnology Information. “PubChem Compound Summary for CID 9941957” PubChem,\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubchem.ncbi.nlm.nih.gov\/compound\/Bpc-157\"\u003ehttps:\/\/pubchem.ncbi.nlm.nih.gov\/compound\/Bpc-157\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eGurtner GC, Werner S, Barrandon Y, Longaker MT. Wound repair and regeneration. Nature. 2008 May 15;453(7193):314-21. doi: 10.1038\/nature07039. PMID: 18480812.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/18480812\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/18480812\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eSantra, M., Zhang, Z. G., Yang, J., Santra, S., Santra, S., Chopp, M., \u0026amp; Morris, D. C. (2014). Thymosin β4 up-regulation of microRNA-146a promotes oligodendrocyte differentiation and suppression of the Toll-like proinflammatory pathway.\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003eThe Journal of biological chemistry\u003c\/em\u003e,\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003e289\u003c\/em\u003e(28), 19508–19518.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/doi.org\/10.1074\/jbc.M113.529966\"\u003ehttps:\/\/doi.org\/10.1074\/jbc.M113.529966\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eSikiric, Predrag et al. “Brain-gut Axis and Pentadecapeptide BPC-157: Theoretical and Practical Implications.” Current neuropharmacology vol. 14,8 (2016): 857-865.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC5333585\/#r1\"\u003ehttps:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC5333585\/#r1\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eChang, Chung-Hsun et al. “The promoting effect of pentadecapeptide BPC-157 on tendon healing involves tendon outgrowth, cell survival, and cell migration.” Journal of applied physiology (Bethesda, Md. : 1985) vol. 110,3 (2011): 774-80. doi:10.1152\/japplphysiol.00945.2010.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/21030672\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/21030672\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eKatherine M. Malinda et.al, Thymosin β4 Accelerates Wound Healing, Journal of Investigative Dermatology, Volume 113, Issue 3, 1999, Pages 364-368, ISSN 0022-202X,\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/www.sciencedirect.com\/science\/article\/pii\/S0022202X15405950\"\u003ehttps:\/\/www.sciencedirect.com\/science\/article\/pii\/S0022202X15405950\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eStudy of Thymosin Beta 4 in Patients With Pressure Ulcers.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/www.clinicaltrials.gov\/ct2\/show\/NCT00382174\"\u003ehttps:\/\/www.clinicaltrials.gov\/ct2\/show\/NCT00382174\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eS Seiwerth, et al. “BPC-157’s effect on healing.” Journal of physiology, Paris vol. 91,3-5 (1997): 173-8. doi:10.1016\/s0928-4257(97)89480-6.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/9403790\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/9403790\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eXu B, Yang M, Li Z, Zhang Y, Jiang Z, Guan S, Jiang D. Thymosin β4 enhances the healing of medial collateral ligament injury in rat. Regul Pept. 2013 Jun 10;184:1-5. doi: 10.1016\/j.regpep.2013.03.026.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/23523891\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/23523891\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003ePevec D, Novinscak T, Brcic L, Sipos K, Jukic I, Staresinic M, Mise S, Brcic I, Kolenc D, Klicek R, Banic T, Sever M, Kocijan A, Berkopic L, Radic B, Buljat G, Anic T, Zoricic I, Bojanic I, Seiwerth S, Sikiric P. Impact of pentadecapeptide BPC-157 on muscle healing impaired by systemic corticosteroid application. Med Sci Monit. 2010 Mar;16(3):BR81-88. PMID: 20190676.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/20190676\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/20190676\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eSrivastava, D., Ieda, M., Fu, J., \u0026amp; Qian, L. (2012). Cardiac repair with thymosin β4 and cardiac reprogramming factors.\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003eAnnals of the New York Academy of Sciences\u003c\/em\u003e,\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003e1270\u003c\/em\u003e, 66–72.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/doi.org\/10.1111\/j.1749-6632.2012.06696.x\"\u003ehttps:\/\/doi.org\/10.1111\/j.1749-6632.2012.06696.x\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eBock-Marquette, I., Saxena, A., White, M. D., Dimaio, J. M., \u0026amp; Srivastava, D. (2004). Thymosin beta4 activates integrin-linked kinase and promotes cardiac cell migration, survival and cardiac repair.\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003eNature\u003c\/em\u003e,\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003e432\u003c\/em\u003e(7016), 466–472.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/doi.org\/10.1038\/nature03000\"\u003ehttps:\/\/doi.org\/10.1038\/nature03000\u003c\/a\u003e\n\u003c\/li\u003e\n\u003c\/ol\u003e","brand":"PureX Labs","offers":[{"title":"20mg","offer_id":47487346573556,"sku":null,"price":85.0,"currency_code":"USD","in_stock":false},{"title":"10mg","offer_id":48098748727540,"sku":null,"price":45.0,"currency_code":"USD","in_stock":false}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0804\/5802\/3156\/files\/BPC-157_TB500.png?v=1769105968"},{"product_id":"ghk-cu","title":"GHK-CU","description":"\u003cp dir=\"ltr\"\u003eGHK-Cu is a naturally occurring copper-binding peptide composed of 3 amino acids, i.e. glycyl-L-histidyl-L-lysine.\u003csup dir=\"ltr\"\u003e(1)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003e-Cu refers to the chemical addition of copper. GHK-Cu (Copper) is a small tripeptide found in plasma and reportedly releases at the time of injury. The concentration of GHK-Cu declines with age. At 20 years, the average concentration of GHK-Cu of 200 ng\/mL declines to 80 ng\/mL by 60 years.\u003csup dir=\"ltr\"\u003e(1)\u003c\/sup\u003e\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eStudies\u003csup dir=\"ltr\"\u003e(4)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003ehave suggested when the plasma GHK peptide is added to the cell culture in nanomolar amounts; the peptide has the potential to induce a wide range of responses from growth stimulation to toxic cell differentiation. During the isolation of the peptide, researchers suggested that it exhibited potential chelating properties and might co-isolate with almost the same amount of copper ions and a fifth of the amount of iron found in the cells. When the peptide was incubated in the isolated cells as a bound complex with copper and iron molecules, maximal potential was reported.\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eStudies\u003csup dir=\"ltr\"\u003e(5)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003ehave suggested that the peptide exhibits potential in gene expression and may to reset elements of the genome. By this potential mechanism, GHK-Cu peptide may restore impaired cells, including carcinogenic cells and COPD cells. GHK-Cu peptide has been researched for its potential across a variety of functions\u003csup dir=\"ltr\"\u003e(1)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eincluding that it may tighten and reverse the thinning of aging skin structure, supporting the extracellular matrix, that it may restore the skin barrier and moderate texture, hyperpigmentation and lesions, may support tissue repair and mitigate inflammation, may stimulate increasing hair follicle size, may exert antioxidant properties and, finally, may exhibit gene restructuring potential.\u003c\/p\u003e\n\u003ch3\u003eSpecifications\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003e\u003cstrong dir=\"ltr\"\u003eMolecular Formula:\u003c\/strong\u003e\u003cspan\u003e \u003c\/span\u003eC\u003csub dir=\"ltr\"\u003e14\u003c\/sub\u003eH\u003csub dir=\"ltr\"\u003e23\u003c\/sub\u003eCuN\u003csub dir=\"ltr\"\u003e6\u003c\/sub\u003eO\u003csub dir=\"ltr\"\u003e4\u003c\/sub\u003e\u003cbr dir=\"ltr\"\u003e\u003cstrong dir=\"ltr\"\u003eMolecular Weight:\u003c\/strong\u003e\u003cspan\u003e \u003c\/span\u003e340.38 g\/mol\u003cbr dir=\"ltr\"\u003e\u003cstrong dir=\"ltr\"\u003eOther Known Titles:\u003c\/strong\u003e\u003cspan\u003e \u003c\/span\u003eglycyl-L-histidyl-L-lysine-copper 2+\u003c\/p\u003e\n\u003ch2\u003eResearch and Clinical Studies\u003c\/h2\u003e\n\u003ch3\u003e\u003cem\u003eGHK Peptide Initial Research\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eThis 1980s study\u003csup dir=\"ltr\"\u003e(6)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003esuggested the biological potential of the naturally occurring peptide in tissue repair. GHK peptide may host copper (II) ions due to possible copper affinity and may thereby stimulate the synthesis of collagen and increase the accumulation of total proteins and DNA at the injury site. Dermal wounded rats were used for this study. At the time of injury, the release of GHK peptide was induced. ‘Emergency response molecules’ were released from the matrix at the site of injury. Once released, GHK appeared to bind with Cu ions found in the blood and then stimulate the synthesis of decorin protein. Decorin protein is responsible for the synthesis of collagen and regulation of wound healing and anti-tumor defense mechanism. Further studies in the 2000s,\u003csup dir=\"ltr\"\u003e(7)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003esuggested that the GHK-Cu peptide hosts the potential to not only stimulate the collagen synthesis but also stimulate the production of tissue inhibitors, TIMP-1 and TIMP-2.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eGHK Peptide and Tissue Repair\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eIn this study,\u003csup dir=\"ltr\"\u003e(8)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003ethe main aim was to understand the action of the GHK-Cu peptide complex when applied to the open wounds in comparison to zinc oxide. 18 New Zealand white rabbits were used for this study, divided into three groups – one group was presented with GHK-Cu, second group with zinc oxide and third group with placebo. Woulds were induced on each rabbit and the rabbits were presented with the respective compounds for 21 consecutive days. After 21 days, it was suggested by the researchers that the group delivered with the GHK-Cu peptide complex appeared to exhibit increased healing compared to the group given zinc oxide or placebo.\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eIn this study,\u003csup dir=\"ltr\"\u003e(9)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003ethe main aim was to understand the action of the GHK-Cu peptide complex as compared to helium neon laser. Laser applications were measured at 1 J cm2 and 3 J cm2. 24 New Zealand white rabbits were used for this study, divided into three groups and presented with respective concentrations of the GHK-Cu peptide complex and helium neon laser application. Experimental wounds were created on all the rabbits and all rabbits were studied for 28 consecutive days with the respective compounds. After the study, it was suggested by the researchers that rabbits studied with GHK-Cu peptide and higher concentration of the laser application appeared more receptive toward wound healing than the other group. The rabbits presented with GHK-Cu peptide exhibited an apparent decline in neutrophil counts and increase in neovascularization.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eGHK Peptide and Metastasis\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eIn this 1983 study,\u003csup dir=\"ltr\"\u003e(1)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003ethe actions of the mixture of GHK-Cu complex and ascorbic acid (Vitamin C) on the growth of the sarcoma (tumor) cells was observed. 180 mice with cancerous growths were exposed to this mixture. Researchers suggested the mixture had the potential to induce a decline in the growth of carcinogenic cells in the subject mice. It was later reported by the researchers that GHK-Cu peptide complex exhibited some potential in increasing the expression of caspase and the associated genes, as well as gene expression associated with DNA repair. Specifically, this peptide seemed to suppress the growth of two types of cancer cells in experimental settings: SH-SY5Y neuroblastoma cells, which are a model for studying nerve cell behavior and pathology, and U937 histiocytic lymphoma cells, which are used to study the immune system's response to cancer. Additionally, the peptide might have reactivated the apoptosis pathway, a type of programmed cell death crucial for removing faulty cells, as evidenced by activity in caspases 3 and 7, which are enzymes that play key roles in apoptosis. Conversely, in a study of non-cancerous cells, GHK appeared to promote the growth of NIH-3T3 fibroblasts, which are healthy cells often used as a standard model to examine cell division and growth.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eGHK Peptide and Ulcers\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eThis clinical study\u003csup dir=\"ltr\"\u003e(10)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003ewas carried out in diabetic subjects with neuropathic ulcers. All subjects were enrolled in a standard wound care protocol, where only the subjects with sharp ulcer wound or debridement were entered into this randomized, placebo controlled clinical trial. The study was carried out using GHK-Cu peptide complex gel. All subjects were divided into different groups, where one group was presented with the peptide gel, whereas others were given standard care with a placebo application. Following the study, researchers suggested that the subjects given the gel exhibited apparently elevated healing at 98%+. The gel complex appeared to have the potential to induce closure of 98.5% of plantar ulcers whereas the control only reportedly induced 60.8% of ulcer healing.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eGHK Peptide and Behavioral Properties\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eIn this study,\u003csup dir=\"ltr\"\u003e(1)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eGHK-Cu was delivered to mice to measure pain mitigation. Mice were placed on a moderately hot plate. Due to heat and the pain, it would usually take longer for mice to lick their paws; however, upon delivery the peptide, the time taken to lick their paws reduced compared to control environments. Researchers suggested the mice got ‘comfortable’ and their pain was eased faster with the presence of GHK-Cu.\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eIn this study,\u003csup dir=\"ltr\"\u003e(11)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003emale rats were deposited into a maze, which was intended to induce anxiety and cause behavioral changes. If anxious, rats were observed to restrict arm movement, keeping \"close arms\"; whereas \"open arm\" behavior was shown in rats with lessened levels of anxiety. As a part of the study, once the peptide was delivered, the time spent by the rats in \"open arms\" state in the maze was monitored. After the study, it was reported by the researchers that the peptide exhibited some potential in increasing \"open arms\" states in the subjects.\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eIn an additional study,\u003csup dir=\"ltr\"\u003e(12)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003etwo rats were placed in a small cage and were then given minor electric shocks. As a result of these shocks, the rat would become agitated and attack the second rat. Twelve minutes before this experiment, GHK-Cu peptide was delivered to both rats. It was noted by the researchers that the number of attacks, after the electric shocks, reduced by 5 times than usual.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eGHK-Cu and Antioxidative potential\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eA study has investigated the potential of Glycyl-L-histidyl-L-lysine (GHK) to regulate the presence of reactive oxygen species (ROS) within laboratory cells, with a focus on its ability to mitigate oxidative stress through interactions with various ROS types.\u003csup dir=\"ltr\"\u003e(13)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eGHK is proposed to act as an endogenous antioxidant, potentially due to its selective targeting and neutralization of certain radicals, specifically hydroxyl (·OH) and peroxyl (ROO·) radicals. The antioxidant properties of GHK were assessed using two primary techniques: flow cytometry, a method for analyzing various cellular characteristics, and electron spin resonance (ESR) spin-trapping, which is employed to detect free radicals. Throughout these evaluations, GHK appeared to lower ROS levels induced by tert-butyl hydroperoxide (t-BOPD), a chemical known to promote oxidative stress within cells. The ESR data revealed that GHK was notably positive in reducing the concentrations of ·OH and ROO· radicals, although it had a seemingly modest action on superoxide (O2 -·) radicals. Additional examinations utilizing ESR assessed the relative potential of GHK in neutralizing ·OH radicals compared to other antioxidants like carnosine and reduced glutathione (GSH), both recognized for their antioxidant capabilities. Preliminary results suggest that GHK could be more proficient at neutralizing ·OH radicals compared to these alternatives.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eGHK-Cu and Antioxidative potential\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eA study has investigated the possible mechanisms through which the peptide complex GHK-Cu could influence anti-inflammatory actions, particularly against lung tissue inflammation induced by cigarette smoke (CS).\u003csup dir=\"ltr\"\u003e(14)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eIt is hypothesized that GHK-Cu may influence various biochemical pathways and molecular markers related to inflammation and oxidative stress, although the specific mechanisms remain somewhat uncertain. In experiments involving mouse models exposed to CS, exposure to GHK-Cu was linked to a potential decrease in the production of pro-inflammatory cytokines, including interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), found in bronchoalveolar lavage fluid—fluid used to capture cells and soluble factors from the airways and lung tissues. These results tentatively suggest that GHK-Cu might help mitigate the inflammatory responses triggered by cigarette smoke. Additionally, there was a noted possible reduction in the activity of myeloperoxidase (MPO), an enzyme that serves as a marker for neutrophil-driven inflammation and oxidative stress, in lung tissues that received GHK-Cu exposure. This observation could indicate a potential role of GHK-Cu in limiting the activation or mobilization of neutrophils, possibly curtailing the oxidative bursts and consequent inflammation. At the molecular level, the research proposes that GHK-Cu may interact with the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathway. NF-κB plays a critical role in the initiation and perpetuation of inflammation. The peptide complex is thought to possibly inhibit NF-κB activation by affecting the phosphorylation of IκBα, a protein that inhibits NF-κB. This interaction could hypothetically result in lower expression of genes that promote inflammation, controlled by NF-κB. Furthermore, the study suggests that GHK-Cu could potentially influence the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway. Nrf2 is integral to cellular defenses against oxidative damage. GHK-Cu is posited to possibly boost the expression and nuclear translocation of Nrf2 in lung tissues, thereby promoting the transcription of genes that combat oxidative stress and possibly enhancing the cellular resilience against oxidative damage. The investigation further examines how GHK-Cu interacts with markers of oxidative stress, such as malondialdehyde (MDA) and glutathione (GSH). MDA is a product of lipid peroxidation and an indicator of oxidative stress, while GSH is a vital antioxidant that plays a crucial role in cellular defense mechanisms. The experimentation with GHK-Cu is associated with a tentative reduction in MDA levels and a possible restoration of GSH levels, suggesting a potential ameliorative action on oxidative stress.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eGHK-Cu and Lipid Peroxidation\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eA theoretical model posits that GHK could play a role in mitigating the discharge of iron from ferritin.\u003csup dir=\"ltr\"\u003e(15)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eFerritin, a protein complex that stores iron, releases it in a form that can facilitate lipid peroxidation, a process where free radicals attack lipids, leading to cell damage. It is suggested that GHK might inhibit the assembly of iron complexes within injured tissues, which could, in turn, decrease inflammation. Further exploration of GHK's role reveals that it may interact with specific biological pathways that govern the release of iron from ferritin. This interaction might restrict the release of iron by up to 87%, although this is a provisional estimate. Such a significant reduction in iron release could conceivably diminish both inflammation and oxidative stress, the latter being a condition where damaging oxidative processes occur more rapidly than the body's ability to counteract them, in the affected tissues.\u003c\/p\u003e\n\u003cp\u003e\u003cem\u003e\u003cstrong dir=\"ltr\"\u003eGHK-Cu peptide is available for research and laboratory purposes only.\u003c\/strong\u003e\u003c\/em\u003e\u003c\/p\u003e\n\u003ch3\u003eReferences:\u003c\/h3\u003e\n\u003col\u003e\n\u003cli\u003ePickart, Loren, and Anna Margolina. “Regenerative and Protective Actions of the GHK-Cu Peptide in the Light of the New Gene Data.” International journal of molecular sciences vol. 19,7 1987. 7 Jul. 2018, doi:10.3390\/ijms19071987.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC6073405\/\"\u003ehttps:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC6073405\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003ePickart L, Freedman JH, Loker WJ, Peisach J, Perkins CM, Stenkamp RE, Weinstein B. Growth-modulating plasma tripeptide may function by facilitating copper uptake into cells. Nature. 1980 Dec 25;288(5792):715-7. doi: 10.1038\/288715a0. PMID: 7453802.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/7453802\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/7453802\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eL.O. Pilgeram, L.R. Pickart, Control of fibrinogen biosynthesis: The role of free fatty acid, Journal of Atherosclerosis Research, Volume 8, Issue 1, 1968, Pages 155-166, ISSN 0368-1319,\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/doi.org\/10.1016\/S0368-1319(68)80089-4\"\u003ehttps:\/\/doi.org\/10.1016\/S0368-1319(68)80089-4\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003ePickart L, Freedman JH, Loker WJ, Peisach J, Perkins CM, Stenkamp RE, Weinstein B. Growth-modulating plasma tripeptide may function by facilitating copper uptake into cells. Nature. 1980 Dec 25;288(5792):715-7. doi: 10.1038\/288715a0. PMID: 7453802.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/7453802\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/7453802\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003ePickart L, Vasquez-Soltero JM, Margolina A. GHK and DNA: resetting the human genome to health. Biomed Res Int. 2014;2014:151479. doi: 10.1155\/2014\/151479. Epub 2014 Sep 11. PMID: 25302294; PMCID: PMC4180391.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/25302294\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/25302294\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eMaquart FX, Pickart L, Laurent M, Gillery P, Monboisse JC, Borel JP. Stimulation of collagen synthesis in fibroblast cultures by the tripeptide-copper complex glycyl-L-histidyl-L-lysine-Cu2+. FEBS Lett. 1988 Oct 10;238(2):343-6. doi: 10.1016\/0014-5793(88)80509-x. PMID: 3169264.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/3169264\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/3169264\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eSiméon A, Emonard H, Hornebeck W, Maquart FX. The tripeptide-copper complex glycyl-L-histidyl-L-lysine-Cu2+ stimulates matrix metalloproteinase-2 expression by fibroblast cultures. Life Sci. 2000 Sep 22;67(18):2257-65. doi: 10.1016\/s0024-3205(00)00803-1. PMID: 11045606.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/11045606\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/11045606\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eCangul IT, Gul NY, Topal A, Yilmaz R. Evaluation of the effects of tripeptide-copper complex and zinc oxide on open-wound healing in rabbits. Vet Dermatol. 2006 Dec;17(6):417-23. doi: 10.1111\/j.1365-3164.2006.00551.x. PMID: 17083573.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/17083573\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/17083573\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eGul NY, Topal A, Cangul IT, Yanik K. The effects of tripeptide copper complex and helium-neon laser on wound healing in rabbits. Vet Dermatol. 2008 Feb;19(1):7-14. doi: 10.1111\/j.1365-3164.2007.00647.x. PMID: 18177285.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/18177285\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/18177285\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eMulder GD, Patt LM, Sanders L, Rosenstock J, Altman MI, Hanley ME, Duncan GW. Enhanced healing of ulcers in patients with diabetes by treatment with glycyl-l-histidyl-l-lysine copper. Wound Repair Regen. 1994 Oct;2(4):259-69. doi: 10.1046\/j.1524-475X.1994.20406.x. PMID: 17147644.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/17147644\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/17147644\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eBobyntsev II, Chernysheva OI, Dolgintsev ME, Smakhtin MY, Belykh AE. Anxiolytic effects of Gly-His-Lys peptide and its analogs. Bull Exp Biol Med. 2015 Apr;158(6):726-8. doi: 10.1007\/s10517-015-2847-3. Epub 2015 Apr 23. PMID: 25900608.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/25900608\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/25900608\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eSever'yanova LА, Dolgintsev ME. Effects of Tripeptide Gly-His-Lys in Pain-Induced Aggressive-Defensive Behavior in Rats. Bull Exp Biol Med. 2017 Dec;164(2):140-143. doi: 10.1007\/s10517-017-3943-3. Epub 2017 Nov 27. PMID: 29181666.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/29181666\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/29181666\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eSakuma, S., Ishimura, M., Yuba, Y., Itoh, Y., \u0026amp; Fujimoto, Y. (2018). The peptide glycyl-ʟ-histidyl-ʟ-lysine is an endogenous antioxidant in living organisms, possibly by diminishing hydroxyl and peroxyl radicals. International journal of physiology, pathophysiology and pharmacology, 10(3), 132–138.\u003c\/li\u003e\n\u003cli\u003eZhang, Q., Yan, L., Lu, J., \u0026amp; Zhou, X. (2022). Glycyl-L-histidyl-L-lysine-Cu2+ attenuates cigarette smoke-induced pulmonary emphysema and inflammation by reducing oxidative stress pathway. Frontiers in molecular biosciences, 9, 925700.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/doi.org\/10.3389\/fmolb.2022.925700\"\u003ehttps:\/\/doi.org\/10.3389\/fmolb.2022.925700\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eMiller, D. M., DeSilva, D., Pickart, L., \u0026amp; Aust, S. D. (1990). Effects of glycyl-histidyl-lysyl chelated Cu(II) on ferritin dependent lipid peroxidation. Advances in experimental medicine and biology, 264, 79–84.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/doi.org\/10.1007\/978-1-4684-5730-8_11\"\u003ehttps:\/\/doi.org\/10.1007\/978-1-4684-5730-8_11\u003c\/a\u003e\n\u003c\/li\u003e\n\u003c\/ol\u003e","brand":"PureX Labs","offers":[{"title":"50mg","offer_id":47487353553140,"sku":null,"price":25.0,"currency_code":"USD","in_stock":true},{"title":"100mg","offer_id":47487358173428,"sku":null,"price":50.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0804\/5802\/3156\/files\/GHK-CU_50MG.png?v=1769106141"},{"product_id":"tirzepatide","title":"Tirzepatide","description":"\u003cp\u003e\u003cmeta charset=\"utf-8\"\u003e\u003cspan\u003eTirzepatide is a synthetic peptide that functions as a dual agonist of the glucose-dependent insulinotropic polypeptide (GIP) receptor and the glucagon-like peptide-1 (GLP-1) receptor. In research models it is used to study incretin biology, metabolic regulation, and the integrated control of glucose homeostasis, appetite signaling, and energy balance.\u003c\/span\u003e\u003cspan\u003e\u003c\/span\u003e\u003c\/p\u003e","brand":"PureX Labs","offers":[{"title":"20mg","offer_id":47487366758644,"sku":null,"price":80.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0804\/5802\/3156\/files\/Tirzepatide.png?v=1769106211"},{"product_id":"ipamorelin","title":"Ipamorelin","description":"\u003cp dir=\"ltr\"\u003eIpamorelin is a synthetic peptide that is composed of five amino acids, otherwise known as a pentadecapeptide (Aib-His-D-2-Nal-D-Phe-Lys-NH2), formally classified as a Growth Hormone Secretagogue (GHS). Its name is derived from the intention of its development. Ipamorelin peptide was designed to act via ghrelin receptor binding. The ghrelin receptors on the pituitary gland (the gland naturally involved with growth hormone, or hGH synthesis) are also known as Growth Hormone Secretagogue receptors (GHS-R). Through its implied action, Ipamorelin may host the potential to trigger the GHS-Rs on the pituitary gland and potentially stimulate the release of growth hormone.\u003csup dir=\"ltr\"\u003e(1)\u003c\/sup\u003e\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eIpamorelin is the first synthetic GHS that appears highly selective and may have the potential to augment the production of hGH without affecting other pituitary hormones such as prolactin or adrenocorticotropic hormone (ACTH). The potential increase in hGH might promote lipolysis and insulin-like growth factor-1 (IGF-1) production synthesis. Consequently, IGF-1 may become a mediator of hGH’s anabolic actions, and thereby the peptide may act to increase cellular proliferation and bone and muscle anabolism.\u003csup dir=\"ltr\"\u003e(1)\u003c\/sup\u003e\u003c\/p\u003e\n\u003ch3\u003eChemical Makeup\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003e\u003cstrong dir=\"ltr\"\u003eMolecular Formula:\u003c\/strong\u003e\u003cspan\u003e \u003c\/span\u003eC\u003csub dir=\"ltr\"\u003e38\u003c\/sub\u003eH\u003csub dir=\"ltr\"\u003e49\u003c\/sub\u003eN\u003csub dir=\"ltr\"\u003e9\u003c\/sub\u003eO\u003csub dir=\"ltr\"\u003e5\u003c\/sub\u003e\u003cbr dir=\"ltr\"\u003e\u003cstrong dir=\"ltr\"\u003eMolecular Weight:\u003c\/strong\u003e\u003cspan\u003e \u003c\/span\u003e711.86 g\/mol\u003cbr dir=\"ltr\"\u003e\u003cstrong dir=\"ltr\"\u003eOther Known Titles:\u003c\/strong\u003e\u003cspan\u003e \u003c\/span\u003eNNC 26-0161\u003c\/p\u003e\n\u003ch2\u003eResearch and Clinical Studies\u003c\/h2\u003e\n\u003ch3\u003e\u003cem\u003eIpamorelin Peptide and Selective Agonism\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eBased on one 1998 murine model-based research study, researchers suggested that Ipamorelin may release growth hormones from the pituitary cells. When Ipamorelin was presented to swine and pentobarbitone anesthetized rats, it reportedly exhibited release in growth hormones. Upon further observation, the researchers hypothesized that similar to other growth hormone (GH) stimulating peptides, Ipamorelin may be a growth receptor agonist stimulating GH release through potential affinity in growth hormone receptors. Moreover, the researchers commented that Ipamorelin appears to be the first GHS-R “\u003cem dir=\"ltr\"\u003eagonist with a selectivity for GH release similar to that displayed by GHRH. The specificity of Ipamorelin makes this compound a very interesting candidate for future clinical development.\u003c\/em\u003e”\u003csup dir=\"ltr\"\u003e(1)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eScientific research studies have also suggested that Ipamorelin may lead to increased hGH secretion, possibly without significantly affecting other pituitary hormones such as the levels of prolactin or ACTH.\u003csup dir=\"ltr\"\u003e(2)\u003c\/sup\u003e\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eIpamorelin Peptide and Growth Hormone Synthesis\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eStudies conducted\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003ein vitro\u003cspan\u003e \u003c\/span\u003e\u003c\/em\u003esuggest that the interaction of Ipamorelin with GHS receptors may potentially affect somatotroph cells in the anterior pituitary gland by triggering a series of cellular signaling events.\u003csup dir=\"ltr\"\u003e(3)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eThis theorized pathway involves the activation of phospholipase C (PLC), which some researchers believe may lead to the increased release of inositol triphosphate (IP3) and diacylglycerol (DAG). This release of secondary messenger molecules such as IP3 might potentially stimulate the discharge of calcium ions (Ca2+) from the cell's internal stores, while DAG might activate protein kinase C (PKC). The subsequent rise in intracellular calcium levels and the possible activation of PKC are thought to result in the exocytosis of vesicles filled with growth hormones from these pituitary cells.\u003csup dir=\"ltr\"\u003e(3)\u003c\/sup\u003e\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eIn late 1999, a clinical trial was carried out on eight test subjects where Ipamorelin was presented every 15 minutes for a set period. Two hours post-study, it was suggested by the researchers that the levels of growth hormone had apparently increased. More specifically, Ipamorelin appeared to have tended to boost growth hormone levels, potentially soaring to as much as 80mIU\/l (roughly equivalent to a concentration of about 26.6ng\/ml). When this increase is measured as a percentage compared to a placebo (with a baseline of 1.31mIU\/l or 0.4ng\/ml), the enhancement appeared to have exceeded a 60-fold uplift.\u003csup dir=\"ltr\"\u003e(4)\u003c\/sup\u003e\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eIpamorelin Peptide and Bone Tissue\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eIt is conceivable that Ipamorelin may positively influence bone mineral density. The theory posits that Ipamorelin might stimulate osteoblasts (cells responsible for bone formation) via hGH-mediated mechanisms, potentially leading to their enhanced proliferation, growth, and specialization. In a particular study, murine models were exposed to either Ipamorelin or a placebo.\u003csup dir=\"ltr\"\u003e(5)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eThe impact of Ipamorelin on bone mineral density in these mice was monitored closely through real-time dual X-ray absorptiometry (DEXA) assessments at critical sites, including the femur and L6 vertebra. Post-experiment, the femur bones were further examined using mid-diaphyseal peripheral quantitative computed tomography (pQCT) scans. Preliminary findings implied that the peptide may have contributed to increased body mass and a probable elevation in the overall tibial and vertebral BMC (bone mineral content) as detected by DEXA compared to the placebo group. Further, the pQCT data appeared to suggest that the observed augmentation in cortical BMC may have stemmed from an enlargement in the cross-sectional area of the bone. In contrast, the cortical volumetric bone mineral density (BMD, which denotes the ratio of BMC to area) appeared to remain steady. Thus, there may have been an enlargement in the volumes of the femur and the L6 vertebrae since BMC appeared to increase while the volumetric BMDs appeared unchanged.\u003csup dir=\"ltr\"\u003e(5)\u003c\/sup\u003e\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eIpamorelin Peptide and Digestion\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eResearchers have delved into the potential of Ipamorelin in the functionality of the stomach, with a keen interest in its ability to possibly expedite the process of gastric emptying. For example, one study employed a technique to ascertain gastric emptying rates, which entailed monitoring the proportion of a marked substance that lingered in the stomach 15 minutes after its introduction through intragastric gavage.\u003csup dir=\"ltr\"\u003e(6)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eThe scientists conducted surgeries to purposefully decelerate the gastric emptying process in murine models. This deceleration was particularly noticeable in the control group. In contrast, Ipamorelin appeared to have markedly accelerated the emptying process compared to the control. This observation led the team to hypothesize that Ipamorelin might be able to increase the velocity of gastric emptying. Additional research was initiated to delve deeper into the action of the compound on the contractile potential of the stomach's smooth muscles, which were activated by acetylcholine and electrical field stimulation. Indeed, the decelerated peristalsis appeared to be mitigated when Ipamorelin and ghrelin were studied together, suggesting the idea that Ipamorelin may enhance the contractility of gastric smooth muscles.\u003csup dir=\"ltr\"\u003e(6)\u003c\/sup\u003e\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eIpamorelin Peptide and Appetite\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eThe potential actions of Ipamorelin on ghrelin receptors may lead to an enhancement in hunger signals and, perhaps, an ensuing augmentation in body mass. Research suggests that research models exposed to Ipamorelin were observed to sustain an estimated 15% surge in body weight.\u003csup dir=\"ltr\"\u003e(7)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eResearchers speculate that this substance might have led to a proportional increase in the weight of fat pads in comparison to the total body weight. Consequently, DEXA scans might indicate a comparative rise in body fat percentage. Moreover, there is speculation among researchers that Ipamorelin might elevate serum leptin levels, a hormone considered to play a crucial role in energy balance and hunger regulation. This observation has prompted scientists to consider increased food consumption as a potential contributor to the weight gain noted in research models exposed to Ipamorelin. They have posited that \"\u003cem dir=\"ltr\"\u003eGHSs increase body fat by GH-independent mechanisms that may include increased feeding.\u003c\/em\u003e”\u003csup dir=\"ltr\"\u003e(7)\u003c\/sup\u003e\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eIpamorelin Peptide and Nitrogen Balance\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eResearchers have suggested that Ipamorelin may potentially mediate anabolic action, which may be due to its potential in hGH and IGF-1 synthesis and may be assessed through its impact on nitrogen balance. In a distinct investigation, researchers aimed to explore the action of Ipamorelin on specific liver markers associated with alpha-amino-nitrogen conversion during induced catabolic states.\u003csup dir=\"ltr\"\u003e(8)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eThe study focused on the liver’s capacity to synthesize urea-N (CUNS), which may serve as an indicator of the organ's ability to process nitrogen. The levels of messenger RNA (mRNA) related to liver urea cycle enzymes were scrutinized, alongside an assessment of the overall nitrogen balance and a hypothesis regarding nitrogen distribution across various organs. The findings suggested that Ipamorelin might have contributed to a possible 20% reduction in CUNS compared to the artificially induced catabolic condition. Furthermore, it might have diminished the expression of urea cycle enzymes, possibly restored nitrogen balance, and, in theory, altered or improved nitrogen concentrations in different organs.\u003csup dir=\"ltr\"\u003e(8)\u003c\/sup\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cem\u003e\u003cstrong dir=\"ltr\"\u003eIpamorelin peptide is available for research and laboratory purposes only.\u003c\/strong\u003e\u003c\/em\u003e\u003c\/p\u003e\n\u003ch3\u003eReferences:\u003c\/h3\u003e\n\u003col\u003e\n\u003cli\u003eK. Raun et al., Ipamorelin, the first selective growth hormone secretagogue, Endocrinology, November 1998.\u003c\/li\u003e\n\u003cli\u003eSinha DK, Balasubramanian A, Tatem AJ, Rivera-Mirabal J, Yu J, Kovac J, Pastuszak AW, Lipshultz LI. Beyond the androgen receptor: the role of growth hormone secretagogues in the modern management of body composition in hypogonadal males. Transl Androl Urol. 2020 Mar;9(Suppl 2):S149-S159. doi: 10.21037\/tau.2019.11.30. PMID: 32257855; PMCID: PMC7108996\u003ca href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC7108996\/\" rel=\"noopener\" dir=\"ltr\"\u003e\u003cspan\u003e \u003c\/span\u003ehttps:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC7108996\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eJiménez-Reina, L., Cañete, R., de la Torre, M. J., \u0026amp; Bernal, G. (2002). Influence of chronic treatment with the growth hormone secretagogue Ipamorelin, in young female rats: somatotroph response in vitro. Histology and histopathology, 17(3), 707–714.\u003cspan\u003e \u003c\/span\u003e\u003ca href=\"https:\/\/doi.org\/10.14670\/HH-17.707\" rel=\"noopener\" dir=\"ltr\"\u003ehttps:\/\/doi.org\/10.14670\/HH-17.707\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eGobburu, J.V.S., Agersø, H., Jusko, W.J. et al. Pharmacokinetic-Pharmacodynamic Modeling of Ipamorelin, a Growth Hormone Releasing Peptide, in Human Volunteers. Pharm Res 16, 1412–1416 (1999).\u003c\/li\u003e\n\u003cli\u003eSvensson, J., Lall, S., Dickson, S. L., Bengtsson, B. A., Rømer, J., Ahnfelt-Rønne, I., Ohlsson, C., \u0026amp; Jansson, J. O. (2000). The GH secretagogues ipamorelin and GH-releasing peptide-6 increase bone mineral content in adult female rats.\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003eThe Journal of endocrinology\u003c\/em\u003e,\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003e165\u003c\/em\u003e(3), 569–577.\u003cspan\u003e \u003c\/span\u003e\u003ca href=\"https:\/\/doi.org\/10.1677\/joe.0.1650569\" rel=\"noopener\" dir=\"ltr\"\u003ehttps:\/\/doi.org\/10.1677\/joe.0.1650569\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eGreenwood-Van Meerveld, B., Tyler, K., Mohammadi, E., \u0026amp; Pietra, C. (2012). Efficacy of ipamorelin, a ghrelin mimetic, on gastric dysmotility in a rodent model of postoperative ileus. Journal of experimental pharmacology, 4, 149–155.\u003cspan\u003e \u003c\/span\u003e\u003ca href=\"https:\/\/doi.org\/10.2147\/JEP.S35396\" rel=\"noopener\" dir=\"ltr\"\u003ehttps:\/\/doi.org\/10.2147\/JEP.S35396\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eLall, S., Tung, L. Y., Ohlsson, C., Jansson, J. O., \u0026amp; Dickson, S. L. (2001). Growth hormone (GH)-independent stimulation of adiposity by GH secretagogues. Biochemical and biophysical research communications, 280(1), 132–138.\u003cspan\u003e \u003c\/span\u003e\u003ca href=\"https:\/\/doi.org\/10.1006\/bbrc.2000.4065\" rel=\"noopener\" dir=\"ltr\"\u003ehttps:\/\/doi.org\/10.1006\/bbrc.2000.4065\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eAagaard, N. K., Grøfte, T., Greisen, J., Malmlöf, K., Johansen, P. B., Grønbaek, H., Ørskov, H., Tygstrup, N., \u0026amp; Vilstrup, H. (2009). Growth hormone and growth hormone secretagogue effects on nitrogen balance and urea synthesis in steroid treated rats.\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003eGrowth hormone \u0026amp; IGF research: official journal of the Growth Hormone Research Society and the International IGF Research Society\u003c\/em\u003e,\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003e19\u003c\/em\u003e(5), 426–431.\u003cspan\u003e \u003c\/span\u003e\u003ca href=\"https:\/\/doi.org\/10.1016\/j.ghir.2009.01.001\" rel=\"noopener\" dir=\"ltr\"\u003ehttps:\/\/doi.org\/10.1016\/j.ghir.2009.01.001\u003c\/a\u003e\n\u003c\/li\u003e\n\u003c\/ol\u003e","brand":"PureX Labs","offers":[{"title":"10mg","offer_id":47487371313396,"sku":null,"price":50.0,"currency_code":"USD","in_stock":true},{"title":"5mg","offer_id":48098749939956,"sku":null,"price":30.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0804\/5802\/3156\/files\/Ipamorelin.png?v=1769106217"},{"product_id":"igf-1-lr3","title":"IGF-1 LR3","description":"\u003cp dir=\"ltr\"\u003eInsulin-like Growth factor-1, or IGF-1, is a naturally produced protein with 70 amino acids. Receptor Grade IGF-1 LR3 is a synthetic variant of the naturally occurring IGF-1, which contains an extended N-terminal structure of 13 amino acids and a replacement of the glutamic acid at residue 3 with arginine. Hence, it is named IGF-1 Long R3.\u003csup dir=\"ltr\"\u003e(1)(2)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eOwing to the altered structure, Receptor Grade IGF-1 LR3 has been suggested to have increased affinity and increased anabolic potential while also binding less to IGF-1 binding proteins (IGF-1BPs). Structurally similar to insulin, this IGF-1 LR3 has the potential primarily to regulate cell tissue growth and development. This potential has been evaluated in cell growth studies, throughout which researchers first prompted the need for developing this high-potency variant. Moreover, the classification of\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003eReceptor Grade\u003c\/em\u003e\u003cspan\u003e \u003c\/span\u003erefers to the purity of the material, which is considered higher than Media Grade IGF-1 LR3.\u003c\/p\u003e\n\u003ch3 dir=\"ltr\"\u003eChemical Makeup\u003csup dir=\"ltr\"\u003e(2,3)\u003c\/sup\u003e\n\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003e\u003cstrong dir=\"ltr\"\u003eMolecular Formula:\u003c\/strong\u003e\u003cspan\u003e \u003c\/span\u003eC\u003csub dir=\"ltr\"\u003e400\u003c\/sub\u003eH\u003csub dir=\"ltr\"\u003e625\u003c\/sub\u003eN\u003csub dir=\"ltr\"\u003e111\u003c\/sub\u003eO\u003csub dir=\"ltr\"\u003e115\u003c\/sub\u003eS\u003csub dir=\"ltr\"\u003e9\u003c\/sub\u003e\u003cbr dir=\"ltr\"\u003e\u003cstrong dir=\"ltr\"\u003eMolecular Weight:\u003c\/strong\u003e\u003cspan\u003e \u003c\/span\u003e9117.5 g\/mol\u003cbr dir=\"ltr\"\u003e\u003cstrong dir=\"ltr\"\u003eOther Known Titles:\u003c\/strong\u003e\u003cspan\u003e \u003c\/span\u003eLong-(arg3) insulin-like growth factor-I, Insulin-like growth factor long chain R3\u003c\/p\u003e\n\u003ch2\u003eResearch and Clinical Studies\u003c\/h2\u003e\n\u003ch3\u003e\u003cem\u003eReceptor Grade IGF-1 LR3 and Anabolic Potential\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eUnfortunately, research on the anabolic potential of IGF-1 LR3 is lacking, as the peptide is aimed towards cell culture studies. Yet, of the few experiments in murine models, researchers have suggested the significant potential of the peptide.\u003csup dir=\"ltr\"\u003e(1)\u003cspan\u003e \u003c\/span\u003e\u003c\/sup\u003eIn one study, experiments were carried out on normal and dexamethasone-induced catabolic murine models. It was noted that IGF-1 LR3 might potentially be 1.5 to 2 times as anabolic as IGF-I in inducing weight gain, increasing visceral organ weights, and possibly enhancing feed use efficiency under continuous delivery conditions. Moreover, IGF-1 LR3 appeared to have retained the potential for greater potency than IGF-I in several metrics, even in studies of only intermittent exposure. Additionally, in murine models exposed to dexamethasone, it was observed that the excretion of Nτ-methylhistidine—a marker indicative of muscle protein breakdown—appeared reduced to a greater extent by IGF-1 LR3, potentially threefold more than by IGF-I. This suggests that IGF-1 LR3 may host the potential, though not consistently equivalent across all parameters, to exhibit enhanced anabolic actions under certain laboratory conditions.\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eTherefore, Receptor Grade IGF-1 LR3 may be posited to exert even greater anabolic potential than IGF-1. To provide a comparison, several studies have researched the anabolic potential of IGF-1. For example, a study\u003csup dir=\"ltr\"\u003e(4)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003ewas conducted in 2005 to study the potential of the peptide in models of IGF-1 deficiency. Following peptide exposure, the length and growth of the models were assessed and analyzed against control thresholds. Based on the study findings, it was observed that total length increased in all peptide-exposed models by a significant margin against the control standards. This study suggests that IGF-1, and possibly also more potent analogs like Receptor Grade IGF-1 LR3 peptide, may have some potential in mitigating growth deficiency.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eReceptor Grade IGF-1 LR3 and Insulin Receptor Sensitivity\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eResearch\u003csup dir=\"ltr\"\u003e(5)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003ehas suggested that IGF proteins typically bind to IGF-1 receptors and may stimulate glucose uptake, potentially through a signaling mechanism involving PI3K and AMPK pathways. However, when studied, peptides like Receptor Grade IGF-1 LR3 appeared to induce glucose uptake not just through IGF-1 receptor interactions but also independently, possibly via other pathways or receptors. This suggests that the mechanism of glucose uptake might involve additional cellular processes beyond the traditional receptor binding. Assefa B Mahmoud\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003eet al. stated, \"Multiple [...] studies reported the role of IGF-1 in enhancing insulin sensitivity and glucose metabolism. A low-serum level of IGF-1 has been associated with insulin resistance, and [...] recombinant IGF-1 has been [hypothesized] to improve insulin sensitivity and glucose metabolism.”\u003c\/em\u003e\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eReceptor Grade IGF-1 LR3 and Cell Lifespan\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eResearch\u003csup dir=\"ltr\"\u003e(6)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eon murine models observed that common markers of physiological decline, such as muscle tears and neurological deficiencies, appeared to be mitigated for an extended period following routine exposure to the peptide. While more detailed studies and clinical trials are pending, the above preliminary study suggests that the peptide may indirectly help to increase lifespan of functional cells. As per William E. Sonntag\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003eet al.,\u003c\/em\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cem\u003e“Based on this review, we conclude that the perceived contradictory roles of growth hormone and insulin-like growth factor-1 in the genesis of the aging phenotype should not be interpreted as a controversy on whether growth hormone or insulin-like growth factor-1 increases or decreases life span but rather as an opportunity to explore the complex roles of these hormones during specific stages of the life span.”\u003c\/em\u003e\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eReceptor Grade IGF-1 LR3 and Muscle Cells\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eA study\u003csup dir=\"ltr\"\u003e(7)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003ewas conducted on female murine models to identify the IGF-1 LR3 peptide’s potential in decreasing the action of myostatin. Myostatin is considered to prevent cellular differentiation; mitigating the actions of this protein may increase lean muscle and reduce fat cell storage and fatty mass. The study's results suggested that the various IGF-1 analogs, including Receptor Grade IGF-1 LR3, appear to potentially reverse adverse myostatin and prevent apoptosis.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eReceptor Grade IGF-1 LR3 and Shorter Action\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eAn experimental mouse model was created for a study\u003csup dir=\"ltr\"\u003e(8)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003ewhere the IGF-1 LR3 peptide was compared to the endogenous IGF-1. Throughout the study, it was observed that when the peptide was exposed to the murine model, it appeared to quickly clear from the serum and evenly distribute into tissue. More specifically, the researchers posited that IGF-1 LR3 cleared faster as it appeared to bind to a lower degree to binding proteins than endogenous IGF-1. This reduced binding affinity means IGF-1 LR3 might circulate more freely than IGF-I. The analysis of tissue distribution patterns of IGF-1 LR3 also suggested a potentially unique localization compared to IGF-I. Elevated levels of the IGF-1 LR3 tracer were observed in tissues such as kidneys, ovaries, and adrenal glands in murine models. This distinct distribution suggests that the organs primarily involved in metabolic and reproductive functions may exhibit varying capacities for the uptake or retention of IGF-1 LR3 in contrast to IGF-I. It is hypothesized that these differences might stem from IGF-1 LR3's diminished propensity to form complexes with IGFBPs, which might influence its bioavailability and interaction with target tissues in experimental models. Nevertheless, further research suggested that a peptide with similar modifications (namely R3) to IGF-1 LR3 may exert increased anabolic potential compared to regular IGF-1 despite the shorter action.\u003csup dir=\"ltr\"\u003e(9)\u003c\/sup\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cem\u003e\u003cstrong dir=\"ltr\"\u003eReceptor Grade IGF-1 LR3 peptide is available for research and laboratory purposes only.\u003c\/strong\u003e\u003c\/em\u003e\u003c\/p\u003e\n\u003ch3\u003eReferences\u003c\/h3\u003e\n\u003col\u003e\n\u003cli\u003eTomas, F. M., Knowles, S. E., Owens, P. C., Chandler, C. S., Francis, G. L., Read, L. C., \u0026amp; Ballard, F. J. (1992). Insulin-like growth factor-I (IGF-I) and especially IGF-I variants are anabolic in dexamethasone-treated rats. The Biochemical journal, 282 ( Pt 1)(Pt 1), 91–97.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC1130894\/\"\u003ehttps:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC1130894\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eHuman Insulin-like growth factor. Protein Data Bank in Europe,\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/www.ebi.ac.uk\/pdbe\/entry\/pdb\/1gzr\"\u003ehttps:\/\/www.ebi.ac.uk\/pdbe\/entry\/pdb\/1gzr\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eNational Center for Biotechnology Information (2023). PubChem Substance Record for SID 381123731, M9L22Y19H9, Source: ChemIDplus. Retrieved January 24, 2023 from\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubchem.ncbi.nlm.nih.gov\/substance\/381123731\"\u003ehttps:\/\/pubchem.ncbi.nlm.nih.gov\/substance\/381123731\u003c\/a\u003e.\u003c\/li\u003e\n\u003cli\u003eAnderson, L. J., Tamayose, J. M., \u0026amp; Garcia, J. M. (2018). Use of growth hormone, IGF-I, and insulin for anabolic purpose: Pharmacological basis, methods of detection, and adverse effects. Molecular and cellular endocrinology, 464, 65–74.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC5723243\/\"\u003ehttps:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC5723243\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eAssefa, B., Mahmoud, A. M., Pfeiffer, A., Birkenfeld, A. L., Spranger, J., \u0026amp; Arafat, A. M. (2017). Insulin-Like Growth Factor (IGF) Binding Protein-2, Independently of IGF-1, Induces GLUT-4 Translocation and Glucose Uptake in 3T3-L1 Adipocytes. Oxidative medicine and cellular longevity, 2017\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC5750484\/\"\u003ehttps:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC5750484\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eWilliam E. Sonntag, Anna Csiszar, Raphael de Cabo, Luigi Ferrucci, Zoltan Ungvari, Diverse Roles of Growth Hormone and Insulin-Like Growth Factor-1 in Mammalian Aging: Progress and Controversies, The Journals of Gerontology: Series A, Volume 67A, Issue 6, June 2012, Pages 587–598,\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/doi.org\/10.1093\/gerona\/gls115\"\u003ehttps:\/\/doi.org\/10.1093\/gerona\/gls115\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eNaisi Li, Qiyuan Yang, Ryan G. Walker, Thomas B. Thompson, Min Du, Buel D. Rodgers, Myostatin Attenuation In Vivo Reduces Adiposity, but Activates Adipogenesis, Endocrinology, Volume 157, Issue 1, 1 January 2016, Pages 282–291.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/doi.org\/10.1210\/en.2015-1546\"\u003ehttps:\/\/doi.org\/10.1210\/en.2015-1546\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eBastian SE, Walton PE, Wallace JC, Ballard FJ. Plasma clearance and tissue distribution of labelled insulin-like growth factor-I (IGF-I) and an analogue LR3IGF-I in pregnant rats. J Endocrinol. 1993 Aug;138(2):327-36.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/doi.org\/10.1677\/joe.0.1380327\"\u003edoi: 10.1677\/joe.0.1380327\u003c\/a\u003e. PMID: 7693845.\u003c\/li\u003e\n\u003cli\u003eElis S, Wu Y, Courtland HW, Cannata D, Sun H, Beth-On M, Liu C, Jasper H, Domené H, Karabatas L, Guida C, Basta-Pljakic J, Cardoso L, Rosen CJ, Frystyk J, Yakar S. Unbound (bioavailable) IGF1 enhances somatic growth. Dis Model Mech. 2011 Sep;4(5):649-58.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/doi.org\/10.1242\/dmm.006775\"\u003edoi: 10.1242\/dmm.006775\u003c\/a\u003e. Epub 2011 May 31. PMID: 21628395; PMCID: PMC3180229.\u003c\/li\u003e\n\u003c\/ol\u003e","brand":"PureX Labs","offers":[{"title":"0.1mg","offer_id":47487377146100,"sku":null,"price":25.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0804\/5802\/3156\/files\/IGF-1_LR3.png?v=1769106217"},{"product_id":"glutathione","title":"Glutathione","description":"\u003cp data-start=\"143\" data-end=\"441\"\u003eGlutathione is a naturally occurring tripeptide antioxidant composed of glutamine, cysteine, and glycine, present in nearly every cell of the body. It is widely regarded as the body’s primary intracellular antioxidant, playing a central role in maintaining cellular balance and defense.\u003c\/p\u003e\n\u003cp data-start=\"443\" data-end=\"772\"\u003eGlutathione is believed to support the neutralization of free radicals, reduction of oxidative stress, and participation in detoxification pathways, particularly within the liver. It is also involved in maintaining cellular redox balance, supporting mitochondrial function, and protecting cells from oxidative damage.\u003c\/p\u003e\n\u003cp data-start=\"774\" data-end=\"1054\"\u003eResearch has explored glutathione’s potential involvement in immune modulation, cellular defense mechanisms, and energy metabolism. Additionally, glutathione has been studied in relation to skin health and pigmentation, as well as broader aging and cellular health models.\u003c\/p\u003e\n\u003cp data-start=\"1056\" data-end=\"1223\"\u003eGlutathione continues to be a compound of interest in research focused on antioxidant activity, detoxification processes, immune function, and cellular resilience.\u003c\/p\u003e","brand":"PureX Labs","offers":[{"title":"600mg","offer_id":47487380685044,"sku":null,"price":80.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0804\/5802\/3156\/files\/Glutathione.png?v=1769106217"},{"product_id":"nad","title":"NAD+","description":"\u003cp dir=\"ltr\"\u003eNAD+ is an acronym for Nicotinamide Adenine Dinucleotide, an endogenous nucleotide that is considered to regulate primary functions such as metabolism, energy production, and DNA repair. It is also considered to act as a secondary messenger via calcium-dependent signaling mechanisms, possibly serving as an immunoregulatory component.\u003csup dir=\"ltr\"\u003e(1)(2)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eNAD+ is considered by researchers to be naturally synthesized via the de novo mechanism of converting the amino acid tryptophan through several enzymatic steps. Researchers posit that there are five components to NAD+ synthesis, including tryptophan, nicotinamide, nicotinic acid, nicotinamide riboside, and nicotinamide mononucleotide.\u003csup dir=\"ltr\"\u003e(3)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eOnce synthesized, research suggests it exerts over 500 enzymatic reactions and cellular processes\u003csup dir=\"ltr\"\u003e(12)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eto aid metabolic activities. Essentially, it is suggested to act as a coenzyme in redox functions, converted to NADH (the energy-carrying form of NAD+), which may involve other metabolic pathways.\u003c\/p\u003e\n\u003cp\u003eResearchers have suggested Nicotinamide Adenine Dinucleotide (NAD+) to act as a coenzyme, with three major classes of enzymes including:\u003c\/p\u003e\n\u003cul\u003e\n\u003cli\u003eDeacetylase enzymes in the sirtuin class (SIRTs)\u003c\/li\u003e\n\u003cli\u003ePoly ADP ribose polymerase (PARPs) enzymes, and\u003c\/li\u003e\n\u003cli\u003eCyclic ADP ribose synthetase (cADPRS)\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003cp\u003eResearch suggests that each class of enzymes interacts with NAD+ in the following possible respects:\u003c\/p\u003e\n\u003cul\u003e\n\u003cli\u003eSIRTs may stimulate mitochondrial homeostasis, stem cell regeneration, loss of stem cells, and nerve degeneration.\u003c\/li\u003e\n\u003cli\u003ePARPs, composed of 17 different enzymes, may act alongside NAD+ enzymes and synthesize poly ADP ribose polymers, which may lead to genome stability.\u003c\/li\u003e\n\u003cli\u003ecADPRS include CD38 and CD157, which are considered to be key immunological cells. cADPRS appears to hydrolyze NAD+ and thereby may stimulate stem cell regeneration and DNA repair, which may be important for maintaining cell cycles.\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003cp dir=\"ltr\"\u003eResearchers suggest the above-mentioned enzymes to be NAD+ dependent enzymes, possibly acting based on the presence of Nicotinamide Adenine Dinucleotide (NAD). Researchers suggest that should all three enzymes be dependent on NAD+, they may potentially compete amongst themselves for bioavailability. It has been posited that the potential function of SIRTs, for instance, may lead to reduced PARPs activity and, thereby, potentially lead to weakened systems. Hence, it may be critical to maintain a balance between the availability and consumption of NAD+ to obtain optimal potential impact.\u003csup dir=\"ltr\"\u003e(5)\u003c\/sup\u003e\u003c\/p\u003e\n\u003ch3\u003eChemical Makeup\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003e\u003cstrong dir=\"ltr\"\u003eMolecular Formula:\u003c\/strong\u003e\u003cspan\u003e \u003c\/span\u003eC\u003csub dir=\"ltr\"\u003e21\u003c\/sub\u003eH\u003csub dir=\"ltr\"\u003e27\u003c\/sub\u003eN\u003csub dir=\"ltr\"\u003e7\u003c\/sub\u003eO\u003csub dir=\"ltr\"\u003e14\u003c\/sub\u003eP\u003csub dir=\"ltr\"\u003e2\u003c\/sub\u003e\u003cbr dir=\"ltr\"\u003e\u003cstrong dir=\"ltr\"\u003eMolecular Weight:\u003c\/strong\u003e\u003cspan\u003e \u003c\/span\u003e663.43 g\/mol\u003cbr dir=\"ltr\"\u003e\u003cstrong dir=\"ltr\"\u003eOther Known Titles:\u003c\/strong\u003e\u003cspan\u003e \u003c\/span\u003enicotinamide adenine dinucleotide\u003c\/p\u003e\n\u003ch2\u003eResearch and Clinical Studies\u003c\/h2\u003e\n\u003ch3\u003e\u003cem\u003eNAD+ Peptide and Productive Aging\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eResearchers suggest that NAD+ has two key intermediates: nicotinamide riboside (NR) and nicotinamide mononucleotide (NMN). Studies have indicated that these intermediates may be potent agents for promoting 'productive aging.' In a study,\u003csup dir=\"ltr\"\u003e(7)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003enormal-aging mice were exposed to the NMN intermediate for 12 months. Following the study, the researchers suggested that NMN may promote NAD+ synthesis in the mice. Peptide exposure may have been the catalyst for the observed reduced weight gain, increased energy metabolism, enhanced physical activity, improved lipid profile, and other physiological impacts in the mice.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eNAD+ Peptide and Neurodegenerative Activity\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eScientists consider mitochondrial dysfunction to lead to various functional limitations in the electron transport chain and ATP (energy) synthesis, possibly resulting in various neurodegenerative diseases. A study\u003csup dir=\"ltr\"\u003e(8)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003ewas conducted where aged mice were exposed to NMN, a NAD+ intermediate, for 3 to 12 months. The study's main aim was to evaluate the potential impact of the peptide on mitochondrial respiratory processes, for which fluorescent NMN protein was presented to the mice models. After peptide introduction, the mitochondrial oxygen consumption rates in the nerve and brain cells of the mice were studied. Upon analysis, it was suggested that mitochondrial functions had been restored in the aged mice, suggesting that NMN may be immediately utilized by the cells to produce NAD+, exerting a possible positive impact.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eNAD+ Peptide and DNA Repair After Ischemic Stress\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eThe main aim of this study\u003csup dir=\"ltr\"\u003e(11)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003ewas to determine the neuroprotective potential of Nicotinamide Adenine Dinucleotide against ischemic stress induced in mice. For this study, ischemic stress was induced in the neuronal cultures in rats via deprivation of oxygen and glucose for about 2 hours. NAD+ was directly replenished into the culture medium before or after the induced ischemic stress. After 72 hours of introducing NAD+ into the cultures, it was reported by the researchers that the DNA base excision repair activity (DNA BER), cell viability, and oxidative DNA damage repair appeared to be significantly improved, irrespective of whether Nicotinamide Adenine Dinucleotide was added before or after inducing the ischemic stress.\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eIndeed, NAD+ appears crucial for DNA integrity, with studies focusing on the enzyme poly(ADP-ribose) polymerase (PAR polymerase or PARP), which might depend on NAD+ for activating DNA repair. In the event of DNA damage, it is thought that PARP might be triggered, potentially attaching itself to the DNA's damaged parts. Researchers suggest that PARP might utilize NAD+ molecules to add ADP-ribose units to itself and other proteins in a process known as\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003ePARylation\u003c\/em\u003e, potentially aiding in the attraction and activation of other DNA repair proteins and thereby assisting in repairing DNA damage.\u003csup dir=\"ltr\"\u003e(15)\u003cspan\u003e \u003c\/span\u003e\u003c\/sup\u003eThis PARylation may lead to the formation of PAR chains, which might signal the DNA repair systems to identify and address DNA damage. PARP is also considered to have a role in detecting and mending single-strand DNA breaks. If NAD+ is confirmed as a necessary cofactor, PARP may be important in preserving genomic stability by initiating DNA repair mechanisms. However, this activity could also reduce NAD+ levels within cells, potentially affecting other NAD+-dependent processes like energy production and cellular signaling. It has been noted that DNA damage may cause a rapid increase in PAR synthesis, possibly using up significant amounts of NAD+. Consequently, researchers are exploring the idea that NAD+ depletion, triggered by PAR polymerase activation, might influence the NAD+\/SIRT1 pathway, potentially affecting mitochondrial function, ROS production, DNA repair, and cell survival.\u003csup dir=\"ltr\"\u003e(16)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eConsequently, the reintroduction of NAD+ in such settings may compensate for this and may be posited to support the process of DNA repair and cell survival.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eNAD+ Peptide and the Liver, Kidney\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eUpon introducing experimental mice with the NAD+ peptide and stimulating an increase in Nicotinamide Adenine Dinucleotide levels up to normal concentrations, researchers suggested the peptide exhibited positive potential in preventing obesity and alcoholic hepatitis while possibly improving glucose homeostasis and overall liver function. When aged mice kidney cells were supplemented with NAD+, the results indicated that adding the peptide possibly promoted SIRTs activity, which exhibited neuroprotective potential against glucose-induced kidney cell hypertrophy. Furthermore, when presented with NMN, NAD+ intermediate, it appeared to promote neuroprotective impact against cisplatin-induced kidney injury.\u003csup dir=\"ltr\"\u003e(12)\u003c\/sup\u003e\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eNAD+ Peptide and Skeletal Function\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eUpon presenting aged mice with NMN daily for 7 days, researchers suggested that the peptide possibly increased ATP production, reduced inflammation, and elevated mitochondrial functions.\u003csup dir=\"ltr\"\u003e(13)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eThe researchers considered this may have been due to the role that NAD+ appears to play in cellular respiration and energy production, specifically acting as a helper molecule in redox reactions, which may be vital to converting nutrients into energy. This process, known as cellular respiration, is thought to allow cells to produce usable energy through a series of steps, and NAD+ is believed to play a key role in two specific phases: glycolysis and the citric acid cycle (or Krebs cycle). In glycolysis, the initial breakdown of glucose into pyruvate is suggested to be produced by a small amount of ATP and NADH. Here, NAD+ is thought to accept electrons and a hydrogen ion from glucose, turning into NADH. This transformation might allow NADH to transport these high-energy electrons to a later stage of energy production. Following glycolysis, pyruvate is further broken down in the citric acid cycle, potentially releasing more energy. NAD+ is implicated in various reactions during this cycle, possibly accepting electrons and hydrogen ions to form NADH. These crucial steps are considered to happen directly within the mitochondria. The NADH formed during both glycolysis and the citric acid cycle is presumed to carry high-energy electrons to the electron transport chain, the last step of cellular respiration. At this stage, NADH may give up its electrons, creating an electrochemical gradient and a chain reaction that drives protons across the mitochondrial membrane. This action appears to lead to the combination of electrons and protons with oxygen to produce water, and the energy released during this process may be used to generate ATP through oxidative phosphorylation. As NADH relinquishes its electrons, it may be transformed back into NAD+, ready to assist in another glycolysis and citric acid cycle. This regeneration of NAD+ is considered to be crucial for the ongoing production of ATP, thus maintaining the cell's energy supply.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eNAD+ Peptide and Cardiac Functions\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eResearchers have suggested Nicotinamide Adenine Dinucleotide deficiency may lead to reduced SIRT activity, which may in turn cause reduced energy production and aortic constriction. When mice were exposed to NMN 30 minutes prior to induced-ischemia, the peptide reportedly produced a cardioprotective function against ischemic injury.\u003csup dir=\"ltr\"\u003e(14)\u003c\/sup\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cem dir=\"ltr\"\u003eNAD+ peptide is available for research and laboratory purposes only.\u003c\/em\u003e\u003c\/strong\u003e\u003c\/p\u003e\n\u003ch3\u003eReferences:\u003c\/h3\u003e\n\u003col\u003e\n\u003cli\u003eSchultz, Michael B, and David A Sinclair. \"Why NAD(+) Declines during Aging: It's Destroyed.\" Cell metabolism vol. 23,6 (2016): 965-966.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC5088772\/\"\u003ehttps:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC5088772\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eBraidy N, Liu Y. NAD+ therapy in age-related degenerative disorders: A benefit\/risk analysis. Exp Gerontol. 2020 Apr;132:110831. doi: 10.1016\/j.exger.2020.110831.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/31917996\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/31917996\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eJohnson, Sean, and Shin-Ichiro Imai. \"NAD + biosynthesis, aging, and disease.\" F1000Research vol. 7 132. 1 Feb 2018.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC5795269\/\"\u003ehttps:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC5795269\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eBieganowski P, Brenner C. Discoveries of nicotinamide riboside as a nutrient and conserved NRK genes establish a Preiss-Handler independent route to NAD+ in fungi and humans. Cell. 2004 May 14;117(4):495-502.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/15137942\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/15137942\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eFang, E. F., Lautrup, S., Hou, Y., Demarest, T. G., Croteau, D. L., Mattson, M. P., \u0026amp; Bohr, V. A. (2017). NAD+ in Aging: Molecular Mechanisms and Translational Implications. Trends in molecular medicine, 23(10), 899–916.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC7494058\/\"\u003ehttps:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC7494058\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eHarden, A; Young, WJ (24 October 1906). \"The alcoholic ferment of yeast-juice Part II.--The coferment of yeast-juice\". Proceedings of the Royal Society of London. Series B, Containing Papers of a Biological Character. 78 (526): 369–375.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/royalsocietypublishing.org\/doi\/10.1098\/rspb.1906.0070\"\u003ehttps:\/\/royalsocietypublishing.org\/doi\/10.1098\/rspb.1906.0070\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eMills KF, Yoshida S, Stein LR, Grozio A, Kubota S, Sasaki Y, Redpath P, Migaud ME, Apte RS, Uchida K, Yoshino J, Imai SI. Long-Term Administration of Nicotinamide Mononucleotide Mitigates Age-Associated Physiological Decline in Mice. Cell Metab. 2016 Dec 13;24(6):795-806.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/28068222\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/28068222\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eLong AN, Owens K, Schlappal AE, Kristian T, Fishman PS, Schuh RA. Effect of nicotinamide mononucleotide on brain mitochondrial respiratory deficits in an Alzheimer's disease-relevant murine model. BMC Neurol. 2015 Mar 1;15:19.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/25884176\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/25884176\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eSafety \u0026amp; Efficacy of Nicotinamide Riboside Supplementation for Improving Physiological Function in Middle-Aged and Older Adults.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/clinicaltrials.gov\/ct2\/show\/NCT02921659\"\u003ehttps:\/\/clinicaltrials.gov\/ct2\/show\/NCT02921659\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eBraidy N, Liu Y. NAD+ therapy in age-related degenerative disorders: A benefit\/risk analysis. Exp Gerontol. 2020 Apr;132:110831.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/31917996\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/31917996\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eWang S, Xing Z, Vosler PS, Yin H, Li W, Zhang F, Signore AP, Stetler RA, Gao Y, Chen J. Cellular NAD replenishment confers marked neuroprotection against ischemic cell death: role of enhanced DNA repair. Stroke. 2008 Sep;39(9):2587-95.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/18617666\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/18617666\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eRajman, Luis et al. \"Therapeutic Potential of NAD-Boosting Molecules: The In Vivo Evidence.\" Cell metabolism vol. 27,3 (2018): 529-547.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC6342515\/\"\u003ehttps:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC6342515\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eHeer C, et al, Coronavirus infection and PARP expression dysregulate the NAD metabolome: An actionable component of innate immunity. Journal of Biological Chemistry. Volume 295, Issue 52, Dec 2020.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/www.jbc.org\/article\/S0021-9258(17)50676-6\/fulltext\"\u003ehttps:\/\/www.jbc.org\/article\/S0021-9258(17)50676-6\/fulltext\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eMehmel, Mario et al. \"Nicotinamide Riboside-The Current State of Research and Therapeutic Uses.\" Nutrients vol. 12,6 1616. 31 May. 2020, doi:10.3390\/nu12061616\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC7352172\/\"\u003ehttps:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC7352172\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eLeung A, Todorova T, Ando Y, Chang P. Poly(ADP-ribose) regulates post-transcriptional gene regulation in the cytoplasm. RNA Biol. 2012 May;9(5):542-8. doi: 10.4161\/rna.19899. Epub 2012 May 1. PMID: 22531498; PMCID: PMC3495734.\u003c\/li\u003e\n\u003cli\u003eCroteau DL, Fang EF, Nilsen H, Bohr VA. NAD\u003csup dir=\"ltr\"\u003e+\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003ein DNA repair and mitochondrial maintenance. Cell Cycle. 2017 Mar 19;16(6):491-492. doi: 10.1080\/15384101.2017.1285631. Epub 2017 Feb 1. PMID: 28145802; PMCID: PMC5384578.\u003c\/li\u003e\n\u003c\/ol\u003e\n\u003cp\u003e\u003ca title=\"NAD+ COA\" href=\"https:\/\/purexlabs.io\/pages\/nad-coa\"\u003eCOA\u003c\/a\u003e\u003c\/p\u003e","brand":"PureX Labs","offers":[{"title":"100mg","offer_id":48231476789492,"sku":null,"price":25.0,"currency_code":"USD","in_stock":true},{"title":"500mg","offer_id":47487383011572,"sku":null,"price":60.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0804\/5802\/3156\/files\/NAD.png?v=1769106217"},{"product_id":"bac-water","title":"Bac Water","description":"\u003cdiv class=\"wp-block-post-excerpt\"\u003e\n\u003cp class=\"wp-block-post-excerpt__excerpt\"\u003eBacteriostatic water (commonly called “bac water”) is a sterile, non-pyrogenic water solution that contains 0.9% benzyl alcohol, which acts as a preservative to inhibit bacterial growth. It’s specifically designed for diluting or reconstituting medications, especially lyophilized (freeze-dried) peptides, before injection.\u003c\/p\u003e\n\u003c\/div\u003e","brand":"PureX Labs","offers":[{"title":"3ml","offer_id":48044982337780,"sku":null,"price":2.5,"currency_code":"USD","in_stock":true},{"title":"10ml","offer_id":47487385239796,"sku":null,"price":5.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0804\/5802\/3156\/files\/Bac_Water.png?v=1769106562"},{"product_id":"retatrutide","title":"Retatrutide","description":"\u003cp\u003e\u003cmeta charset=\"utf-8\"\u003e\u003cspan\u003eRetatrutide is a synthetic tri-agonist peptide that activates GLP-1, GIP, and glucagon receptors. It has been studied for its potential effects on glucose regulation, energy balance, and body weight in preclinical and clinical research.\u003c\/span\u003e\u003cspan\u003e\u003c\/span\u003e\u003c\/p\u003e\n\u003cp\u003e\u003ca href=\"https:\/\/purexlabs.io\/pages\/retatrutide-10mg-coa\" title=\"10MG COA\"\u003e\u003cspan\u003e10MG COA\u003c\/span\u003e\u003c\/a\u003e\u003c\/p\u003e\n\u003cp\u003e\u003ca href=\"https:\/\/purexlabs.io\/pages\/retatrutide-30mg-coa\" title=\"30MG COA\"\u003e\u003cspan\u003e30MG COA\u003c\/span\u003e\u003c\/a\u003e\u003c\/p\u003e","brand":"PureX Labs","offers":[{"title":"10mg","offer_id":48045007929588,"sku":null,"price":50.0,"currency_code":"USD","in_stock":true},{"title":"20mg","offer_id":47548287451380,"sku":null,"price":100.0,"currency_code":"USD","in_stock":true},{"title":"30mg","offer_id":47548287484148,"sku":null,"price":150.0,"currency_code":"USD","in_stock":true},{"title":"40mg","offer_id":48045007962356,"sku":null,"price":200.0,"currency_code":"USD","in_stock":true},{"title":"50mg","offer_id":48318197170420,"sku":null,"price":250.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0804\/5802\/3156\/files\/Render_Mockup_1920_1920_2026-01-31.png?v=1769799169"},{"product_id":"mt-2-melanotan-ii","title":"MT-2 (Melanotan II)","description":"\u003cdiv class=\"wp-block-woocommerce-product-details alignwide is-style-minimal\" data-hide-tab-title=\"true\" data-block-name=\"woocommerce\/product-details\"\u003e\n\u003cdiv\u003e\n\u003cdiv class=\"woocommerce-tabs wc-tabs-wrapper\"\u003e\n\u003cdiv aria-labelledby=\"tab-title-description\" role=\"tabpanel\" id=\"tab-description\" class=\"woocommerce-Tabs-panel woocommerce-Tabs-panel--description panel entry-content wc-tab\"\u003e\n\u003cp\u003eMelanotan II (MT-2) is a synthetic peptide analog of the naturally occurring hormone α-MSH (alpha-melanocyte-stimulating hormone). Research has explored MT-2 for its ability to bind to melanocortin receptors, which play a role in skin pigmentation and tanning responses. Studies have also investigated its potential influence on appetite and sexual function through these receptor pathways. MT-2 is commonly evaluated in laboratory settings for its possible applications in photoprotection, tanning, and metabolic research. It is intended strictly for scientific study and is not approved for human consumption or cosmetic use.\u003c\/p\u003e\n\u003c\/div\u003e\n\u003c\/div\u003e\n\u003c\/div\u003e\n\u003c\/div\u003e\n\u003cdiv class=\"wp-block-woocommerce-product-collection alignwide is-layout-flow wp-block-woocommerce-product-collection-is-layout-flow\" data-tag-name=\"div\" data-query='{\"perPage\":3,\"pages\":1,\"offset\":0,\"postType\":\"product\",\"order\":\"asc\",\"orderBy\":\"title\",\"search\":\"\",\"exclude\":[],\"inherit\":false,\"taxQuery\":[],\"isProductCollectionBlock\":true,\"featured\":false,\"woocommerceOnSale\":false,\"woocommerceStockStatus\":[\"instock\"],\"woocommerceAttributes\":[],\"woocommerceHandPickedProducts\":[],\"filterable\":true,\"relatedBy\":{\"categories\":true,\"tags\":true}}' data-query-id=\"2\" data-query-context-includes='[\"collection\"]' data-hide-controls='[\"inherit\"]' data-display-layout='{\"type\":\"flex\",\"columns\":3,\"shrinkColumns\":false}' data-dimensions='{\"widthType\":\"fill\"}' data-collection=\"woocommerce\/product-collection\/related\" data-block-name=\"woocommerce\/product-collection\" data-__private-preview-state='{\"isPreview\":true,\"previewMessage\":\"Actual products will vary depending on the product being viewed.\"}' data-wp-router-region=\"wc-product-collection-2\" data-wp-interactive=\"woocommerce\/product-collection\" data-wp-init=\"callbacks.onRender\" data-wp-context='{\"notices\":[],\"hideNextPreviousButtons\":false,\"isDisabledPrevious\":true,\"isDisabledNext\":false,\"ariaLabelPrevious\":\"Previous products\",\"ariaLabelNext\":\"Next products\",\"collection\":\"woocommerce\\\/product-collection\\\/related\"}'\u003e\n\u003cdiv class=\"wc-block-components-notices alignwide\" data-wp-interactive=\"woocommerce\/store-notices\"\u003e\u003cbr\u003e\u003c\/div\u003e\n\u003c\/div\u003e\n\u003cp dir=\"ltr\"\u003e\u003cmeta charset=\"utf-8\"\u003eMelanotan II (MT-2) likely serves as a non-selective agonist with the potential to bind with four out of the five different subtypes of melanocortin receptors (MC-R).\u003csup dir=\"ltr\"\u003e(3)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eDepending on the localization, the receptor-Melanotan 2 bond may induce different actions. Namely, the four receptors that Melanotan 2 may interact with include:\u003c\/p\u003e\n\u003cul\u003e\n\u003cli\u003eThe melanocortin 1 receptor (MC1R) may be expressed in melanocytes, which are cells found in tissues such as dermal tissues, hair, and possibly cells and tissues found in the eye.\u003c\/li\u003e\n\u003cli\u003eThe melanocortin 3 receptor (MC3R) might be found in a range of tissues, potentially including the brain and the placenta. Initial observations suggest that MC3R might be involved in modulating appetite under certain experimental conditions.\u003c\/li\u003e\n\u003cli\u003eThe melanocortin 4 receptor (MC4R) may be localized within the central nervous system, perhaps in the hypothalamus. Some early indications suggest that this receptor may impact neurons that are believed to have some influence over mating behaviors and general arousal.\u003c\/li\u003e\n\u003cli\u003eThe melanocortin 5 receptor (MC5R) appears to be distributed across multiple tissues, although what role it might serve remains unclear.\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003cp dir=\"ltr\"\u003eFor example, the potential interaction between Melanotan 2 and the MC1Rs may lead to increased production of eumelanin, which causes darkening of the epidermal layer’s pigment.\u003csup dir=\"ltr\"\u003e(4)\u003c\/sup\u003e\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eOn the other hand, when Melanotan 2 binds with the MC4R, it may induce supraspinal centers in the brain, which may lead to increased libido. These signals may then be carried to the sympathetic and parasympathetic centers in the spinal cord and thoracolumbar region.\u003csup dir=\"ltr\"\u003e(3)\u003c\/sup\u003e\u003c\/p\u003e\n\u003ch2\u003eChemical Makeup\u003c\/h2\u003e\n\u003cp dir=\"ltr\"\u003e\u003cstrong dir=\"ltr\"\u003eOther Known Titles:\u003c\/strong\u003e\u003cspan\u003e \u003c\/span\u003eMT-II\u003cbr dir=\"ltr\"\u003e\u003cstrong dir=\"ltr\"\u003eMolecular Weight:\u003c\/strong\u003e\u003cspan\u003e \u003c\/span\u003e1024.19 g\/mol\u003cbr dir=\"ltr\"\u003e\u003cstrong dir=\"ltr\"\u003eMolecular Formula:\u003c\/strong\u003e\u003cspan\u003e \u003c\/span\u003eC\u003csub dir=\"ltr\"\u003e50\u003c\/sub\u003eH\u003csub dir=\"ltr\"\u003e69\u003c\/sub\u003eN\u003csub dir=\"ltr\"\u003e15\u003c\/sub\u003eO\u003csub dir=\"ltr\"\u003e9\u003c\/sub\u003e\u003c\/p\u003e\n\u003ch2\u003eResearch and Clinical Studies\u003c\/h2\u003e\n\u003ch3\u003e\u003cem\u003eMelanotan 2 Peptide and Nerve Cell Regeneration\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eResearch\u003csup dir=\"ltr\"\u003e(5)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003ein a murine model of an induced peripheral nerve injury has been employed to investigate the neurotrophic potential of Melanotan 2. 48 hours after half of the murine models were presented with the peptide, it was noted that the Melanotan 2 research models appeared to indicate a recovery in their sensory function. Furthermore, when the murine models were presented with a chemotherapeutic compound, Melanotan 2 appeared to exhibit neuroprotective properties, which protected the nerves from the compound's induced neurotoxicity to a certain extent. This potential is posited to be mediated via the MC4 receptors, which might even promote neurite outgrowth and possibly support the intrinsic capacity of neuronal tissue to recover after injury.\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eAlthough the exact signaling pathways are not fully understood, it is often suggested that the pro-opiomelanocortin (POMC)-derived melanocortin peptides, including compounds analogous to a-melanocyte-stimulating hormone (a-MSH), may influence neuronal structures by increasing the number and length of neurites and potentially promoting nerve sprouting in damaged regions. Since Melanotan 2 is considered a potent melanocortin receptor agonist, it may trigger a cascade of intracellular events that theoretically lead to a better-supported ability of nerve fibers to regenerate after various forms of insult, as well as a partial protective response against toxic neuropathic conditions. Therefore, the researchers concluded that they “\u003cem dir=\"ltr\"\u003eobserved that Melanotan-II also possesses neuroprotective properties, as it partially protected the nerve from a toxic neuropathy induced by cisplatin.\u003c\/em\u003e”\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eMelanotan 2 Peptide and Arousal Neurosignaling\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eIn a clinical study,\u003csup dir=\"ltr\"\u003e(6)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eMelanotan 2 has been suggested to induce increased arousal neuron signaling in more than 80% of cases, compared to only 20% success with a placebo. This research peptide may act via the MC4 receptors and downstream of established neuromodulators, including dopaminergic and oxytocinergic signals, possibly integrating their actions within discrete hypothalamic centers. These regions are thought to coordinate various homeostatic and motivational behaviors, and the introduction of an agonist like Melanotan 2 may potentially reframe the balance of neuronal activity. These researchers also posit that the involvement of MC5 receptors in certain peripheral glands may potentially provide a parallel route that links central neuro signaling with peripheral modulatory factors. However, this remains an area where mechanisms are only hypothesized.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eMelanotan 2 Peptide and Neurodevelopmental Modulation\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eResearchers have said that Melanotan 2 may potentially influence aberrant neural mechanisms by possibly stimulating populations of neurons that may govern social cognition through endogenous oxytocinergic signaling.\u003csup dir=\"ltr\"\u003e(7)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eThese MC4R-sensitive circuits, potentially located in regions such as the paraventricular nucleus of the hypothalamus, might release endogenous oxytocin in response to Melanotan 2, possibly recalibrating imbalanced neurochemical activity thought to underlie key aspects of social impairment. This oxytocin release may, in turn, modulate neurotransmission involving serotonin, glutamate, dopamine, and GABA, all of which are implicated in shaping social adaptation.\u003c\/p\u003e\n\u003cp\u003eBy engaging these systems, Melanotan 2 may alter the functional connectivity of cortical and subcortical networks—regions including, for instance, the anterior cingulate cortex—where oxytocin receptor distribution may differ in atypical neurodevelopmental contexts. In doing so, researchers have been able to hypothesize that Melanotan 2 might restore or modify synaptic communication and synaptic plasticity, which may go so far as to reshape the underlying neuroarchitecture.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eMelanotan 2 Peptide and Models of Sunless Tanning\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eMelanotan 2 may increase melanin production and thereby induce darker pigmentation without the need for ultraviolet irradiation by engaging the MC1R on melanocytes.\u003csup dir=\"ltr\"\u003e(8)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eMoreover, the peptide's cyclic structure supports a more prolonged metabotropic activity compared to other MSH analogs.\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eAlthough the precise intracellular signaling cascades remain incompletely understood, current data suggest that receptor interactions might lead to the elevated synthesis of eumelanin. This might offer a potential pathway for the development of sunless tanning models in a controlled research environment. Specifically, researchers have made comments about their observation of outcomes in research models, such as “\u003cem dir=\"ltr\"\u003eincreased [darkened] pigmentation in the face, upper body, and buttock\u003c\/em\u003e” in experimental settings.\u003c\/p\u003e\n\u003cp\u003e\u003cem\u003e\u003cstrong dir=\"ltr\"\u003eMelanotan 2 peptide is available for research and laboratory purposes only. \u003c\/strong\u003e\u003c\/em\u003e\u003c\/p\u003e\n\u003ch3\u003eReferences:\u003c\/h3\u003e\n\u003col\u003e\n\u003cli\u003eRyakhovsky, Vladimir V et al. “The first preparative solution phase synthesis of Melanotan II.” Beilstein Journal of Organic Chemistry vol. 4 (2008): 39. doi:10.3762\/bjoc.4.39.\u003cspan\u003e \u003c\/span\u003e\u003ca href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/19043625\/\" rel=\"noopener\" dir=\"ltr\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/19043625\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eMac E. Hadley, Discovery that a melanocortin regulates sexual functions in male and female humans, Peptides, Volume 26, Issue 10, 2005, Pages 1687-1689, ISSN 0196-9781,\u003cspan\u003e \u003c\/span\u003e\u003ca href=\"https:\/\/doi.org\/10.1016\/j.peptides.2005.01.023\" rel=\"noopener\" dir=\"ltr\"\u003ehttps:\/\/doi.org\/10.1016\/j.peptides.2005.01.023\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eKing, Stephen H et al. “Melanocortin receptors, melanotropic peptides and penile erection.” Current topics in medicinal chemistry vol. 7,11 (2007): 1098-1106.\u003cspan\u003e \u003c\/span\u003e\u003ca href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC2694735\/\" rel=\"noopener\" dir=\"ltr\"\u003ehttps:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC2694735\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003ePeters, Björn, et al. “Melanotan II: a possible cause of renal infarction: review of the literature and case report.” CEN case reports vol. 9,2 (2020): 159-161. doi:10.1007\/s13730-020-00447-z.\u003cspan\u003e \u003c\/span\u003e\u003ca href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC7148395\/\" dir=\"ltr\"\u003ehttps:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC7148395\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eTer Laak, Mariël P, et al. “The potent melanocortin receptor agonist melanotan-II promotes peripheral nerve regeneration and has neuroprotective properties in the rat.” European Journal of Pharmacology vol. 462,1-3 (2003): 179-83. doi:10.1016\/s0014-2999(02)02945-x.\u003cspan\u003e \u003c\/span\u003e\u003ca href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/12591111\" rel=\"noopener\" dir=\"ltr\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/12591111\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eWessells, H et al. “Melanocortin receptor agonists, penile erection, and sexual motivation: human studies with Melanotan II.” International journal of impotence research vol. 12 Suppl 4 (2000): S74-9. doi:10.1038\/sj.ijir.3900582.\u003cspan\u003e \u003c\/span\u003e\u003ca href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/11035391\/\" rel=\"noopener\" dir=\"ltr\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/11035391\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eMinakova E, Lang J, Medel-Matus JS, Gould GG, Reynolds A, Shin D, Mazarati A, Sankar R. Melanotan-II reverses autistic features in a maternal immune activation mouse model of autism. PLoS One. 2019 Jan 10;14(1):e0210389. Doi: 10.1371\/journal.pone.0210389. PMID: 30629642; PMCID: PMC6328175.\u003c\/li\u003e\n\u003cli\u003eDorr RT, Lines R, Levine N, Brooks C, Xiang L, Hruby VJ, Hadley ME. Evaluation of melanotan-II, a superpotent cyclic melanotropic peptide in a pilot phase-I clinical study. Life Sci. 1996;58(20):1777-84. doi: 10.1016\/0024-3205(96)00160-9. PMID: 8637402.\u003c\/li\u003e\n\u003c\/ol\u003e","brand":"PureX Labs","offers":[{"title":"10mg","offer_id":47548289220852,"sku":null,"price":25.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0804\/5802\/3156\/files\/Render_Mockup_1920_1920_2026-01-31_3.png?v=1769802134"},{"product_id":"tb-500","title":"TB-500","description":"\u003cp dir=\"ltr\"\u003e\u003cmeta charset=\"utf-8\"\u003e\u003cspan\u003eTB-500 is a synthetic peptide modeled after a portion of the thymosin beta-4 protein, a naturally occurring peptide found in nearly all human and animal cells. Research has focused on its possible influence on actin regulation, a protein critical to cellular structure and movement. TB-500 is of particular interest in studies exploring wound healing, muscle and tendon repair, and recovery from tissue injury. Its ability to encourage cell migration and blood vessel formation has made it a valuable compound for research into regenerative science. As with other peptides, TB-500 is intended solely for laboratory and research purposes and is not approved for human use.\u003c\/span\u003e\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eBesides being highly soluble in water and light in weight, TB-500 is a 43 amino acid-containing peptide found in abundance in the wound fluid comprising multiple blood platelets. This peptide may exhibit possible anti-inflammatory potential and may support neurological healing, as well as potentially supporting healing processes in the spinal cord, heart, and epidermis.\u003csup dir=\"ltr\"\u003e(1)\u003c\/sup\u003e\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eTB-500 peptide, also known as thymosin β(4), includes a distinct peptide segment (17)LKKTETQ(23), which acts as the active site and which researchers consider potentially impactful in actin binding, cell migration, and wound healing.\u003csup dir=\"ltr\"\u003e(2)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eThe amino acid sequence of TB-500 is:\u003cbr dir=\"ltr\"\u003eAc-Ser-Asp-Lys-Pro-Asp-Met-Ala-Glu-Ile-Glu-Lys-Phe-Asp-Lys-Ser-Lys-Leu-Lys-Lys-Thr-Glu-Thr-Gln-Glu-Lys-Asn-Pro-Leu-Pro-Ser-Lys-Glu-Thr-Ile-Glu-Gln-Glu-Lys-Gln-Ala-Gly-Glu-Ser-OH.\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eActins are essential proteins that form a key component of the cytoskeleton within cells, serving not only to maintain cellular structure but also to facilitate various cellular functions, including movement. Actin is suggested to be critical in supporting these cellular structures and processes. Thymosin beta-4 and, thus, TB-500 are believed to interact with actin, potentially by binding to globular actin (G-actin), a precursor to filamentous actin (F-actin). This interaction is thought to hinder the transformation of G-actin into F-actin, a process known as actin sequestration, and is likely to increase the availability of G-actin. The inhibition of F-actin formation by thymosin beta-4 may conceivably modify the structure of the cellular cytoskeleton, impacting cellular abilities for movement and morphological changes. Such changes are tentatively linked to various physiological and pathological states where cell motility is essential, including wound healing, tissue regeneration, and the progression of cancer through metastasis.\u003csup dir=\"ltr\"\u003e(3)\u003c\/sup\u003e\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eFurthermore, Thymosin beta-4 has been detected not only within cells but also extracellularly, such as in blood plasma and wound exudates. Preliminary studies involving vascular cells suggest that Thymosin beta-4 is extracellular, it might influence cellular functions like motility and the formation of new blood vessels (angiogenesis).\u003csup dir=\"ltr\"\u003e(11,12)\u003cspan\u003e \u003c\/span\u003e\u003c\/sup\u003eIt is postulated that Thymosin beta-4 might exert this potential through its interactions with ATP synthase enzymes located on the cell surface, which are critical for cellular energy production. These findings indicate a broader scope of action for thymosin beta-4, impacting both intra- and extracellular processes.\u003c\/p\u003e\n\u003ch3\u003eChemical Makeup\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003e\u003cstrong dir=\"ltr\"\u003eMolecular Formula:\u003c\/strong\u003e\u003cspan\u003e \u003c\/span\u003eC\u003csub dir=\"ltr\"\u003e212\u003c\/sub\u003eH\u003csub dir=\"ltr\"\u003e350\u003c\/sub\u003eN\u003csub dir=\"ltr\"\u003e56\u003c\/sub\u003eO\u003csub dir=\"ltr\"\u003e78\u003c\/sub\u003eS\u003cbr dir=\"ltr\"\u003e\u003cstrong dir=\"ltr\"\u003eMolecular Weight:\u003c\/strong\u003e\u003cspan\u003e \u003c\/span\u003e4963 g\/mol\u003cbr dir=\"ltr\"\u003e\u003cstrong dir=\"ltr\"\u003eOther Known Titles:\u003c\/strong\u003e\u003cspan\u003e \u003c\/span\u003eThymosin Beta 4\u003c\/p\u003e\n\u003ch2\u003eResearch and Clinical Studies\u003c\/h2\u003e\n\u003ch3\u003e\u003cem\u003eTB-500 Peptide and Inflammation\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eTβ4, and thus TB-500, is thought to potentially increase the levels of microRNA-146a (miR-146a), which might function as a suppressive regulator of specific cellular signaling pathways, particularly those associated with the functions of inflammation-related cytokines, including L-1 receptor-linked kinase 1 (IRAK1) and tumor necrosis factor receptor-associated factor 6 (TRAF6). The researchers of a study investigating the potential of the peptide on these factors propose this as a possible mechanism of action for TB-500. More specifically, the authors observed that \"\u003cem dir=\"ltr\"\u003etransfection of anti-miR-146a nucleotides reversed the inhibitory effect of Tβ4 on IRAK1 and TRAF6,\u003c\/em\u003e\" thus suggesting this as a potential mechanism. Consequently, it is suggested that TB-500 may contribute to anti-inflammatory potential via these mechanisms.\u003csup dir=\"ltr\"\u003e(4)\u003c\/sup\u003e\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eTB-500 Peptide and Acute Wounds\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eIn 1999, a research study was conducted on wounded murine test models, who were introduced to TB-500 as a form of synthetic Thymosin Beta 4.\u003csup dir=\"ltr\"\u003e(5)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eFour days after the presentation, it was reported by the researchers that the TB-500 peptide rats exhibited an apparent 41% increase in re-epithelialization than control murine models presented with saline. Seven days after the study, the TB-500 wounds were reported to be contracted by at least 11% more than the saline wounds. Upon analysis, it was concluded that TB-500 may possibly induce angiogenesis and collagen deposition, increasing the wound healing rate.The authors commented that their observations “\u003cem dir=\"ltr\"\u003esuggest that Tβ4 is a potent wound healing factor with multiple activities...\u003c\/em\u003e”\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eTB-500 Peptide and Chronic Wounds\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eResearch studies were carried out on normal rats and mice, diabetic mice, aged mice, and steroid-influenced rats. All these animals were served full-thickness punch wounds and introduced to the TB-500 peptide. It was reported that the TB-500 appeared to accelerate the wound-healing process in all test models, regardless of the stated pre-existing conditions. Furthermore, phase 2 clinical trials were conducted on models of stasis and pressure ulcers. It was reported that TB-500 might accelerate the healing process by as much as one month.\u003csup dir=\"ltr\"\u003e(6)\u003c\/sup\u003e\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eTB-500 Peptide and Heart Cells\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003ePulmonary hypertension is considered by scientists to be a progressive cardiac disease where the pulmonary arteries restrict the blood ejection by the right ventricle. This may result in increased pulmonary vascular resistance and pressure, potentially leading to ventricular failure of the heart. It was reported by researchers that TB-500 might be action specific on the Notch3-Col 3A-CTGF gene axis in MCT-influenced mice, which appeared to result in the case of the test study in decreasing the right ventricular heart cell hypertrophy by a significant amount.\u003csup dir=\"ltr\"\u003e(7)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eBased on Tβ4 research, TB-500 might also influence the regeneration of cardiac cells. Preliminary research indicates that TB-500 may enhance the resilience of myocardial cells under hypoxic conditions and may also promote angiogenesis, which could facilitate the repair of cardiac cells. There is a suggestion from researchers that cardiac fibroblasts could potentially differentiate into cells akin to cardiomyocytes.\u003csup dir=\"ltr\"\u003e(8)\u003cspan\u003e \u003c\/span\u003e\u003c\/sup\u003eFurthermore, it has been proposed that the combination of TB-500 with cardiac reprogramming methods could synergistically mitigate damage to cardiac cells and support their regeneration by activating intrinsic cells in the heart area. Further experimentation employing mouse models, in which coronary arteries were ligated, suggested that TB-500 could potentially increase the activity of integrin-linked kinase (ILK) and protein kinase B (Akt) in cardiac tissue. This observation indicates a possible enhancement in the early survival of cardiomyocytes and an apparent improvement in cardiac function.\u003csup dir=\"ltr\"\u003e(9)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eFurther, the research indicates that TB-500 may facilitate the migration of myocardial and endothelial cells in the fetal heart, and this function appears to be preserved in adult cardiomyocytes.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eTB-500 and Hair Follicle Growth\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eIn 2003, studies were carried out on mice to examine the potential of TB-500 in hair growth. Under the influence of the TB-500 peptide, it was reported by the researchers that, via histological examination of the mouse skin cells, the peptide appeared to increase the number of hair shafts and hair follicles, thereby inducing hair growth. Upon real-time PCR and western blotting techniques, changes in the expression of m-RNA cells were observed between the TB500 and control mice. The m-RNA and protein levels were reported elevated in TB-500 mice, which might have significantly induced hair growth.\u003csup dir=\"ltr\"\u003e(10)\u003c\/sup\u003e\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eTB-500 and Blood Vessel Formation\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eIt is hypothesized that TB-500 might influence angiogenesis via several molecular interactions. This is based on studies involving TB-500 overexpression lentiviral vector in transfecting umbilical vein endothelial cells (HUVEC) and murine critical limb ischemia (CLI) models.\u003csup dir=\"ltr\"\u003e(13)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eResearchers have also employed inhibitors such as DAPT, targeting the Notch pathway, and BMS, affecting the NF-κB pathway, in both HUVEC and murine CLI experiments to probe the intricate biological processes involved. The potential of TB-500 on angiogenesis and cellular migration were evaluated using MTT assays to measure cell viability, alongside tube formation and wound healing assays to assess angiogenic and migratory capabilities, respectively. Additionally, a variety of molecular methodologies were utilized, including Western blotting, reverse transcription, quantitative PCR, immunofluorescence, and immunohistochemistry. These techniques were instrumental in investigating the expression levels of angiogenesis-associated markers and elements related to the Notch\/NF-κB pathways. Preliminary findings indicate that TB-500 might enhance not only the viability, angiogenesis, and migration of HUVEC but could also elevate the expression of angiopoietin-2 (Ang2), TEK receptor tyrosine kinase 2 (tie2), vascular endothelial growth factor A (VEGFA), NOTCH1 intracellular domain (N1ICD), Notch receptor 3 (Notch3), NF-κB, and phosphorylated (p)-p65 in these cells. In the muscle tissues of murine CLI models, similar increases in the expression of CD31, α-smooth muscle actin (α-SMA), Ang2, tie2, VEGFA, N1ICD, and p-p65 were observed, suggesting a regulatory potential of TB-500 on these molecular targets. Interestingly, the application of DAPT and BMS in these studies seemed to counteract the actions of TB-500, potentially indicating that the mechanisms of action of TB-500 in promoting angiogenesis might be mediated through its interactions with the Notch and NF-κB pathways. Moreover, the apparent reversal of the actions of DAPT and BMS by TB-500 could underscore its role in modulating these pathways, supporting the proposition of its regulatory functions in angiogenesis. Researchers have noted that these observations might imply a role for Tβ4 in promoting angiogenesis through regulation of these critical pathways.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eTB-500 and Corneal Tissues\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eStudies have posited that TB-500 may modulate cytokine production and thus accelerate healing in corneal wound models.\u003csup dir=\"ltr\"\u003e(14)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eFollowing injury, there is some indication that TB-500 could promote increased expression of IL-1β and IL-6 mRNA in the corneas of murine models. Moreover, TB-500 experimentation after alkali injury might lead to a decrease in the expression of chemoattractants such as MIP-2 and KC for polymorphonuclear neutrophils (PMNs) in mouse corneas, potentially resulting in diminished PMN infiltration. Concerning the inflammatory signaling pathways in the cornea, it is speculated that TB-500 may influence NFκB pathways, possibly exerting anti-inflammatory actions. TB-500 is also theorized to possess anti-apoptotic attributes. An overexpression of TB-500 in cellular models is observed to potentially increase growth rates, diminish basal apoptosis, and confer resistance to factors that induce cell death. In corneal epithelial cells, TB-500 could potentially inhibit apoptosis by blocking caspases and curtailing the release of the pro-apoptotic protein bcl-2 from mitochondria. The mechanism of TB-500’s anti-apoptotic action might include reducing the initiation signals of early cell death and activating the survival kinase Akt via complex interactions with PINCH and integrin-linked kinase. It is conceivable that TB-500’s anti-apoptotic influence operates through several molecular pathways. Nonetheless, it is crucial to acknowledge that these mechanisms remain conjectural and warrant further empirical investigation to be substantiated.\u003c\/p\u003e\n\u003cp\u003e\u003cem\u003e\u003cstrong dir=\"ltr\"\u003eTB-500 peptide is available for research and laboratory purposes only.\u003c\/strong\u003e\u003c\/em\u003e\u003c\/p\u003e\n\u003ch3\u003eReferences:\u003c\/h3\u003e\n\u003col\u003e\n\u003cli\u003eKleinman HK, Sosne G. Thymosin β4 Promotes Dermal Healing. Vitam Horm. 2016;102:251-75.\u003cspan\u003e \u003c\/span\u003e\u003ca href=\"https:\/\/www.sciencedirect.com\/science\/article\/abs\/pii\/S008367291630005X\" rel=\"noopener\" dir=\"ltr\"\u003edoi: 10.1016\/bs.vh.2016.04.005\u003c\/a\u003e. Epub 2016 May 24.\u003c\/li\u003e\n\u003cli\u003eHo EN, Kwok WH, Lau MY, Wong AS, Wan TS, Lam KK, Schiff PJ, Stewart BD. Doping control analysis of TB-500, a synthetic version of an active region of thymosin β₄, in equine urine and plasma by liquid chromatography-mass spectrometry. J Chromatogr A. 2012 Nov 23;1265:57-69.\u003cspan\u003e \u003c\/span\u003e\u003ca href=\"https:\/\/doi.org\/10.1016\/j.chroma.2012.09.043\" rel=\"noopener\" dir=\"ltr\"\u003edoi: 10.1016\/j.chroma.2012.09.043\u003c\/a\u003e. Epub 2012 Sep 23.\u003c\/li\u003e\n\u003cli\u003eGurtner GC, Werner S, Barrandon Y, Longaker MT. Wound repair and regeneration. Nature. 2008 May 15;453(7193):314-21.\u003cspan\u003e \u003c\/span\u003e\u003ca href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/18480812\/\" rel=\"noopener\" dir=\"ltr\"\u003edoi: 10.1038\/nature07039\u003c\/a\u003e. PMID: 18480812.\u003c\/li\u003e\n\u003cli\u003eSantra, M., Zhang, Z. G., Yang, J., Santra, S., Santra, S., Chopp, M., \u0026amp; Morris, D. C. (2014). Thymosin β4 up-regulation of microRNA-146a promotes oligodendrocyte differentiation and suppression of the Toll-like proinflammatory pathway.\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003eThe Journal of biological chemistry\u003c\/em\u003e,\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003e289\u003c\/em\u003e(28), 19508–19518.\u003cspan\u003e \u003c\/span\u003e\u003ca href=\"https:\/\/doi.org\/10.1074\/jbc.M113.529966\" rel=\"noopener\" dir=\"ltr\"\u003ehttps:\/\/doi.org\/10.1074\/jbc.M113.529966\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eKatherine M. Malinda et.al, Thymosin β4 Accelerates Wound Healing, Journal of Investigative Dermatology, Volume 113, Issue 3, 1999, Pages 364-368, ISSN 0022-202X.\u003c\/li\u003e\n\u003cli\u003eTreadwell T, Kleinman HK, Crockford D, Hardy MA, Guarnera GT, Goldstein AL. The regenerative peptide thymosin β4 accelerates the rate of dermal healing in preclinical animal models and in patients. Ann N Y Acad Sci. 2012 Oct.\u003c\/li\u003e\n\u003cli\u003eWei C, Kim IK, Li L, Wu L, Gupta S. Thymosin Beta 4 protects mice from monocrotaline-induced pulmonary hypertension and right ventricular hypertrophy. PLoS One. 2014 Nov 20;9(11):e110598.\u003c\/li\u003e\n\u003cli\u003eSrivastava, D., Ieda, M., Fu, J., \u0026amp; Qian, L. (2012). Cardiac repair with thymosin β4 and cardiac reprogramming factors.\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003eAnnals of the New York Academy of Sciences\u003c\/em\u003e,\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003e1270\u003c\/em\u003e, 66–72.\u003cspan\u003e \u003c\/span\u003e\u003ca href=\"https:\/\/doi.org\/10.1111\/j.1749-6632.2012.06696.x\" rel=\"noopener\" dir=\"ltr\"\u003ehttps:\/\/doi.org\/10.1111\/j.1749-6632.2012.06696.x\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eBock-Marquette, I., Saxena, A., White, M. D., Dimaio, J. M., \u0026amp; Srivastava, D. (2004). Thymosin beta4 activates integrin-linked kinase and promotes cardiac cell migration, survival and cardiac repair.\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003eNature\u003c\/em\u003e,\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003e432\u003c\/em\u003e(7016), 466–472.\u003cspan\u003e \u003c\/span\u003e\u003ca href=\"https:\/\/doi.org\/10.1038\/nature03000\" rel=\"noopener\" dir=\"ltr\"\u003ehttps:\/\/doi.org\/10.1038\/nature03000\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eGao, Xy., Hou, F., Zhang, Zp. et al. Role of thymosin beta 4 in hair growth. Mol Genet Genomics 291, 1639–1646 (2016).\u003c\/li\u003e\n\u003cli\u003eHuff, T., Müller, C. S., Otto, A. M., Netzker, R., \u0026amp; Hannappel, E. (2001). beta-Thymosins, small acidic peptides with multiple functions.\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003eThe international journal of biochemistry \u0026amp; cell biology\u003c\/em\u003e,\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003e33\u003c\/em\u003e(3), 205–220.\u003cspan\u003e \u003c\/span\u003e\u003ca href=\"https:\/\/doi.org\/10.1016\/s1357-2725(00)00087-x\" rel=\"noopener\" dir=\"ltr\"\u003ehttps:\/\/doi.org\/10.1016\/s1357-2725(00)00087-x\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eFreeman, K. W., Bowman, B. R., \u0026amp; Zetter, B. R. (2011). Regenerative protein thymosin beta-4 is a novel regulator of purinergic signaling.\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003eFASEB journal : official publication of the Federation of American Societies for Experimental Biology\u003c\/em\u003e,\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003e25\u003c\/em\u003e(3), 907–915.\u003cspan\u003e \u003c\/span\u003e\u003ca href=\"https:\/\/doi.org\/10.1096\/fj.10-169417\" rel=\"noopener\" dir=\"ltr\"\u003ehttps:\/\/doi.org\/10.1096\/fj.10-169417\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eLv, S., Cai, H., Xu, Y., Dai, J., Rong, X., \u0026amp; Zheng, L. (2020). Thymosin‑β 4 induces angiogenesis in critical limb ischemia mice via regulating Notch\/NF‑κB pathway.\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003eInternational journal of molecular medicine\u003c\/em\u003e,\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003e46\u003c\/em\u003e(4), 1347–1358.\u003cspan\u003e \u003c\/span\u003e\u003ca href=\"https:\/\/doi.org\/10.3892\/ijmm.2020.4701\" rel=\"noopener\" dir=\"ltr\"\u003ehttps:\/\/doi.org\/10.3892\/ijmm.2020.4701\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eSosne, G., Qiu, P., \u0026amp; Kurpakus-Wheater, M. (2007). Thymosin beta 4: A novel corneal wound healing and anti-inflammatory agent.\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003eClinical ophthalmology (Auckland, N.Z.)\u003c\/em\u003e,\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003e1\u003c\/em\u003e(3), 201–207.\u003c\/li\u003e\n\u003c\/ol\u003e","brand":"PureX Labs","offers":[{"title":"5mg","offer_id":47548294758644,"sku":null,"price":45.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0804\/5802\/3156\/files\/Render_Mockup_1920_1920_2026-01-31_4.png?v=1769802134"},{"product_id":"tesamorelin","title":"Tesamorelin","description":"\u003cp dir=\"ltr\"\u003eTesamorelin is a synthetic polypeptide composed of 44 amino acids analogous to growth hormone-releasing hormone. The N-terminus of the compound has been modified compared to growth hormone-releasing hormone, the modification of which researchers suggest may lead to improved stability.\u003csup dir=\"ltr\"\u003e(1)\u003c\/sup\u003e\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eTesamorelin has been studied for its potential mechanism of action, posited to be similar to growth hormone-releasing hormones (GHRH) receptors located at the anterior pituitary gland, possibly leading to increased production and secretion of growth hormones. Growth hormones may act on several cells, including hepatocytes, stimulating the systemic synthesis of insulin-like growth factor-1 (IGF-1). In addition, growth hormone may also stimulate IGF-1 production locally, inside various tissues.\u003csup dir=\"ltr\"\u003e(1)\u003c\/sup\u003e\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eIGF-1 has been posited to be the main anabolic mediator of growth hormone, potentially working to stimulate growth and inhibit programmed cell death.\u003csup dir=\"ltr\"\u003e(1)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eOn the other hand, growth hormone itself is suggested to be lipolytic, inducing fat breakdown at specific adipose depots, such as abdominal and visceral fat depositions. Tesamorelin appears to stimulate the release of growth hormone, and consequently IGF-1, by potentially interacting with the GHRH receptors in the anterior pituitary gland cells. When Tesamorelin interacts with the GHRH receptor, it is hypothesized that this interaction might alter the receptor's structure, potentially initiating communication pathways within the cell. It is also theorized that Tesamorelin might enhance the production of cyclic adenosine monophosphate (cAMP) in certain cells. This process may occur through the stimulation of adenylate cyclase, an enzyme that converts adenosine triphosphate (ATP) into cAMP. Increased cAMP levels may lead to the activation of protein kinase A (PKA), an enzyme deemed critical for transmitting signals within cells. Activated PKA may phosphorylate various target proteins, triggering a cascade of cellular responses. The conjectural stimulation of the GHRH receptor by Tesamorelin and the cAMP-PKA signaling pathway might promote the secretion and distribution of growth hormone (hGH) from somatotroph cells in the pituitary gland. Research indicates that this peptide may lead to an estimated 69% increase in overall growth hormone levels, measured by the area under the curve (AUC), and a reported 55% increase in the mean pulse area of the growth hormone. However, it does not seem to influence the frequency or peak levels of growth hormone pulses. Additionally, IGF-1 levels apparently surged by 122%.\u003csup dir=\"ltr\"\u003e(3)\u003c\/sup\u003e\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eThe N-terminus and C-terminus of the GHRH molecule are altered in Tesamorelin, potentially lending stability to the peptide and possibly increasing the compound's resistance to enzyme deactivation compared to natural GHRH.\u003csup dir=\"ltr\"\u003e(4)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eFocusing on the specific alterations, the C-terminus of Tesamorelin is modified by the addition of a trans-3-hexenoic acid group. This particular change, often referred to as an omega-amino acid modification, is believed to potentially reinforce the peptide's defense against enzymatic breakdown. On the other end, the N-terminus is modified by the attachment of an acetyl group, represented by the chemical notation CH₃CO-. This acetylation might enhance not only the molecule's stability but also its biological activity. As a result of these specific modifications, Tesamorelin is designated chemically as N-(trans-3-hexenoyl)-[Tyr1]hGRF(1–44)NH2 acetate, highlighting the specific alterations made to the peptide.\u003c\/p\u003e\n\u003ch3\u003eChemical Makeup\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003e\u003cstrong dir=\"ltr\"\u003eMolecular Formula:\u003c\/strong\u003e\u003cspan\u003e \u003c\/span\u003eC\u003csub dir=\"ltr\"\u003e221\u003c\/sub\u003eH\u003csub dir=\"ltr\"\u003e366\u003c\/sub\u003eN\u003csub dir=\"ltr\"\u003e72\u003c\/sub\u003eO\u003csub dir=\"ltr\"\u003e67\u003c\/sub\u003eS\u003cbr dir=\"ltr\"\u003e\u003cstrong dir=\"ltr\"\u003eMolecular Weight:\u003c\/strong\u003e\u003cspan\u003e \u003c\/span\u003e5136 g\/mol\u003cbr dir=\"ltr\"\u003e\u003cstrong dir=\"ltr\"\u003eOther Known Titles:\u003c\/strong\u003e\u003cspan\u003e \u003c\/span\u003e(3E)-hex-3-enoylsomatoliberin\u003c\/p\u003e\n\u003ch2\u003eResearch and Clinical Studies\u003c\/h2\u003e\n\u003ch3\u003e\u003cem\u003eTesamorelin Peptide and Lipodystrophy\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp\u003eLipodystrophy models refer to abnormal or pathological fat distribution and metabolism. The primary feature of lipodystrophy is the irregular distribution of fat into depots, leading to loss of fat (lipoatrophy) from specefic areas, and accumulation of excess fat (lipohypertrophy) in other regions. This abnormal fat distribution is often associated with serious negative metabolic changes, including insulin resistance, elevated cholesterol and triglyceride levels. Test models exhibiting lipodystrophy report low levels of GH and IGF-1. Researchers studying Tesamorelin's action and potential impact, suggest that the peptide may positively influence lipid metabolism, especially in lipodystrophy models.\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eFor example, two phase III studies\u003csup dir=\"ltr\"\u003e(6)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003ewere conducted with 806 test subjects over 26 weeks, followed by another 26-week extension. Each of the 806 test subjects had immunodeficiencies and lipodystrophy. The subjects were divided into two groups; one group with 543 subjects was presented with Tesamorelin, and the remaining 263 subjects were presented with a placebo for 26 weeks. After this duration, the Tesamorelin subjects were again randomly divided into 2 groups, in which one group continued Tesamorelin influence, and the other half was presented with a placebo for another 26 weeks. At week 26, the researchers observed a significant decrease in visceral adipose tissue level amongst the Tesamorelin subjects, at least 15.4%. Additionally, the levels of triglyceride and cholesterol were reported significantly decreased compared to the placebo group.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eTesamorelin Peptide and Immunodeficient Fat Fractions\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eResearchers posit that serious immunodeficiencies may induce non-alcoholic fatty liver disease (NAFLD), which in clinical cases is reported in nearly 40% of HIV-positive test models.\u003csup dir=\"ltr\"\u003e(7)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eIn this study,\u003csup dir=\"ltr\"\u003e(5)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003e61 test subjects with HIV and a high hepatic fat fraction (HFF) were selected as test models. These subjects were influenced with Tesamorelin or a placebo for 12 months. The rate of HFF was monitored at the end of the study. After 12 months, it was reported by the researchers that 35% of subjects presented with Tesamorelin exhibited an apparent reduction in HFF rate by less than 5% vs. only 4% of subjects receiving placebo exhibited any HFF reduction. There was no reported alteration in the glucose levels.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eTesamorelin Peptide and Cognition\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eIn this clinical study,\u003csup dir=\"ltr\"\u003e(8)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eimmunodeficient models with mild cognitive impairment were observed. The main intent of this study was to determine Tesamorelin's potential effect on neurological functioning. 100 subjects, aged more than 40 years, participated in this trial and underwent Tesamorelin presentation daily for 6 months, followed by all absence of Tesamorelin influence for the next 6 months. Then Tesamorelin was re-introduced once a day for another 6 months. The primary outcome of this study was reported in changes in neurocognitive performance measured by the Global Deficit Score (GDS) after 6 and 12 months. This study is underway, and the final results have not been published.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eTesamorelin Peptide and Insulin\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eThe main aim of this study\u003csup dir=\"ltr\"\u003e(9)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003ewas to determine any potential Tesamorelin might exhibit in altering insulin sensitivity. In this clinical trial setting, 53 test subjects with Type II diabetes were observed in this 12-week randomized trial. The subjects were divided into three groups, each receiving a lower or higher concentration of Tesamorelin or a placebo. Following the study period of 12 weeks, the concentration of fasting glucose, glycosylated hemoglobin, and diabetes control was measured. There was no reported significant reduction in either of these parameters. The results of all three groups appeared to be indifferent.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eTesamorelin Peptide and Muscle Tissue\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eIn a research investigation, the possible impacts of Tesamorelin on the structural quality of muscle tissues were evaluated using computed tomography (CT) scans.\u003csup dir=\"ltr\"\u003e(10)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eComputed tomography (CT) is an imaging tool that combines X-rays and computer technology to produce detailed pictures of internal structures. The findings from this study tentatively suggested a potential association between Tesamorelin and improvements in the density and overall volume of muscle tissues. It was observed that specific muscle groups, particularly the\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003erectus abdominis\u003c\/em\u003e,\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003epsoas major\u003c\/em\u003e, and\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003eparaspinal muscles\u003c\/em\u003e, exhibited more noticeable variations. These variations consisted of either increased muscle density and volume or decreased fat within the muscle tissue. From a statistical perspective, the alterations in muscle density and size or the reduction in fat content in these specific muscles were significantly different when compared to results from a control group receiving a placebo.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eTesamorelin Peptide and Visceral Fat\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eVisceral obesity involves the accumulation of excess fat around and within internal organs, a condition often observed in models of lipodystrophy—a disorder characterized by abnormal distribution of fat cells. This form of excessive fat accumulation is potentially linked to several metabolic issues. These issues include insulin resistance, a diminished ability to respond to insulin leading to elevated blood glucose levels. Additionally, visceral obesity is associated with the development of atherosclerosis, a condition where plaque builds up in the arteries, elevated levels of low-density lipoprotein (LDL) cholesterol, and hyperuricemia, an excess of uric acid. The significance of these models extends beyond aesthetic concerns, indicating that lipodystrophy may precipitate profound metabolic disturbances. In addressing these challenges, Tesamorelin, a synthetic form of the growth-hormone-releasing factor, has been proposed as a possibly positive avenue for further development. Research into Tesamorelin has suggested it may lead to a reduction of up to 25% in visceral fat among lipodystrophy models.\u003csup dir=\"ltr\"\u003e(11)\u003c\/sup\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cem\u003e\u003cstrong dir=\"ltr\"\u003eTesamorelin peptide is available for research and laboratory purposes only. Please review and adhere to our\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" href=\"https:\/\/www.corepeptides.com\/terms\/\"\u003eTerms and Conditions\u003c\/a\u003e\u003cspan\u003e \u003c\/span\u003ebefore ordering.\u003c\/strong\u003e\u003c\/em\u003e\u003c\/p\u003e\n\u003ch3\u003eReferences:\u003c\/h3\u003e\n\u003col\u003e\n\u003cli\u003eClinical and Research Information on Drug-Induced Liver Injury [Internet]. Bethesda (MD): National Institute of Diabetes and Digestive and Kidney Diseases; 2012-. Tesamorelin. [Updated 2018 Oct 20].\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/www.ncbi.nlm.nih.gov\/books\/NBK548730\/\"\u003ehttps:\/\/www.ncbi.nlm.nih.gov\/books\/NBK548730\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eSpooner, L. M., \u0026amp; Olin, J. L. (2012). Tesamorelin: a growth hormone-releasing factor analogue for HIV-associated lipodystrophy. The Annals of pharmacotherapy, 46(2), 240–247.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/doi.org\/10.1345\/aph.1Q629\"\u003ehttps:\/\/doi.org\/10.1345\/aph.1Q629\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eStanley TL, Chen CY, Branch KL, Makimura H, Grinspoon SK. Effects of a growth hormone-releasing hormone analog on endogenous GH pulsatility and insulin sensitivity in healthy men. J Clin Endocrinol Metab. 2011 Jan;96(1):150-8. doi: 10.1210\/jc.2010-1587. Epub 2010 Oct 13. PMID: 20943777; PMCID: PMC3038486.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC3038486\/\"\u003ehttps:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC3038486\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eFerdinandi ES, Brazeau P, High K, Procter B, Fennell S, Dubreuil P. Non-clinical pharmacology and safety evaluation of TH9507, a human growth hormone-releasing factor analogue. Basic Clin Pharmacol Toxicol. 2007 Jan;100(1):49-58. doi: 10.1111\/j.1742-7843.2007.00008.x. PMID: 17214611.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/17214611\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/17214611\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eStanley, T. L., Fourman, L. T., Feldpausch, M. N., Purdy, J., Zheng, I., Pan, C. S., Aepfelbacher, J., Buckless, C., Tsao, A., Kellogg, A., Branch, K., Lee, H., Liu, C. Y., Corey, K. E., Chung, R. T., Torriani, M., Kleiner, D. E., Hadigan, C. M., \u0026amp; Grinspoon, S. K. (2019). Effects of tesamorelin on non-alcoholic fatty liver disease in HIV: a randomised, double-blind, multicentre trial. The lancet. HIV, 6(12), e821–e830.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC6981288\/\"\u003ehttps:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC6981288\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eFalutz J, Mamputu JC, Potvin D, Moyle G, Soulban G, Loughrey H, Marsolais C, Turner R, Grinspoon S. Effects of tesamorelin (TH9507), a growth hormone-releasing factor analog, in human immunodeficiency virus-infected patients with excess abdominal fat: a pooled analysis of two multicenter, double-blind placebo-controlled phase 3 trials with safety extension data. J Clin Endocrinol Metab. 2010 Sep;95(9):4291-304. doi: 10.1210\/jc.2010-0490. Epub 2010 Jun 16. PMID: 20554713.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/20554713\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/20554713\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eTesamorelin Effects on Liver Fat and Histology in HIV.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/clinicaltrials.gov\/ct2\/show\/NCT02196831\"\u003ehttps:\/\/clinicaltrials.gov\/ct2\/show\/NCT02196831\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003ePhase II Trial of Tesamorelin for Cognition in Aging HIV-Infected Persons.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/clinicaltrials.gov\/ct2\/show\/record\/NCT02572323\"\u003ehttps:\/\/clinicaltrials.gov\/ct2\/show\/record\/NCT02572323\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eClemmons, D. R., Miller, S., \u0026amp; Mamputu, J. C. (2017). Safety and metabolic effects of tesamorelin, a growth hormone-releasing factor analogue, in patients with type 2 diabetes: A randomized, placebo-controlled trial. PloS one, 12(6), e0179538.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC5472315\/\"\u003ehttps:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC5472315\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eAdrian S, Scherzinger A, Sanyal A, Lake JE, Falutz J, Dubé MP, Stanley T, Grinspoon S, Mamputu JC, Marsolais C, Brown TT, Erlandson KM. The Growth Hormone Releasing Hormone Analogue, Tesamorelin, Decreases Muscle Fat and Increases Muscle Area in Adults with HIV. J Frailty Aging. 2019;8(3):154-159. doi: 10.14283\/jfa.2018.45. PMID: 31237318; PMCID: PMC6766405.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC6766405\/\"\u003ehttps:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC6766405\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eSivakumar T, Mechanic O, Fehmie DA, Paul B. Growth hormone axis treatments for HIV-associated lipodystrophy: a systematic review of placebo-controlled trials. HIV Med. 2011 Sep;12(8):453-62.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/doi.org\/10.1111\/j.1468-1293.2010.00906.x\"\u003edoi: 10.1111\/j.1468-1293.2010.00906.x\u003c\/a\u003e. Epub 2011 Jan 25. PMID: 21265979.\u003c\/li\u003e\n\u003c\/ol\u003e\n\u003cp\u003e\u003ca title=\"Tesamorelin 10MG COA\" href=\"https:\/\/purexlabs.io\/pages\/tesamorelin-10mg-coa\"\u003eCOA\u003c\/a\u003e\u003c\/p\u003e","brand":"PureX Labs","offers":[{"title":"5mg","offer_id":48358718931188,"sku":null,"price":70.0,"currency_code":"USD","in_stock":true},{"title":"10mg","offer_id":47548295807220,"sku":null,"price":120.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0804\/5802\/3156\/files\/Render_Mockup_1920_1920_2026-01-31_2_e451d656-de7c-4087-b18e-5f114f3a1594.png?v=1769799798"},{"product_id":"sermorelin","title":"Sermorelin","description":"\u003cp dir=\"ltr\"\u003eSermorelin is a 29 amino acid peptide, the shortest synthetically developed peptide that may potentially induce biological activity at the receptors for the growth hormone-releasing hormone (GHRH).\u003csup dir=\"ltr\"\u003e(2)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eSermorelin polypeptide is an analog of the GHRH factor consisting of GHRH (1-29 acid)-amide. Due to this structural and functional mimicry, Sermorelin has been studied across multiple branches of scientific research involving growth hormone deficiency models.\u003csup dir=\"ltr\"\u003e(3)\u003c\/sup\u003e\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eIt was in the early 1980s that the action of Sermorelin, classified as a growth hormone-releasing fragment GHRF (1-29) amide, was first explored. Several research studies were conducted on rats where exogenous GHRF (1-29) amide was introduced in conscious and anesthetized rats. It was observed that the presence of GHRF appeared to stimulate the pituitary gland and promote growth. Following this theory, Sermorelin and similar compounds have become the subject of further research in growth hormone deficiency models.\u003csup dir=\"ltr\"\u003e(4)\u003c\/sup\u003e\u003c\/p\u003e\n\u003cp\u003eSermorelin is suggested to be a growth hormone analog constituting the first 29 amino acids out of the usual 44 amino acids found in growth hormone-releasing hormone (GHRH). Researchers posit that Sermorelin binds with the GHRH receptors found on the pituitary gland and suggest further that the synthetic peptide may stimulate secretion of growth hormone (hGH). Thus, Sermorelin is believed to maintain the fundamental function of GHRH, possibly stimulating the GHRH receptors in the pituitary gland and leading to sporadic release of growth hormone despite its reduced amino acid sequence. This mechanism is thought to result in increased levels of insulin-like growth factor-1 (IGF-1), primarily recognized for its role in the anabolic actions of growth hormone. The estimated half-life of Sermorelin is around 11 to 12 minutes.\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eA major potential advantage of the peptide is that due to its apparent GHRH receptor specificity, it may not induce any significant change in the levels of other endocrine markers such as prolactin, insulin, cortisol, glucose, or thyroid hormones.\u003csup dir=\"ltr\"\u003e(6)\u003c\/sup\u003e\u003c\/p\u003e\n\u003ch3\u003eChemical Makeup\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003e\u003cstrong dir=\"ltr\"\u003eMolecular Formula:\u003cspan\u003e \u003c\/span\u003e\u003c\/strong\u003eC\u003csub dir=\"ltr\"\u003e149\u003c\/sub\u003eH\u003csub dir=\"ltr\"\u003e246\u003c\/sub\u003eN\u003csub dir=\"ltr\"\u003e44\u003c\/sub\u003eO\u003csub dir=\"ltr\"\u003e42\u003c\/sub\u003eS\u003cbr dir=\"ltr\"\u003e\u003cstrong dir=\"ltr\"\u003eMolecular Weight:\u003c\/strong\u003e\u003cspan\u003e \u003c\/span\u003e3357.93 g\/mol\u003cbr dir=\"ltr\"\u003e\u003cstrong dir=\"ltr\"\u003eOther Known Titles:\u003cspan\u003e \u003c\/span\u003e\u003c\/strong\u003eGRF 1-29\u003c\/p\u003e\n\u003ch2\u003eResearch and Clinical Studies\u003c\/h2\u003e\n\u003ch3\u003e\u003cem\u003eSermorelin and GHRH Receptors\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eSermorelin is thought to interact with GHRH receptors through complex molecular mechanisms, possibly triggering various cellular signaling pathways. It is hypothesized that upon binding to the GHRH receptor, Sermorelin may alter the receptor's structure, potentially initiating a series of intracellular signaling events.\u003csup dir=\"ltr\"\u003e(12)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eSome researchers propose that Sermorelin might enhance the production of cyclic adenosine monophosphate (cAMP) in specific cells. This enhancement may occur through the activation of adenylate cyclase, which is suggested to convert ATP into cAMP. Higher levels of cAMP might lead to the activation of protein kinase A (PKA), a key enzyme in cellular signaling processes. PKA might phosphorylate various target proteins, thereby initiating further cellular responses. The potential activation of the GHRH receptor by Sermorelin, along with the ensuing cAMP-PKA signaling cascade, is thought to possibly promote the secretion and distribution of growth hormone (hGH) from somatotroph cells in the pituitary gland. The secreted hGH is also believed to contribute to the synthesis of insulin-like growth factor-1 (IGF-1).\u003csup dir=\"ltr\"\u003e(12)\u003c\/sup\u003e\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eSermorelin Peptide and Growth Velocity\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eResearchers reported positive results in the idiopathic GH deficiency when Sermorelin was presented to underdeveloped animal models. Increased growth and height velocity rate was observed within 12 months of consistent, continuous peptide presence. These elevated levels were reported to be sustained for an average of 36 months after continuous presence.\u003csup dir=\"ltr\"\u003e(7)\u003c\/sup\u003e\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eSermorelin Peptide and Anabolic Research Outcomes\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003ePreliminary findings from one investigation indicate that Sermorelin may lead to an 82% enhancement in average growth hormone levels, with actions persisting for approximately two hours.\u003csup dir=\"ltr\"\u003e(13)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eA separate study conducted over 16 weeks hypothesizes that Sermorelin might elevate growth hormone levels by as much as 107%, and increase IGF-1 levels by about 28%.\u003csup dir=\"ltr\"\u003e(14)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eThe research further suggests a possible increase in lean body mass of approximately 2.78 lbs (1.26 kg), with no significant change in fat mass. These actions are tentatively attributed to the peptide's capacity to boost growth hormone levels, and in turn, IGF-1, which is considered a potential anabolic agent influencing growth hormone activity. The most noteworthy outcomes identified by the researchers include observations that there was “\u003cem dir=\"ltr\"\u003ea gain of 1.26 ± 0.52 kg (P \u0026lt; 0.05) in LBM\u003c\/em\u003e” and that “\u003cem dir=\"ltr\"\u003eskin thickness increased significantly.\u003c\/em\u003e”\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eSermorelin Peptide and Lipodystrophy\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eScientists carried out a controlled clinical study involving 31 HIV-positive subjects with lipodystrophy, to investigate the potential impact of Sermorelin.\u003csup dir=\"ltr\"\u003e(8)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eAll 31 subjects were divided into two groups, where one was presented with Sermorelin, and the other group with a placebo for 12 weeks. Following the study, it was suggested by the research team that growth hormone levels appeared significantly increased in Sermorelin subjects as compared to the ones given a placebo. Levels of insulin-like growth factor (IGF-1) had apparently increased – resulting in increased lean body mass in the peptide group. Abdominal visceral fat and the ratio of trunk to lower extremity fat were reported by the researchers to be significantly reduced. There was no other reported change in the glucose or insulin levels.\u003csup dir=\"ltr\"\u003e(8)\u003c\/sup\u003e\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eSermorelin Peptide and Cognition\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eIn the early 2000s, clinical research studies were conducted with 89 subjects between 68 and 69 years of age to explore the correlation (if any) between tapering growth hormone release and impaired cognition. Scientists consider that with increasing age, levels of growth hormone naturally decline, which may result in reduced physiological functions, including cognition (i.e. ability to collect, process, and recollect information). Following the introduction of Sermorelin, it was observed that there was an apparent improved performance in the Wechsler Adult Intelligence Scale (WAIS) – i.e. improved IQ levels, picture arrangement tests, and verbal tests - amongst the test subjects.\u003csup dir=\"ltr\"\u003e(9)\u003c\/sup\u003e\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eSermorelin Peptide and Tumor Cells\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eA clinical study was designed where 1,018 glioma subjects were presented with over 4,000 compounds each, and following each presentation, a DRS was determined for all compounds, for each subject. Following the results of the study, it appeared that the Sermorelin compound reportedly induced the most sensitivity in the test subjects. Upon analysis, it was suggested by the researchers that this may be due to the potential of Sermorelin to block the tumor cell cycles, thereby possibly preventing tumor cell proliferation.\u003csup dir=\"ltr\"\u003e(10)\u003c\/sup\u003e\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eSermorelin Peptide and Hypogonadism\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp\u003eInitial research into the peptide suggested that Sermorelin might be impactful in increasing lean mass. One study sought to explore if Sermorelin had potential in hypogonadism (which is considered to stem from additional fat mass). Test models were divided into two groups where one group was presented with Sermorelin followed by GHRH 1-40, with a one week interval between the two compounds, whereas the other group was given the same combination in reverse order. Following the study, it was reported by the researchers that for both groups, the Sermorelin appeared to stimulate the release of FSH and LH, which might stimulate testosterone production.\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eThis initial research spawned additional studies, including one clinical study that included 19 male subjects, 9 of whom were aged between 22 and 33 years of age, and 10 were aged between 60 and 78 years of age. The more elderly subjects were presented with one of two concentrations of Sermorelin for a period of 28 days, with an interval of 14 days in between the two instances. Testosterone levels in the elderly subjects reportedly increased after the presentation of Sermorelin; however, it should be noted that the levels were not statistically significant. Furthermore, researchers suggested that elevated levels of growth hormones, possibly induced by Sermorelin presence, appeared to be at peak during the night time, for all test subjects, as compared during the day.\u003csup dir=\"ltr\"\u003e(11)\u003c\/sup\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cem\u003e\u003cstrong dir=\"ltr\"\u003eSermorelin peptide is available for research and laboratory purposes only.\u003c\/strong\u003e\u003c\/em\u003e\u003c\/p\u003e\n\u003ch3\u003eReferences:\u003c\/h3\u003e\n\u003col\u003e\n\u003cli\u003eGarcia JM, Merriam GR, Kargi AY. Growth Hormone in Aging. [Updated 2019 Oct 7]. In: Feingold KR, Anawalt B, Boyce A, et al., editors. Endotext [Internet]. South Dartmouth (MA): MDText.com, Inc.; 2000.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/www.ncbi.nlm.nih.gov\/books\/NBK279163\/?report=reader\"\u003ehttps:\/\/www.ncbi.nlm.nih.gov\/books\/NBK279163\/?report=reader\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003ePrakash, A, and K L Goa. “Sermorelin: a review of its use in the diagnosis and treatment of children with idiopathic growth hormone deficiency.” BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy vol. 12,2 (1999): 139-57.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/18031173\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/18031173\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eNational Center for Biotechnology Information. \"PubChem Compound Summary for CID 16129620, Sermorelin\" PubChem\u003c\/li\u003e\n\u003cli\u003eClark, R G, and I C Robinson. “Growth induced by pulsatile infusion of an amidated fragment of human growth hormone releasing factor in normal and GHRF-deficient rats.” Nature vol. 314,6008 (1985): 281-3.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/2858818\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/2858818\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eDrugs at FDA: FDA Approved Drugs.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/www.accessdata.fda.gov\/scripts\/cder\/daf\/index.cfm?event=overview.process\u0026amp;ApplNo=020443\"\u003ehttps:\/\/www.accessdata.fda.gov\/scripts\/cder\/daf\/index.cfm?event=overview.process\u0026amp;ApplNo=020443\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eJunichi I. et al, Growth hormone secretagogues: history, mechanism of action, and clinical development, JSCM Rapid Communications Vol. 3 Issue 1, 09 February 2020.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" href=\"https:\/\/onlinelibrary.wiley.com\/doi\/full\/10.1002\/rco2.9\"\u003ehttps:\/\/onlinelibrary.wiley.com\/doi\/full\/10.1002\/rco2.9\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003ePrakash, A, and K L Goa. “Sermorelin: a review of its use in the diagnosis and treatment of children with idiopathic growth hormone deficiency.” BioDrugs : clinical immunotherapeutics, biopharmaceuticals and gene therapy vol. 12,2 (1999): 139-57.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/18031173\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/18031173\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eKoutkia, Polyxeni et al. “Growth hormone-releasing hormone in HIV-infected men with lipodystrophy: a randomized controlled trial.” JAMA vol. 292,2 (2004): 210-8.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/15249570\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/15249570\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eVitiello, Michael V et al. “Growth hormone releasing hormone improves the cognition of healthy older adults.” Neurobiology of aging vol. 27,2 (2006): 318-23.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/16399214\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/16399214\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eChang, Yuanhao et al. “A potentially effective drug for patients with recurrent glioma: sermorelin.” Annals of translational medicine vol. 9,5 (2021): 406. doi:10.21037\/atm-20-6561.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC8033379\/\"\u003ehttps:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC8033379\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eSinha, Deepankar K et al. “Beyond the androgen receptor: the role of growth hormone secretagogues in the modern management of body composition in hypogonadal males.” Translational andrology and urology vol. 9,Suppl 2 (2020): S149-S159. doi:10.21037\/tau.2019.11.30.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC7108996\/\"\u003ehttps:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC7108996\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eZhou, F., Zhang, H., Cong, Z., Zhao, L. H., Zhou, Q., Mao, C., Cheng, X., Shen, D. D., Cai, X., Ma, C., Wang, Y., Dai, A., Zhou, Y., Sun, W., Zhao, F., Zhao, S., Jiang, H., Jiang, Y., Yang, D., Eric Xu, H., … Wang, M. W. (2020). Structural basis for activation of the growth hormone-releasing hormone receptor. Nature communications, 11(1), 5205.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/doi.org\/10.1038\/s41467-020-18945-0\"\u003ehttps:\/\/doi.org\/10.1038\/s41467-020-18945-0\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eVittone, J., Blackman, M. R., Busby-Whitehead, J., Tsiao, C., Stewart, K. J., Tobin, J., Stevens, T., Bellantoni, M. F., Rogers, M. A., Baumann, G., Roth, J., Harman, S. M., \u0026amp; Spencer, R. G. (1997). Effects of single nightly injections of growth hormone-releasing hormone (GHRH 1-29) in healthy elderly men.\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003eMetabolism: clinical and experimental\u003c\/em\u003e,\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003e46\u003c\/em\u003e(1), 89–96.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/doi.org\/10.1016\/s0026-0495(97)90174-8\"\u003ehttps:\/\/doi.org\/10.1016\/s0026-0495(97)90174-8\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eKhorram, O., Laughlin, G. A., \u0026amp; Yen, S. S. (1997). Endocrine and metabolic effects of long-term administration of [Nle27]growth hormone-releasing hormone-(1-29)-NH2 in age-advanced men and women.\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003eThe Journal of clinical endocrinology and metabolism\u003c\/em\u003e,\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003e82\u003c\/em\u003e(5), 1472–1479.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/doi.org\/10.1210\/jcem.82.5.3943\"\u003ehttps:\/\/doi.org\/10.1210\/jcem.82.5.3943\u003c\/a\u003e\n\u003c\/li\u003e\n\u003c\/ol\u003e","brand":"PureX Labs","offers":[{"title":"5mg","offer_id":47548296528116,"sku":null,"price":40.0,"currency_code":"USD","in_stock":true},{"title":"10mg","offer_id":47548297019636,"sku":null,"price":65.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0804\/5802\/3156\/files\/Render_Mockup_1920_1920_2026-01-31_5.png?v=1769802134"},{"product_id":"cjc-1295-ipamorelin","title":"CJC-1295 + Ipamorelin","description":"\u003cp dir=\"ltr\"\u003eIpamorelin and CJC-1295 are both considered to be growth hormone secretagogues. Ipamorelin is a synthetic pentapeptide,\u003csup dir=\"ltr\"\u003e(1)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eand CJC-1295 peptide consists of 29 amino acids.\u003csup dir=\"ltr\"\u003e(2)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eIpamorelin appears to fall into a category of peptides classified as growth hormone secretagogues (GHSs). These are peptides that are assumed to stimulate the release of the growth hormones, however are not considered growth hormone releasing peptides themselves. On the other hand, CJC-1295 has also been suggested by researchers to stimulate the release of growth hormone, primarily by mimicking the actions of the naturally occurring growth hormone-releasing hormone (GHRH). Both Ipamorelin and CJC-1295 peptides have been assigned by researchers to this class, studied for similar potential actions and apparently differing only in terms of their half-life and pharmacokinetic profiles.\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eCJC-1295 \u0026amp; Ipamorelin peptides both are suggested by researchers to augment the levels of the growth hormones through a possible triggering of the anterior pituitary gland. Scientists consider that once triggered, growth hormones may be naturally secreted, maintaining levels of growth hormones in the organism.\u003csup dir=\"ltr\"\u003e(3)\u003c\/sup\u003e\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eCJC-1295 peptide is a tetrasubstituted version of GHRH 1-29, developed to represent the shortest functional sequence of GHRH. GHRH 1-29 consists of the first 29 amino acids of the native GHRH peptide, and may potentially stimulate growth hormone production in pituitary gland cells, called somatotrophs. The peptide has four amino acid substitutions in its structure, which scientists suggest may enhance its activity and resistance towards proteolytic enzymes. More specifically, the amino acids which are replaced appear to be the 2nd, 8th, 15th, and 27th amino acids. Owing to these substitutions, the peptide might be able to bind covalently to blood albumin, with trace amounts possibly able to bind to fibrinogen and immunoglobulin G (IgG). As a result, the apparent half-life of the peptide may increase from 10 mins to 30 mins.\u003csup dir=\"ltr\"\u003e(4)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eThis may lead to elevated levels of plasma growth hormone and insulin-like growth factor 1 (IGF-1).\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eCJC-1295 might also be linked with the purported drug affinity complex (DAC) element, which may attach to plasma proteins. In particular, the DAC element in CJC-1295 alludes to the connection of N-epsilon-3-maleimidopropionamide derivative of lysine at the C-terminal end. Merging the tetrasubstituted amino acid chain and the DAC element, CJC-1295 appears to display enhanced pharmacokinetics yet retains a comparable attraction to the GHRH receptors in the pituitary gland, similar to natural GHRH.\u003csup dir=\"ltr\"\u003e(5)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eMore specifically, researchers comment that when the peptide was “\u003ci dir=\"ltr\"\u003eselected for further pharmacokinetic evaluation, where it was found to be present in plasma beyond 72 h.\u003c\/i\u003e”\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003e\u003ca title=\"Ipamorelin for Sale - 5mg\" href=\"https:\/\/www.corepeptides.com\/peptides\/ipamorelin-5mg\/\" dir=\"ltr\"\u003eIpamorelin\u003c\/a\u003e\u003cspan\u003e \u003c\/span\u003eis a man-made pentapeptide, also known as NNC 26-0161, that is believed to associate with a specific receptor in the pituitary gland cells, termed the growth hormone secretagogue receptor (GHS-R1a). These receptors are considered to be located in the hypothalamus. Moreover, GHS-R1a is often referred to as the ghrelin receptors because ghrelin seems to be its primary natural ligand. Ipamorelin appears to stand out from other GHSs as a potentially more selective compound, which may possibly stimulate the release of GH levels by somatotroph cells without also increasing other hormones produced by the anterior pituitary gland, such as prolactin.\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eWhen the peptide blend, sometimes also called the peptide stack, is presented in combination, research studies typically report that the Ipamorelin exerts initial action, exhibiting some sign of impact within the first two hours of presentation, and as it starts to wean off, the CJC-1295 peptide may gradually supplement action.\u003csup dir=\"ltr\"\u003e(6)\u003c\/sup\u003e\u003c\/p\u003e\n\u003ch3\u003eChemical Makeup\u003c\/h3\u003e\n\u003cp\u003e\u003cstrong\u003eMolecular Formula:\u003c\/strong\u003e\u003c\/p\u003e\n\u003cul\u003e\n\u003cli\u003e\n\u003cb dir=\"ltr\"\u003e\u003cem dir=\"ltr\"\u003eCJC-1295:\u003c\/em\u003e\u003c\/b\u003e\u003cem dir=\"ltr\"\u003e\u003cspan\u003e \u003c\/span\u003eC\u003c\/em\u003e\u003csub dir=\"ltr\"\u003e\u003cem dir=\"ltr\"\u003e152\u003c\/em\u003e\u003c\/sub\u003eH\u003csub dir=\"ltr\"\u003e\u003cem dir=\"ltr\"\u003e252\u003c\/em\u003e\u003c\/sub\u003eN\u003csub dir=\"ltr\"\u003e\u003cem dir=\"ltr\"\u003e44\u003c\/em\u003e\u003c\/sub\u003eO\u003csub dir=\"ltr\"\u003e\u003cem dir=\"ltr\"\u003e42\u003c\/em\u003e\u003c\/sub\u003e\n\u003c\/li\u003e\n\u003cli\u003e\n\u003cb dir=\"ltr\"\u003e\u003cem dir=\"ltr\"\u003eIpamorelin:\u003c\/em\u003e\u003c\/b\u003e\u003cem dir=\"ltr\"\u003e\u003cspan\u003e \u003c\/span\u003eC\u003c\/em\u003e\u003csub dir=\"ltr\"\u003e\u003cem dir=\"ltr\"\u003e38\u003c\/em\u003e\u003c\/sub\u003eH\u003csub dir=\"ltr\"\u003e\u003cem dir=\"ltr\"\u003e49\u003c\/em\u003e\u003c\/sub\u003eN\u003csub dir=\"ltr\"\u003e\u003cem dir=\"ltr\"\u003e9\u003c\/em\u003e\u003c\/sub\u003eO\u003csub dir=\"ltr\"\u003e\u003cem dir=\"ltr\"\u003e5\u003c\/em\u003e\u003c\/sub\u003e\n\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003cp\u003e\u003cstrong\u003eMolecular Weight:\u003c\/strong\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cstrong\u003eOther Known Titles\u003c\/strong\u003e\u003c\/p\u003e\n\u003cul\u003e\n\u003cli\u003e\n\u003cb dir=\"ltr\"\u003e\u003cem dir=\"ltr\"\u003eCJC-1295:\u003c\/em\u003e\u003c\/b\u003e\u003cem dir=\"ltr\"\u003e\u003cspan\u003e \u003c\/span\u003eCJC-1295 NO DAC; Mod GRF 1-29\u003c\/em\u003e\n\u003c\/li\u003e\n\u003cli\u003e\n\u003cb dir=\"ltr\"\u003e\u003cem dir=\"ltr\"\u003eIpamorelin:\u003c\/em\u003e\u003c\/b\u003e\u003cem dir=\"ltr\"\u003e\u003cspan\u003e \u003c\/span\u003eNNC 26-0161\u003c\/em\u003e\n\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003ch2\u003eResearch and Clinical Studies\u003c\/h2\u003e\n\u003ch3\u003e\u003cem\u003eCJC-1295 \u0026amp; Ipamorelin Blend and Half Life Determination\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eClinical studies have been conducted on test subjects to determine the half life of and individual pharmacokinetic profiles of the two peptides. In one late 1990s study,\u003csup dir=\"ltr\"\u003e(6)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003ea clinical trial was conducted on eight male test subjects with a concentration escalation design. The level of growth hormones was monitored after every instance of peptide presentation. At the end of the study, it was suggested by the researchers that there was a single episode of growth hormone release with the highest peak at 0.67 hours, after which there was an exponential decline up to negligible concentrations of the compound. This study concluded that the Ipamorelin peptide appeared to exhibit a short half-life of 2 hours, after which the potential action appears to begin to decline.\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003e\u003ca title=\"CJC-1295 for Sale - 5mg\" href=\"https:\/\/www.corepeptides.com\/peptides\/cjc-1295-no-dac-mod-grf-1-29\/\" dir=\"ltr\"\u003eCJC-1295\u003c\/a\u003e, by contrast, appears to have a much longer half-life. Researchers comment that a single introduction of the peptide may upregulate growth hormone production by somatotrophs for prolonged periods of time, thus apparently contributing “\u003ci dir=\"ltr\"\u003eto an overall increase in [growth hormone] secretion … by 46%\u003c\/i\u003e” and also potentially upregulating its main anabolic mediator insulin-like growth factor-1 (IGF-1) by 45% on average.\u003csup dir=\"ltr\"\u003e(7)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eAnother publication also observes that CJC-1295 may potentially upregulate “\u003ci dir=\"ltr\"\u003e[growth hormone] concentrations by 2- to 10-fold,\u003c\/i\u003e” and estimates that the half-life of the peptide ranges between 5.8 – 8.1 days.\u003csup dir=\"ltr\"\u003e(8)\u003c\/sup\u003e\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eCJC-1295 \u0026amp; Ipamorelin Blend General Research\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eIn this early 2000s study,\u003csup dir=\"ltr\"\u003e(7)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003ea clinical trial was conducted on male test subjects aged between 20 and 40 years old. Test subjects were divided into two groups; one group was presented with the placebo and the other with the peptide. Blood was sampled from the subjects one week before and after the presentation of CJC-1295 peptide (and placebo) to monitor the levels of growth hormone pulsatility. At the end of the study, it was suggested that CJC-1295 contributed to a 7.5-fold increase in the growth hormone pulsatility levels as compared to that of the placebo. Apart from apparently affecting the synthesis of growth hormone, scientists also suggest that CJC-1295 may interact with the survival and proliferation of the cells that synthesize it - the somatotroph cells in the anterior pituitary gland.\u003csup dir=\"ltr\"\u003e(9)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eIn one study on murine models, the authors commented that \"\u003ci dir=\"ltr\"\u003eCJC-1295 caused an increase in total pituitary RNA and GH mRNA, suggesting that proliferation of somatotroph cells had occurred, as confirmed by immunohistochemistry images.\u003c\/i\u003e”\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eTo exert these apparent effects, CJC-1295 appears to interact with specific binding sites on the GHRH receptor protein, leading to conformational changes in the receptor structure and potentially initiating a cascade of molecular events. The binding appears to activate intracellular signaling proteins that potentially act as molecular toggles.\u003csup dir=\"ltr\"\u003e(10)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eThese proteins are often referred to as G-proteins, which, upon activation, might drive the generation of secondary messengers like cyclic adenosine monophosphate (cAMP) or inositol trisphosphate (IP3.\u003csup dir=\"ltr\"\u003e(11)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eSecondary messengers such as cAMP may set in motion protein kinases, enzymes believed to alter distinct proteins. These kinases possess a modulatory capacity for cellular activities and might phosphorylate transcription regulators, or proteins overseeing gene modulation. Once phosphorylated, these transcription regulators could migrate into the nucleus of somatotroph cells, possibly impacting genes associated with growth hormone formation.\u003csup dir=\"ltr\"\u003e(7)\u003c\/sup\u003e\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eOn the other hand, Ipamorelin appears to interact with the anterior pituitary gland cells via the N-terminus of GHS-R1a, which has binding sites that appear to recognize specific sequences in the secretagogue. When Ipamorelin meets this receptor, it may attach in a non-permanent way through forces like hydrogen bonds and forces between molecules called van der Waals forces. This attachment might make the receptor change its shape, which could start cell signals, mainly those involving G-proteins. GHS-R1a might work with a specific part of G-proteins called Gαq\/11.\u003csup dir=\"ltr\"\u003e(12)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eA main process started by GHS-R1a involves an enzyme called phospholipase C (PLC). Gαq\/11 interacts with PLC, which may split a fat-like molecule, phosphatidylinositol 4,5-bisphosphate (PIP2), into two messaging molecules: IP3 (Inositol trisphosphate) and DAG (Diacylglycerol). IP3 appears to attach to places on a cell part called the endoplasmic reticulum, causing calcium ions (Ca2+) to be released. Also, DAG might turn on an enzyme called protein kinase C (PKC), which may add phosphate groups to other signaling molecules. All these steps might end with the ‘turning on’ of proteins that help release growth hormone from certain cells in the pituitary gland.\u003csup dir=\"ltr\"\u003e(13)\u003c\/sup\u003e\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eCJC-1295 \u0026amp; Ipamorelin Blend and Nitrogen Balance\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eThe apparent synergistic action of CJC-1295 and Ipamorelin on the production of growth hormone by the somatotroph cells in the anterior pituitary gland appears to result in a positive nitrogen balance and potential increase in lean mass in test models. In a particular study, investigators sought to probe the metabolic capabilities of Ipamorelin within the context of certain hepatic markers related to alpha-amino-nitrogen processing during an artificlaly triggered catabolism. The team evaluated the liver's ability to produce urea-N (CUNS), a potential metric of nitrogen processing within the liver. They examined the observable levels of messenger RNA (mRNA) linked to enzymes of the urea cycle in the liver, gauged the overall nitrogen equilibrium, and postulated the nitrogen quantities in different organs. It was proposed that Ipamorelin might have led to a 20% decline in CUNS, in contrast to the catabolic condition that was artificially prompted by the researchers. Moreover, it could have conceivably decreased the manifestation of urea cycle enzymes, reinstated nitrogen equilibrium, and theoretically adjusted or enhanced the nitrogen values in organs.\u003csup dir=\"ltr\"\u003e(14)\u003c\/sup\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cem dir=\"ltr\"\u003eCJC-1295 \u0026amp; Ipamorelin peptide blend is available for research and laboratory purposes only.\u003c\/em\u003e\u003c\/strong\u003e\u003c\/p\u003e\n\u003ch3\u003eReferences:\u003c\/h3\u003e\n\u003col\u003e\n\u003cli\u003eRaun K, Hansen BS, Johansen NL, Thøgersen H, Madsen K, Ankersen M, Andersen PH. Ipamorelin, the first selective growth hormone secretagogue. Eur J Endocrinol. 1998 Nov;139(5):552-61. doi: 10.1530\/eje.0.1390552. PMID: 9849822.\u003ca href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/9849822\/\" rel=\"noopener\" dir=\"ltr\"\u003e\u003cspan\u003e \u003c\/span\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/9849822\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eLucie Jette et al, hGRF1-29-Albumin Bioconjugates Activate the GRF Receptor on the Anterior Pituitary in Rats: Identification of CJC-1295 as a Long Lasting GRF Analog, ResearchGate, January 2005.\u003c\/li\u003e\n\u003cli\u003eRaun K, Hansen BS, Johansen NL, Thøgersen H, Madsen K, Ankersen M, Andersen PH. Ipamorelin, the first selective growth hormone secretagogue. Eur J Endocrinol. 1998 Nov;139(5):552-61. doi: 10.1530\/eje.0.1390552. PMID: 9849822\u003ca href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/9849822\/\" rel=\"noopener\" dir=\"ltr\"\u003e\u003cspan\u003e \u003c\/span\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/9849822\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eThe Discovery of Growth Hormone-Releasing Hormone: An Update\u003ca href=\"https:\/\/onlinelibrary.wiley.com\/doi\/full\/10.1111\/j.1365-2826.2008.01740.x\" rel=\"noopener\" dir=\"ltr\"\u003e\u003cspan\u003e \u003c\/span\u003ehttps:\/\/onlinelibrary.wiley.com\/doi\/full\/10.1111\/j.1365-2826.2008.01740.x\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eJetté, L., Léger, R., Thibaudeau, K., Benquet, C., Robitaille, M., Pellerin, I., Paradis, V., van Wyk, P., Pham, K., \u0026amp; Bridon, D. P. (2005). Human growth hormone-releasing factor (hGRF)1-29-albumin bioconjugates activate the GRF receptor on the anterior pituitary in rats: identification of CJC-1295 as a long-lasting GRF analog. Endocrinology, 146(7), 3052–3058.\u003cspan\u003e \u003c\/span\u003e\u003ca href=\"https:\/\/doi.org\/10.1210\/en.2004-1286\" rel=\"noopener\" dir=\"ltr\"\u003ehttps:\/\/doi.org\/10.1210\/en.2004-1286\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eGobburu JV, Agersø H, Jusko WJ, Ynddal L (September 1999). “Pharmacokinetic-pharmacodynamic modeling of ipamorelin, a growth hormone releasing peptide, in human volunteers”. Pharmaceutical Research. 16 (9): 1412–6. doi:10.1023\/A:1018955126402\u003c\/li\u003e\n\u003cli\u003eIonescu M, Frohman LA. Pulsatile secretion of growth hormone (GH) persists during continuous stimulation by CJC-1295, a long-acting GH-releasing hormone analog. J Clin Endocrinol Metab. 2006 Dec;91(12):4792-7. doi: 10.1210\/jc.2006-1702. Epub 2006 Oct 3. PMID: 17018654.\u003ca href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/17018654\/\" rel=\"noopener\" dir=\"ltr\"\u003e\u003cspan\u003e \u003c\/span\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/17018654\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eTeichman SL, Neale A, Lawrence B, Gagnon C, Castaigne JP, Frohman LA. Prolonged stimulation of growth hormone (GH) and insulin-like growth factor I secretion by CJC-1295, a long-acting analog of GH-releasing hormone, in healthy adults. J Clin Endocrinol Metab. 2006 Mar;91(3):799-805. doi: 10.1210\/jc.2005-1536. Epub 2005 Dec 13. PMID: 16352683.\u003ca href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/16352683\/\" rel=\"noopener\" dir=\"ltr\"\u003e\u003cspan\u003e \u003c\/span\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/16352683\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eAlba, M., Fintini, D., Sagazio, A., Lawrence, B., Castaigne, J. P., Frohman, L. A., \u0026amp; Salvatori, R. (2006). Once-daily administration of CJC-1295, a long-acting growth hormone-releasing hormone (GHRH) analog, normalizes growth in the GHRH knockout mouse.\u003cspan\u003e \u003c\/span\u003e\u003ci dir=\"ltr\"\u003eAmerican journal of physiology. Endocrinology and metabolism\u003c\/i\u003e,\u003cspan\u003e \u003c\/span\u003e\u003ci dir=\"ltr\"\u003e291\u003c\/i\u003e(6), E1290–E1294.\u003cspan\u003e \u003c\/span\u003e\u003ca href=\"https:\/\/doi.org\/10.1152\/ajpendo.00201.2006\" rel=\"noopener\" dir=\"ltr\"\u003ehttps:\/\/doi.org\/10.1152\/ajpendo.00201.2006\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eMartin, B., Lopez de Maturana, R., Brenneman, R., Walent, T., Mattson, M. P., \u0026amp; Maudsley, S. (2005). Class II G protein-coupled receptors and their ligands in neuronal function and protection.\u003cspan\u003e \u003c\/span\u003e\u003ci dir=\"ltr\"\u003eNeuromolecular medicine\u003c\/i\u003e,\u003cspan\u003e \u003c\/span\u003e\u003ci dir=\"ltr\"\u003e7\u003c\/i\u003e(1-2), 3–36.\u003cspan\u003e \u003c\/span\u003e\u003ca href=\"https:\/\/doi.org\/10.1385\/nmm:7:1-2:003\" rel=\"noopener\" dir=\"ltr\"\u003ehttps:\/\/doi.org\/10.1385\/nmm:7:1-2:003\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eNewton, A. C., Bootman, M. D., \u0026amp; Scott, J. D. (2016). Second Messengers.\u003cspan\u003e \u003c\/span\u003e\u003ci dir=\"ltr\"\u003eCold Spring Harbor perspectives in biology\u003c\/i\u003e,\u003cspan\u003e \u003c\/span\u003e\u003ci dir=\"ltr\"\u003e8\u003c\/i\u003e(8), a005926.\u003cspan\u003e \u003c\/span\u003e\u003ca href=\"https:\/\/doi.org\/10.1101\/cshperspect.a005926\" rel=\"noopener\" dir=\"ltr\"\u003ehttps:\/\/doi.org\/10.1101\/cshperspect.a005926\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eYin, Y., Li, Y., \u0026amp; Zhang, W. (2014). The growth hormone secretagogue receptor: its intracellular signaling and regulation.\u003cspan\u003e \u003c\/span\u003e\u003ci dir=\"ltr\"\u003eInternational journal of molecular sciences\u003c\/i\u003e,\u003cspan\u003e \u003c\/span\u003e\u003ci dir=\"ltr\"\u003e15\u003c\/i\u003e(3), 4837–4855.\u003cspan\u003e \u003c\/span\u003e\u003ca href=\"https:\/\/doi.org\/10.3390\/ijms15034837\" rel=\"noopener\" dir=\"ltr\"\u003ehttps:\/\/doi.org\/10.3390\/ijms15034837\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eBill, C. A., \u0026amp; Vines, C. M. (2020). Phospholipase C.\u003cspan\u003e \u003c\/span\u003e\u003ci dir=\"ltr\"\u003eAdvances in experimental medicine and biology\u003c\/i\u003e,\u003cspan\u003e \u003c\/span\u003e\u003ci dir=\"ltr\"\u003e1131\u003c\/i\u003e, 215–242.\u003cspan\u003e \u003c\/span\u003e\u003ca href=\"https:\/\/doi.org\/10.1007\/978-3-030-12457-1_9\" rel=\"noopener\" dir=\"ltr\"\u003ehttps:\/\/doi.org\/10.1007\/978-3-030-12457-1_9\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eAagaard, N. K., Grøfte, T., Greisen, J., Malmlöf, K., Johansen, P. B., Grønbaek, H., Ørskov, H., Tygstrup, N., \u0026amp; Vilstrup, H. (2009). Growth hormone and growth hormone secretagogue effects on nitrogen balance and urea synthesis in steroid treated rats.\u003cspan\u003e \u003c\/span\u003e\u003ci dir=\"ltr\"\u003eGrowth hormone \u0026amp; IGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society\u003c\/i\u003e,\u003cspan\u003e \u003c\/span\u003e\u003ci dir=\"ltr\"\u003e19\u003c\/i\u003e(5), 426–431.\u003cspan\u003e \u003c\/span\u003e\u003ca href=\"https:\/\/doi.org\/10.1016\/j.ghir.2009.01.001\" rel=\"noopener\" dir=\"ltr\"\u003ehttps:\/\/doi.org\/10.1016\/j.ghir.2009.01.001\u003c\/a\u003e\n\u003c\/li\u003e\n\u003c\/ol\u003e","brand":"PureX Labs","offers":[{"title":"10mg","offer_id":47548298002676,"sku":null,"price":50.0,"currency_code":"USD","in_stock":false},{"title":"20mg","offer_id":48318298063092,"sku":null,"price":100.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0804\/5802\/3156\/files\/Render_Mockup_1920_1920_2026-01-31_7.png?v=1769804832"},{"product_id":"cjc-1295","title":"CJC-1295","description":"\u003cp data-end=\"505\" data-start=\"188\"\u003eCJC-1295 is a synthetic 29–amino acid analog of growth hormone–releasing hormone (GHRH) designed to stimulate the pituitary gland to release endogenous growth hormone (GH). It represents the shortest functional fragment of GHRH capable of activating somatotroph cells, which are responsible for GH production.\u003c\/p\u003e\n\u003cp data-end=\"820\" data-start=\"507\"\u003eThe peptide contains four amino acid substitutions compared to native GHRH. These modifications are theorized to enhance stability, receptor affinity, and resistance to enzymatic degradation, resulting in a longer functional duration than natural GHRH while preserving physiological, pulsatile GH release.\u003c\/p\u003e\n\u003cp data-end=\"1203\" data-start=\"822\"\u003eBy binding to GHRH receptors, CJC-1295 is believed to activate intracellular signaling pathways involving G-proteins and secondary messengers such as cAMP, which may promote GH gene expression. Increased GH secretion may subsequently elevate insulin-like growth factor-1 (IGF-1) levels, a hormone associated with protein synthesis, tissue growth, and cellular regeneration.\u003c\/p\u003e\n\u003cp data-end=\"1489\" data-start=\"1205\"\u003eCJC-1295 has been studied for its potential role in lean muscle support, fat metabolism, bone and connective tissue maintenance, and sleep-related neuroendocrine function. Due to its modified structure, it is reported to have a longer half-life (~30 minutes) than native GHRH.\u003c\/p\u003e\n\u003cp data-end=\"1558\" data-start=\"1491\"\u003eCJC-1295 is intended for research and laboratory purposes only.\u003c\/p\u003e","brand":"PureX Labs","offers":[{"title":"5mg","offer_id":47548299084020,"sku":null,"price":35.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0804\/5802\/3156\/files\/Render_Mockup_1920_1920_2026-01-31_8.png?v=1769804832"},{"product_id":"mots-c","title":"MOTS-c","description":"\u003cp dir=\"ltr\"\u003eMOTS-c (mitochondrial open-reading-frame of the 12S rRNA-c) peptide is a novel mitochondria-derived peptide. It is a short peptide composed of 16 amino acids, expressed in tissues and plasma, indicating a cell-specific and hormonal role.\u003csup dir=\"ltr\"\u003e(1)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eWith the potential to work both as a cell-specific compound and as a hormone, this peptide possibly acts by stimulating the AMP-activated protein kinase (AMPK) pathway. Only two mitochondrial-derived peptides (MDPs) have been studied, Humanin and MOTS-c. When metabolic stress occurs in the organism, the peptide is believed to translocate to the cellular nuclei and alter the gene expression. MOTS-c peptide may also be released extracellularly and is known as \"\u003cem dir=\"ltr\"\u003emitochondrial hormone\u003c\/em\u003e\" or simply as \"\u003cem dir=\"ltr\"\u003emitokine.\u003c\/em\u003e”\u003cspan\u003e \u003c\/span\u003e\u003csup dir=\"ltr\"\u003e(2)(3)\u003c\/sup\u003e\u003c\/p\u003e\n\u003ch3 dir=\"ltr\"\u003eChemical Makeup\u003csup dir=\"ltr\"\u003e(4)\u003c\/sup\u003e\n\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003e\u003cstrong dir=\"ltr\"\u003eMolecular Formula:\u003c\/strong\u003e\u003cspan\u003e \u003c\/span\u003eC\u003csub dir=\"ltr\"\u003e101\u003c\/sub\u003eH\u003csub dir=\"ltr\"\u003e152\u003c\/sub\u003eN\u003csub dir=\"ltr\"\u003e28\u003c\/sub\u003eO\u003csub dir=\"ltr\"\u003e22\u003c\/sub\u003eS\u003csub dir=\"ltr\"\u003e2\u003c\/sub\u003e\u003cbr dir=\"ltr\"\u003e\u003cstrong dir=\"ltr\"\u003eMolecular Weight:\u003c\/strong\u003e\u003cspan\u003e \u003c\/span\u003e2174.64 g\/mol\u003cbr dir=\"ltr\"\u003e\u003cstrong dir=\"ltr\"\u003eOther Titles:\u003c\/strong\u003e\u003cspan\u003e \u003c\/span\u003eMitochondrial-derived peptide MOTS-c, Mitochondrial open reading frame of the 12S rRNA-c\u003c\/p\u003e\n\u003ch2\u003eResearch and Clinical Studies\u003c\/h2\u003e\n\u003cp dir=\"ltr\"\u003eAnimal research models have indicated multiple potential actions from MOTS-c peptide, including increased physical performance, regulated cellular and tissue metabolism, and myoblast adaptation.\u003csup dir=\"ltr\"\u003e(2)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eResearch suggests that these actions may primarily depend on age and age-related changes in MOTS-c expression. The researchers suggest MOTS-c levels and activity might decline, hinting at a role in the cell aging process and the development of age-related metabolic dysfunction. Furthermore, MOTS-c may interact with known aging regulators, such as NAD+ and sirtuins, suggesting its involvement in pathways potentially modulating the lifespan of the cell.\u003csup dir=\"ltr\"\u003e(1)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eAs per Joseph C Reynolds et al.,\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003e“Mitochondria are chief metabolic organelles with strong implications in cell aging that also coordinate broad physiological functions, in part, using peptides that are encoded within their independent genome.”\u003c\/em\u003e\u003csup dir=\"ltr\"\u003e(4)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eThe peptide endogenous expression has also been posited to be boosted via physical activity, potentially enhancing cellular metabolism.\u003csup dir=\"ltr\"\u003e(5)\u003c\/sup\u003e\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eMOTS-c Peptide and Muscle Metabolism\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eWith increasing age, skeletal muscles tend to gain insulin resistance, leading to decreased glucose uptake. Upon peptide exposure, skeletal muscles may be stimulated with an improved response toward AMPK activation. As a result, glucose transporter expression may increase, potentially improving skeletal muscle metabolism and enhancing skeletal muscle functioning and growth. Further, MOTS-c's actions are posited to include targeting metabolic pathways such as the folate-methionine cycle and purine biosynthesis. This targeting may potentially lead to a modulation of cellular metabolism, including actions on glucose uptake and lipid utilization. The peptide's impact might involve a shift in metabolic priorities within the cell, possibly affecting the balance between anabolic and catabolic processes. In systemic metabolism, MOTS-c is posited to function as a mitochondrial hormone, with circulating peptide levels appearing to affect metabolic functions in skeletal muscle and possibly adipose tissue. Its potential regulatory actions on glucose homeostasis and insulin action suggest a broader hormonal role in energy balance and nutrient sensing across different tissues.\u003csup dir=\"ltr\"\u003e(1)\u003c\/sup\u003e\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eMOTS-c Peptide and Fat Cell Metabolism\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eResearch has suggested that the peptide may potentially leave the mitochondrial site, translocate to cellular nuclei, and possibly alter gene expression. More specifically, the peptide may interact with a broad range of genes, particularly those with antioxidant response elements (ARE), hinting at a potential regulatory relationship with stress-responsive transcription factors like NRF2. Such findings suggest a genetically integrated system of mitonuclear communication, where both mitochondrial and nuclear genomes may encode factors that cross-regulate each other. This action, in turn, may alter glucose uptake restriction.\u003csup dir=\"ltr\"\u003e(6)\u003cspan\u003e \u003c\/span\u003e\u003c\/sup\u003eThis hypothesis was first suggested from a study in which the experimental mice were given high-fat food, and only half were presented with the peptide. The researchers indicated that MOTS-c may potentially impact cellular metabolism by inhibiting the folate cycle directly tethered de novo purine biosynthesis, consequently leading to AMPK activation. Such actions hint at a broader role of the peptide in regulating insulin sensitivity and metabolic homeostasis, offering insights into its preventive potential against age-dependent and high-fat-induced insulin resistance and diet-induced obesity. The study presents supportive data to suggest that the peptide may stimulate glucose utilization, affect the methionine-folate cycle, and promote AMPK activation. These cellular actions suggest that MOTS-c might coordinate various metabolic processes, including glucose and lipid metabolism. Consequently, the murine models exposed to the peptide were lean and more energetic than the rest, further indicating that the peptide might prevent fat accumulation and induce glucose uptake via the AMPK pathway.\u003csup dir=\"ltr\"\u003e(3)\u003c\/sup\u003e\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eMOTS-c Peptide and Bone\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eMOTS-c peptide has been suggested to regulate the transforming growth factor beta (TGF-beta)\/SMAD pathway, which may profoundly affect bone tissues.\u003csup dir=\"ltr\"\u003e(7)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eMore specifically, MOTS-c's actions may involve the upregulation of TGF-β\/Smad pathway-related genes, including TGF-β1, TGF-β2, and Smad7, suggesting a pivotal role of this pathway in MOTS-c mediated osteogenic differentiation. This hypothesis is further supported when the osteogenic differentiation promoted by MOTS-c is reversed upon TGF-β1 knockdown, indicating that MOTS-c's actions may be at least partly mediated through the TGF-β\/Smad pathway. The peptide may also stimulate the expression of osteogenesis-related genes such as ALP, Bglap, and Runx2. Thus, this peptide may stimulate the SMAD pathway in the osteoblast cells, possibly improving bone density and strength. When studied in bone marrow cells, this compound appeared to trigger the differentiation of the stem cells, which may lead to bone tissue development.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eMOTS-c Peptide and Cardiac Function\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eThe peptide has not been suggested by researchers to directly influence cardiac function; instead, researchers posit that the peptide exerts potential on the endothelial cells that line the blood vessels inside. These endothelial tissues are considered to affect blood pressure and clotting. The researchers suspect a positive correlation exists between MOTS-c levels and microvascular and epicardial endothelial function. Such findings tentatively suggest MOTS-c as a potential biomarker for endothelial function, with the study revealing a nuanced relationship between MOTS-c levels and vascular reactivity. Further, the research suggested that when mice were exposed to MOTS-c, it appeared to improve the endothelial tissues' functioning, thereby possibly facilitating dysfunction. The mechanistic basis for MOTS-c's action on endothelial function remains speculative but may involve the activation of AMPK.\u003csup dir=\"ltr\"\u003e(8)\u003c\/sup\u003e\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eMOTS-c Peptide and Cell Lifespan\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eResearch has suggested that the peptide may be associated with enhanced longevity on a cellular level. The peptide typically contains glutamate residue, but when this is replaced by lysine, the new compound may exert a functional change. Scientists so far are aware that the functionality of the glutamate and lysine groups are vastly different, but how this specific structural change affects peptide functionality is yet to be understood. Noriyuki Fuku et al. suggests that there is\u003cspan\u003e \u003c\/span\u003e\u003cem dir=\"ltr\"\u003e“a biological link between MOTS-c and extended lifespan through the putative endocrine action of this mitokine. Further mechanistic research is needed to determine the functional significance of polymorphism and the potential influence of MOTS-c in the [...] aging process.”\u003c\/em\u003e\u003cspan\u003e \u003c\/span\u003e\u003csup dir=\"ltr\"\u003e(9)\u003c\/sup\u003e\u003c\/p\u003e\n\u003cp\u003e\u003cem\u003e\u003cstrong dir=\"ltr\"\u003eThe peptide is available for research and laboratory purposes only.\u003c\/strong\u003e\u003c\/em\u003e\u003c\/p\u003e\n\u003ch3\u003eReferences:\u003c\/h3\u003e\n\u003col\u003e\n\u003cli\u003eLee C, Kim KH, Cohen P. MOTS-c: A novel mitochondrial-derived peptide regulating muscle and fat metabolism. Free Radic Biol Med. 2016 Nov;100:182-187. doi: 10.1016\/j.freeradbiomed.2016.05.015. Epub 2016 May 20. PMID: 27216708; PMCID: PMC5116416.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC5116416\/\"\u003ehttps:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC5116416\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eMohtashami Z, Singh MK, Salimiaghdam N, Ozgul M, Kenney MC. Most Recent Mitochondrial Derived Peptide in Human Aging and Age-Related Diseases. Int J Mol Sci. 2022 Oct 9;23(19):11991.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/doi.org\/10.3390\/ijms231911991\"\u003edoi: 10.3390\/ijms231911991\u003c\/a\u003e. PMID: 36233287; PMCID: PMC9570330.\u003c\/li\u003e\n\u003cli\u003eLee C, Zeng J, Drew BG, Sallam T, Martin-Montalvo A, Wan J, Kim SJ, Mehta H, Hevener AL, de Cabo R, Cohen P. The mitochondrial-derived peptide MOTS-c promotes metabolic homeostasis and reduces obesity and insulin resistance. Cell Metab. 2015 Mar 3;21(3):443-54.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/doi.org\/10.1016\/j.cmet.2015.02.009\"\u003edoi: 10.1016\/j.cmet.2015.02.009\u003c\/a\u003e. PMID: 25738459; PMCID: PMC4350682.\u003c\/li\u003e\n\u003cli\u003eLu H, Wei M, Zhai Y, Li Q, Ye Z, Wang L, Luo W, Chen J, Lu Z. MOTS-c peptide regulates adipose homeostasis to prevent ovariectomy-induced metabolic dysfunction. J Mol Med (Berl). 2019 Apr;97(4):473-485. doi: 10.1007\/s00109-018-01738-w. Epub 2019 Feb 6. PMID: 30725119.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/30725119\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/30725119\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eReynolds JC, Lai RW, Woodhead JST, Joly JH, Mitchell CJ, Cameron-Smith D, Lu R, Cohen P, Graham NA, Benayoun BA, Merry TL, Lee C. MOTS-c is an exercise-induced mitochondrial-encoded regulator of age-dependent physical decline and muscle homeostasis. Nat Commun. 2021 Jan 20;12(1):470.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/33473109\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/33473109\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eKim KH, Son JM, Benayoun BA, Lee C. The Mitochondrial-Encoded Peptide MOTS-c Translocates to the Nucleus to Regulate Nuclear Gene Expression in Response to Metabolic Stress. Cell Metab. 2018 Sep 4;28(3):516-524.e7. doi: 10.1016\/j.cmet.2018.06.008. Epub 2018 Jul 5. PMID: 29983246; PMCID: PMC6185997.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC6185997\/\"\u003ehttps:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC6185997\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eHu BT, Chen WZ. MOTS-c improves osteoporosis by promoting osteogenic differentiation of bone marrow mesenchymal stem cells via TGF-β\/Smad pathway. Eur Rev Med Pharmacol Sci. 2018 Nov;22(21):7156-7163. doi: 10.26355\/eurrev_201811_16247. PMID: 30468456.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/30468456\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/30468456\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eQin Q, Delrio S, Wan J, Jay Widmer R, Cohen P, Lerman LO, Lerman A. Downregulation of circulating MOTS-c levels in patients with coronary endothelial dysfunction. Int J Cardiol. 2018 Mar 1;254:23-27. doi: 10.1016\/j.ijcard.2017.12.001. Epub 2017 Dec 6. PMID: 29242099.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/29242099\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/29242099\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eNoriyuki Fuku el al., The mitochondrial-derived peptide: A player in exceptional longevity?,\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/dx.doi.org\/10.1111\/acel.12389\"\u003ehttp:\/\/dx.doi.org\/10.1111\/acel.12389\u003c\/a\u003e.\u003c\/li\u003e\n\u003c\/ol\u003e","brand":"PureX Labs","offers":[{"title":"10mg","offer_id":47548300558580,"sku":null,"price":40.0,"currency_code":"USD","in_stock":true},{"title":"40mg","offer_id":48353466843380,"sku":null,"price":140.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0804\/5802\/3156\/files\/Render_Mockup_1920_1920_2026-01-31_9.png?v=1769804832"},{"product_id":"aod-9604","title":"AOD-9604","description":"\u003cp dir=\"ltr\"\u003eAOD 9604 peptide is a synthetic analog of growth hormone designed with the intention of mitigating obesity and aiding weight loss. The peptide is a modified fragment of the growth hormone where the last 16 amino acids (176-191) have been reproduced as a specific peptide, called GH Fragment 176-191 or simply AOD 9604. It also has a tyrosine residue to replace the first amino acid at the N-terminus, which researchers consider to help increase the stability of the peptide.\u003csup dir=\"ltr\"\u003e(1)\u003c\/sup\u003e\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eMore specifically, AOD 9604 is considered the lipolytic fragment of GH as different parts of the GH molecule appease to have different potentials. For instance, studies suggest that out of its 191 amino acid structure “\u003ci dir=\"ltr\"\u003ethe N-terminal region exhibits an insulin-potentiating action, while amino acids 108 - 129 of hGH were found to evoke high mitogenic responses.\u003c\/i\u003e”\u003csup dir=\"ltr\"\u003e(2)\u003c\/sup\u003e\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eAOD 9604 peptide was developed in the 1990s in an effort to develop proteins which might exhibit anti-obesity properties similar to Growth Hormone (hGH). Rigorous scientific studies and experiments have since been conducted to determine the potential action of AOD 9604 in lipolysis.\u003csup dir=\"ltr\"\u003e(1)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eLipolysis is a term to describe the process through which stored fats or triglycerides in fat cells are broken down into glycerol and free fatty acids, which may be used as an energy source by other cells. Enzymes such as lipase appear to play a critical role in this process, helping in the breakdown of these fats. It's possible that AOD9604 may influence the fat cells and lipolytic receptors, particularly given its observed association with changes in weight and fat in murine models. Research study findings indicate that the fragment seems to have the capacity to amplify lipolytic sensitivity following its introduction. Furthermore, the study hypothesizes a potential interaction of AOD9604 with the beta-adrenergic pathway, especially concerning the beta(3)-adrenergic receptors (beta(3)-AR), which are considered to be key lipolytic receptors found in fat cells. While it is not entirely clear, the expression level of beta(3)-AR RNA, the primary lipolytic receptor in fat cells, was observed to increase in the presence of AOD 9604. This could possibly suggest that the peptide might be playing a role in enhancing the sensitivity of these lipolytic receptors, potentially making them more responsive to lipolytic stimuli. However, it is essential to note that while the peptide appears to elevate the expression of beta(3)-AR, it may not act directly through the beta(3)-AR to induce its potential lipolytic action.\u003c\/p\u003e\n\u003cp\u003eScientists and researchers have suggested that the modified portion of the hGH in the AOD 9604 peptide may be responsible for significantly inducing the fat burning process, possibly without stimulating the production of Insulin-like Growth Factor IGF 1, as opposed to the natural growth hormone.\u003c\/p\u003e\n\u003ch3\u003eChemical Makeup\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003e\u003cstrong dir=\"ltr\"\u003eMolecular Formula:\u003cspan\u003e \u003c\/span\u003e\u003c\/strong\u003eC\u003csub dir=\"ltr\"\u003e78\u003c\/sub\u003eH\u003csub dir=\"ltr\"\u003e123\u003c\/sub\u003eN\u003csub dir=\"ltr\"\u003e23\u003c\/sub\u003eO\u003csub dir=\"ltr\"\u003e23\u003c\/sub\u003eS\u003csub dir=\"ltr\"\u003e2\u003c\/sub\u003e\u003cbr dir=\"ltr\"\u003e\u003cstrong dir=\"ltr\"\u003eMolecular Weight:\u003cspan\u003e \u003c\/span\u003e\u003c\/strong\u003e1815.12 g\/mol\u003cbr dir=\"ltr\"\u003e\u003cstrong dir=\"ltr\"\u003eOther Known Titles:\u003c\/strong\u003e\u003cspan\u003e \u003c\/span\u003eTyr-hGH Fragment 177-191\u003c\/p\u003e\n\u003ch2\u003eResearch and Clinical Studies\u003c\/h2\u003e\n\u003ch3\u003e\u003cem\u003eAOD 9604 Peptide and Lipolytic Activity\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eEarly studies were carried out on obese mice where the AOD 9604 peptide was periodically introduced for 14 days. Following the experiment, the results reported a reduction in weight and excess fat. These results appeared directly correlated with the increased levels of major lipolytic receptors, beta(3)-AR, found in the fat cells. AOD 9604 peptide appeared to exhibit action similar to hGH wherein both may be capable of increasing repressed levels of lipolytic receptors in obese mice as compared to the lean mice. To confirm whether the lipolytic action of AOD 9604 might merely be associated with the increased lipolytic receptor levels, additional studies were carried out where AOD 9604 was given to mice with knocked out lipolytic receptors. Further analysis suggested that the AOD 9604 peptide enacted the lipolytic action via increased energy expenditure and fat oxidation.\u003csup dir=\"ltr\"\u003e(1)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eBoth these findings on chronic and acute action of AOD 9604 suggested that while enhanced beta(3)-AR expression may have played a role in the chronic action of the compound, beta(3)-AR might not be the sole arbiter in this reaction. Oxidation and enhanced energy expenditure appeared to be vital in the proposed action of the peptide.\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eIn 2000, a research study was carried out in obese Zucker rats where the AOD 9604 peptide was given daily for 19 consecutive days. Following the study, it was reported that weight appeared to be reduced in all rats by over 50%, in comparison to the rats given a placebo. Further analysis suggested that the adipose tissues of the AOD 9604 peptide animals had increased lipolytic activity and no marked insulin sensitivity interruption in the animals.\u003csup dir=\"ltr\"\u003e(3)\u003c\/sup\u003e\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eAOD 9604 Peptide and Obesity\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eIn 2004, clinical trials observed the actions of the peptide in 300 obese subjects who were given the peptide for 12 weeks. The rate of weight loss remained consistent throughout the study period. The trial results noted minor improvement exhibited in the subjects’ cholesterol profiles and glucose tolerance levels.\u003csup dir=\"ltr\"\u003e(4)\u003c\/sup\u003e\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eAOD 9604 Peptide and Cell Regeneration\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eAdditional research was conducted to study the regenerative potential of the peptide. In 2015, 32 white rabbits were divided into four groups of eight, and each group was given a placebo, AOD 9604, hyaluronic acid, or a combination of AOD 9604 and hyaluronic acid for 4 to 7 weeks. After the study, these rabbits were assessed morphologically and histopathologically to determine the degree of cartilage degeneration. It was concluded that rabbits given the combination of AOD 9604 with hyaluronic acid apparently exhibited the least degeneration. Thus, it was suggested by the researchers that AOD 9604 might exhibit potential to enhance cartilage regeneration and cartilage repair in some capacity.\u003csup dir=\"ltr\"\u003e(5)\u003c\/sup\u003e\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eThis may be due to the potential role of AOD 9604 in cellular differentiation processes and, potentially, in the synthesis of proteins important for tissue repair. According to an\u003cspan\u003e \u003c\/span\u003e\u003ci dir=\"ltr\"\u003ein vitro\u003cspan\u003e \u003c\/span\u003e\u003c\/i\u003estudy, AOD 9604 may possibly enhance the differentiation of adipose mesenchymal stem cells into bone\u003csup dir=\"ltr\"\u003e(5)\u003c\/sup\u003e. These stem cells, which are typically found within fat tissue, may have the potential to evolve into various cell types. It has been hypothesized that under the influence of AOD 9604, these stem cells may show a predisposition to differentiate into bone cells. Moreover, when the research was conducted on isolated bovine chondrocytes, it appeared that there might be an increased production of proteoglycan and collagen. Chondrocytes are cells believed to be found within cartilage tissue, and they possibly play a role in producing and maintaining the extracellular matrix, which consists of components like collagen and proteoglycans. It is posited that the presence of AOD 9604 could stimulate these chondrocytes to produce more of these vital components. The study also hints at the idea that AOD 9604 might promote the differentiation of myoblasts into C2C12 cells. Myoblasts are thought to be precursor muscle cells, and C2C12 cells are a type of murine model muscle cell line. From what the study suggests, AOD 9604 may assist in the transition of these precursor cells into a more mature form. The research seems to underline the potential role AOD 9604 might have in processes connected to the repair of bone, cartilage, and muscle tissues.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eAOD 9604 and Research in Cancer Cells\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eThe peptide may be able to bind (target) tumor-related proteins to enhance tumor drug accumulation and local cytotoxicity.\u003csup dir=\"ltr\"\u003e(6)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eThe hGH fragment AOD 9604 may potentially play a pivotal role in cancer cell research, as it has been observed to enhance the anticancer efficacy of doxorubicin, a commonly recognized chemotherapeutic agent. One study utilized chitosan nanoparticles, a biocompatible and biodegradable polymer, as a carrier for doxorubicin and AOD 9604.\u003csup dir=\"ltr\"\u003e(6)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eThe research team hypothesized that AOD 9604 possibly enhanced the doxorubicin binding to multiple breast cancer cell protein targets, thereby exhibiting greater anti-proliferative activity against the MCF-7 breast cancer cell line compared to chitosan loaded with doxorubicin alone. This suggests that AOD 9604 may potentially augment the anti-cancer potency of doxorubicin while possibly minimizing unintended actions associated with non-target tissue exposure. In conclusion, multiple clinical studies have suggested that the peptide may significantly induce lipolysis and possibly prevent lipogenesis by mimicking natural hGH.\u003c\/p\u003e\n\u003cp\u003e\u003cem\u003e\u003cstrong dir=\"ltr\"\u003eAOD 9604 is available for research and laboratory purposes only.\u003c\/strong\u003e\u003c\/em\u003e\u003c\/p\u003e\n\u003ch3\u003eReferences:\u003c\/h3\u003e\n\u003col\u003e\n\u003cli\u003eMark Heffernan, Roger J. Summers, Anne Thorburn, Esra Ogru, Robert Gianello, Woei-Jia Jiang, Frank M. Ng, The Effects of Human GH and Its Lipolytic Fragment (AOD 9604) on Lipid Metabolism Following Chronic Treatment in Obese Mice and β 3-AR Knock-Out Mice, Endocrinology, Volume 142, Issue 12, 1 December 2001, Pages 5182–5189.\u003ca href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/11713213\/\" rel=\"noopener\" dir=\"ltr\"\u003e\u003cspan\u003e \u003c\/span\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/11713213\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eMoré, M. I., \u0026amp; Kenley, D. (2014). Safety and metabolism of AOD9604, a novel nutraceutical ingredient for improved metabolic health.\u003cspan\u003e \u003c\/span\u003e\u003ci dir=\"ltr\"\u003eJournal of Endocrinology and Metabolism\u003c\/i\u003e,\u003cspan\u003e \u003c\/span\u003e\u003ci dir=\"ltr\"\u003e4\u003c\/i\u003e(3), 64-77.\u003c\/li\u003e\n\u003cli\u003eFrank M. Ng, J Sun et.al, Metabolic Studies of a Synthetic Lipolytic Domain (AOD 9604) of Human Growth Hormone, Hormone Research, February 2000.\u003c\/li\u003e\n\u003cli\u003eNews, Medical and Life Sciences, Obesity drug codenamed AOD 9604 highly successful in trials, 16 December 2004.\u003c\/li\u003e\n\u003cli\u003eDong Rak Kwon and GI Young Park, Effect of Intra-articular Injection of AOD9604 with or without Hyaluronic Acid in Rabbit Osteoarthritis Model, Annals of Clinical and Laboratory Science, Volume 45, July-August 2015.\u003c\/li\u003e\n\u003cli\u003eHabibullah, M. M., Mohan, S., Syed, N. K., Makeen, H. A., Jamal, Q. M. S., Alothaid, H., Bantun, F., Alhazmi, A., Hakamy, A., Kaabi, Y. A., Samlan, G., Lohani, M., Thangavel, N., \u0026amp; Al-Kasim, M. A. (2022). Human Growth Hormone Fragment 176-191 Peptide Enhances the Toxicity of Doxorubicin-Loaded Chitosan Nanoparticles Against MCF-7 Breast Cancer Cells.\u003cspan\u003e \u003c\/span\u003e\u003ci dir=\"ltr\"\u003eDrug design, development and therapy\u003c\/i\u003e,\u003cspan\u003e \u003c\/span\u003e\u003ci dir=\"ltr\"\u003e16\u003c\/i\u003e, 1963–1974.\u003cspan\u003e \u003c\/span\u003e\u003ca href=\"https:\/\/doi.org\/10.2147\/DDDT.S367586\" rel=\"noopener\" dir=\"ltr\"\u003ehttps:\/\/doi.org\/10.2147\/DDDT.S367586\u003c\/a\u003e\n\u003c\/li\u003e\n\u003c\/ol\u003e","brand":"PureX Labs","offers":[{"title":"5mg","offer_id":47548302196980,"sku":null,"price":60.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0804\/5802\/3156\/files\/Render_Mockup_1920_1920_2026-01-31_10.png?v=1769804832"},{"product_id":"5-amino-1mq","title":"5-Amino-1MQ","description":"\u003cp data-start=\"155\" data-end=\"499\"\u003e5-Amino-1MQ is a research-grade inhibitor of nicotinamide N-methyltransferase (NNMT), an enzyme involved in cellular methylation balance and nicotinamide metabolism. NNMT activity has been associated with regulation of adipocyte energy balance, lipid storage, and insulin signaling, making it a target of interest in metabolic research.\u003c\/p\u003e\n\u003cp data-start=\"501\" data-end=\"883\"\u003eBy inhibiting NNMT, 5-Amino-1MQ is used to investigate NAD⁺-dependent energy pathways, including downstream effects on mitochondrial function and sirtuin signaling. Research models explore its role in fat mass regulation, insulin sensitivity, metabolic rate, and one-carbon metabolism, as well as the interaction between epigenetic regulation and metabolic function.\u003c\/p\u003e","brand":"PureX Labs","offers":[{"title":"5mg","offer_id":47548302983412,"sku":null,"price":35.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0804\/5802\/3156\/files\/Render_Mockup_1920_1920_2026-01-31_15.png?v=1769805238"},{"product_id":"semax","title":"Semax","description":"\u003cp dir=\"ltr\"\u003eSemax peptide is a synthetic polypeptide analog of an adrenocorticotropic hormone fragment 4-7 (ACTH 4-7),\u003csup dir=\"ltr\"\u003e(1)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003ea hormone secreted by the anterior pituitary gland. This fragment has been reported by researchers not to exhibit any action characteristic of ACTH itself but may have a potentially specific action within the brain.\u003csup dir=\"ltr\"\u003e(2)\u003c\/sup\u003e\u003c\/p\u003e\n\u003cp\u003eResearchers find that naturally occurring peptides may occasionally exhibit instability and easy degradation by biological enzymes, such as those found in gastrointestinal and cerebrospinal fluids. Consequently, researchers aim to synthesize analogs of these naturally occurring but potentially unstable peptides to induce similar biological action with the added value of higher stability. Semax is one such synthetically developed derivative of an endogenous adrenocorticotropic hormone fragment. The Met-Glu-His-Phe sequence in Semax is extended by adding a Pro-Gly-Pro (PGP) sequence at its C-terminal end. This modification with PGP may potentially enhance the molecule's ability to cross the blood-brain barrier (BBB) by increasing its lipophilicity. This increase in lipophilicity may facilitate the molecule’s passive diffusion or uptake through mechanisms such as lipid raft-mediated endocytosis, which may circumvent the tight junctions that typically restrict entry into the brain. Furthermore, the presence of PGP at the peptide's C-terminus might also modify its interactions with specific transporters or receptors on the BBB, potentially favoring its transport via receptor-mediated transcytosis. Moreover, the acetylation of Semax may improve its stability by making it more resistant to enzymatic breakdown, thereby extending its half-life in biological settings.\u003c\/p\u003e\n\u003cp\u003eSynthetically developed Semax has been widely researched for its potential mechanism of action and lauded for its apparent biological stability. Researchers suggest it may inhibit select enzymes that regulate the degradation of enkephalins, naturally released neurotransmitters secreted in the brain, which scientists consider may regulate several biological functions. Enkephalins are believed to be significantly involved in nociception (the sensory perception of pain) and stress response. Moreover, an elevation in enkephalin concentrations might potentially impact other neurotransmitter systems due to the intricate interconnections between the opioid system and neurotransmitters such as dopamine and serotonin. This interaction may manifest through modulation or alteration of neurotransmitter release, receptor activity, or signal transduction pathways, indicating a sophisticated and multifaceted relationship that remains an area of active research. In addition to enkephalins, Semax has been evaluated for its potential to inhibit other peptide-degrading secreted enzymes.\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eBased on one specific research study,\u003csup dir=\"ltr\"\u003e(4)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eSemax may induce elevated secretion and release of dopamine as well as possibly increasing the levels of brain-derived neurotrophic factor (BDNF). Based on another study,\u003csup dir=\"ltr\"\u003e(5)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eSemax has been speculated to also host the potential to alter gene expressions that modulate the immune system. In altering gene expression, the levels of immune cells and their mobility may be elevated. Semax was reported by researchers to exhibit altering potential in the encoding of chemokines and immunoglobulins, related to the functioning of the vascular system.\u003c\/p\u003e\n\u003ch3\u003eChemical Makeup\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003e\u003cstrong dir=\"ltr\"\u003eMolecular Formula:\u003c\/strong\u003e\u003cspan\u003e \u003c\/span\u003eC\u003csub dir=\"ltr\"\u003e39\u003c\/sub\u003eH\u003csub dir=\"ltr\"\u003e54\u003c\/sub\u003eN\u003csub dir=\"ltr\"\u003e10\u003c\/sub\u003eO\u003csub dir=\"ltr\"\u003e10\u003c\/sub\u003eS\u003cbr dir=\"ltr\"\u003e\u003cstrong dir=\"ltr\"\u003eMolecular Weight:\u003c\/strong\u003e\u003cspan\u003e \u003c\/span\u003e854.99 g\/mol\u003cbr dir=\"ltr\"\u003e\u003cstrong dir=\"ltr\"\u003eOther Known Titles:\u003c\/strong\u003e\u003cspan\u003e \u003c\/span\u003eACTH (4-7)PGP, HY-P1146\u003c\/p\u003e\n\u003ch2\u003eResearch Studies and Clinical Trials\u003c\/h2\u003e\n\u003ch3\u003e\u003cem\u003eSemax Peptide and Nootropic Action\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eAn initial study\u003csup dir=\"ltr\"\u003e(6)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003ewas conducted on ACTH hormone and its analogs, including Semax, to determine its nootropic potential in murine models. After peptide exposure in the models, 5-hydroxyindoleacetic acid (5-HIAA) levels were monitored. 5-HIAA levels appeared elevated by 25% after 2 hours of Semax presence. The levels appeared to increase gradually up to a maximum of 180% within 4 hours of peptide exposure. It was noted by researchers that the peptide, when introduced 20 minutes before D-amphetamine, appeared to lead to an elevation of 5-HIAA as compared to exposure to Semax alone. 5-HIAA is a primary metabolite of serotonin, which indicates that Semax might enhance serotonergic activity. This hypothetical influence on serotonin metabolism might enhance the functions of serotonin-dependent pathways, which may affect operations within the central nervous system. This speculative action underscores a possible modulation of neurotransmitter systems that play critical roles in mood, cognition, and overall brain function.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eSemax Peptide and Neonatal Anxiety Models\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eThe main aim of this study\u003csup dir=\"ltr\"\u003e(7)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003ewas to expose neonatal murine models to an SSRI and then Semax, to evaluate the interaction. Murine models aged between 1 and 14 days received an SSRI, followed by Semax on days 15 to 28. After 28 days, it was noted that upon exposure to the SSRI, the rats exhibited anxiety-like behavior, with an apparently impaired response to stressors and new stimuli during the first 14 days. Following Semax exposure, these SSRI-induced actions appeared to be mitigated, with the rats even exhibiting improved learning abilities and an overall reduction in anxiety-driven behaviors. Researchers posited that Semax might have reestablished normal levels of monoamines in the brain, which may have been initially decreased by the SSRI. By affecting these neurotransmitter systems, Semax might restore or stabilize neural pathways that were previously disrupted. Such changes might balance the excitatory and inhibitory signals in the brain, creating a state more conducive to reduced anxiety. For instance, by potentially increasing serotonin levels, Semax may improve mood and decrease anxiety, while optimizing dopamine might enhance motivation and reward processing. Furthermore, norepinephrine adjustments might improve attention and vigilance. Behavioral assessments conducted in the experiment indicated that these potential actions of Semax appeared temporally stable. The reduction in anxiety-related behaviors was sustained from adolescence through young adulthood, suggesting that Semax might have a lasting influence on neural circuits. This enduring stability implies that Semax might support creating a protective or corrective action on these circuits that persists beyond immediate exposure.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eSemax Peptide and the Vascular System\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eIn this study,\u003csup dir=\"ltr\"\u003e(8)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eresearchers evaluated the potential of Semax to protect murine heart models from vascular damage after experimental myocardial infarction (MI). The murine models were induced with myocardial infarction, and a cohort of the models were exposed to Semax in an experimental group for the following 6 days. On the 28th day, it was reported by the researchers that the murine models that served as a control group appeared to have developed cardiac hypertrophy along with decreased arterial blood pressure. The Semax-exposed models exhibited signs indicating preventing diastolic pressure growth in the left ventricle, with apparent left ventricle remodeling. Notably, the peptide may have ameliorated both cardiomyocyte hypertrophy and the imbalance between the growth of contractile and mitochondrial apparatus.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eSemax Peptide and Neonatal Deprivation\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eAdolescent rats\u003csup dir=\"ltr\"\u003e(9)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003ewere separated from their mothers for approximately 5 hours per day during postnatal days 1 to 14. From days 15 to 28, these adolescent rats were then exposed to the Semax peptide. After 28 days, it was found that during maternal deprivation, when Semax was not present, there was an apparent increase in anxiety and physical and emotional reactivity in the rats. Upon Semax exposure, researchers reported that reactions and anxiety in the rats appeared restored to control levels.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eSemax Peptide and Neuroprotection\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eThis clinical trial\u003csup dir=\"ltr\"\u003e(10)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003ewas conducted on 100 models of ischemic stroke. A cohort representing 30% of the models was exposed to Semax, whereas the rest were evaluated as a control group. Following the study, researchers reported that following Semax exposure, there appeared to be an improvement in the rate of restoration of damaged neurological functions. All results were analyzed using EEG mapping.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eSemax Peptide and Nootropic Properties\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eA small-scale clinical trial\u003csup dir=\"ltr\"\u003e(11)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003ewas conducted in which research models were given Semax under high-stress conditions, and subsequent brain activity was monitored. At the end of the study, after a total of 24 hours, researchers reported that compared to normal pre-trial thresholds, the models appeared to exhibit increased memory recall and increased focus intervals.\u003c\/p\u003e\n\u003cp\u003e\u003cem\u003e\u003cstrong dir=\"ltr\"\u003eSemax peptide is available for research and laboratory purposes only.\u003c\/strong\u003e\u003c\/em\u003e\u003c\/p\u003e\n\u003ch3\u003eReferences:\u003c\/h3\u003e\n\u003col\u003e\n\u003cli\u003eT. Kolomin et al., A New Generation of Drugs: Synthetic Peptides based on Natural Regulatory peptides. Neuroscience \u0026amp; Medicine, 2013, 223-252. Published Online December 2013.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/dx.doi.org\/10.4236\/nm.2013.44035\"\u003ehttp:\/\/dx.doi.org\/10.4236\/nm.2013.44035\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eDornbush RL, Nikolovski O. ACTH 4-10 and short-term memory. Pharmacol Biochem Behav. 1976;5(Suppl 1):69-72. doi: 10.1016\/0091-3057(76)90331-2. PMID: 189333.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/189333\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/189333\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eKost NV, Sokolov OIu, Gabaeva MV, Grivennikov IA, Andreeva LA, Miasoedov NF, Zozulia AA. Ingibiruiushchee deĭstvie semaksa i selanka na énkefalindegradiruiushchie fermenty syvorotki krovi cheloveka [Semax and selank inhibit the enkephalin-degrading enzymes from human serum]]. Bioorg Khim. 2001 May-Jun;27(3):180-3. Russian. doi: 10.1023\/a:1011373002885. PMID: 11443939.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/11443939\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/11443939\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eShih-Jen Tsai, Semax, an analogue of adrenocorticotropin (4–10), is a potential agent for the treatment of attention-deficit hyperactivity disorder and Rett syndrome, Medical Hypotheses, Volume 68, Issue 5, 2007, Pages 1144-1146.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/doi.org\/10.1016\/j.mehy.2006.07.017\"\u003ehttps:\/\/doi.org\/10.1016\/j.mehy.2006.07.017\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eMedvedeva, E.V., Dmitrieva, V.G., Povarova, O.V. et al. The peptide semax affects the expression of genes related to the immune and vascular systems in rat brain focal ischemia: genome-wide transcriptional analysis. BMC Genomics 15, 228 (2014).\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/doi.org\/10.1186\/1471-2164-15-228\"\u003ehttps:\/\/doi.org\/10.1186\/1471-2164-15-228\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eEremin KO, Kudrin VS, Saransaari P, Oja SS, Grivennikov IA, Myasoedov NF, Rayevsky KS. Semax, an ACTH(4-10) analogue with nootropic properties, activates dopaminergic and serotoninergic brain systems in rodents. Neurochem Res. 2005 Dec;30(12):1493-500.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/doi.org\/10.1007\/s11064-005-8826-8\"\u003edoi: 10.1007\/s11064-005-8826-8\u003c\/a\u003e. PMID: 16362768.\u003c\/li\u003e\n\u003cli\u003eNataliya Yu. Glazova, Daria M. Manchenko, Maria A. Volodina, Svetlana A. Merchieva, Ludmila A. Andreeva, Vladimir S. Kudrin, Nikolai F. Myasoedov, Natalia G. Levitskaya, Semax, synthetic ACTH(4–10) analogue, attenuates behavioural and neurochemical alterations following early-life fluvoxamine exposure in white rats, Neuropeptides, Volume 86, 2021, 102114, ISSN 0143-4179.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/doi.org\/10.1016\/j.npep.2020.102114\"\u003ehttps:\/\/doi.org\/10.1016\/j.npep.2020.102114\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eGavrilova SA, Golubeva AV, Lipina TV, Fominykh ES, Shornikova MV, Postnikov AB, Andrejeva LA, Chentsov IuS, Koshelev VB. [Protective effect of peptide semax (ACTH(4-7)Pro-Gly-Pro) on the rat heart rate after myocardial infarction]. Ross Fiziol Zh Im I M Sechenova. 2006 Nov;92(11):1305-21. Russian. PMID: 17385423.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/17385423\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/17385423\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eVolodina MA, Sebentsova EA, Glazova NY, Levitskaya NG, Andreeva LA, Manchenko DM, Kamensky AA, Myasoedov NF. Semax attenuates the influence of neonatal maternal deprivation on the behavior of adolescent white rats. Bull Exp Biol Med. 2012 Mar;152(5):560-3. English, Russian. doi: 10.1007\/s10517-012-1574-2. PMID: 22803132.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/22803132\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/22803132\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eGusev EI, Skvortsova VI, Miasoedov NF, Nezavibat'ko VN, Zhuravleva EIu, Vanichkin AV. Effektivnost' semaksa v ostrom periode polusharnogo ishemicheskogo insul'ta (klinicheskoe i élektrofiziologicheskoe issledovanie) [Effectiveness of semax in acute period of hemispheric ischemic stroke (a clinical and electrophysiological study)]. Zh Nevrol Psikhiatr Im S S Korsakova. 1997;97(6):26-34. Russian. PMID: 11517472.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/11517472\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/11517472\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eAsmarin IP, Nezavibat'ko VN, Miasoedov NF, Kamenskiĭ AA, Grivennikov IA, Ponomareva-Stepnaia MA, Andreeva LA, Kaplan AIa, Koshelev VB, Riasina TV. Nootropnyĭ analog adrenokortikotropina 4-10-semaks (15-letniĭ opyt razrabotki i izucheniia) [A nootropic adrenocorticotropin analog 4-10-semax (l5 years experience in its design and study)]. Zh Vyssh Nerv Deiat Im I P Pavlova. 1997 Mar-Apr;47(2):420-30. Russian. PMID: 9173745.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/9173745\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/9173745\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003c\/ol\u003e","brand":"PureX Labs","offers":[{"title":"5mg","offer_id":47548303737076,"sku":null,"price":25.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0804\/5802\/3156\/files\/Render_Mockup_1920_1920_2026-01-31_11.png?v=1769804832"},{"product_id":"ss-31","title":"SS-31","description":"\u003cp data-end=\"529\" data-start=\"139\"\u003eSS-31 is a research-grade peptide from the Szeto–Schiller class designed to selectively localize to mitochondria and interact with cardiolipin within the inner mitochondrial membrane. Through modulation of cardiolipin–protein interactions, SS-31 is used to investigate electron transport chain (ETC) efficiency, membrane organization, and mitochondrial structural integrity.\u003c\/p\u003e\n\u003cp data-end=\"880\" data-start=\"531\"\u003eResearch models suggest SS-31 may help preserve cristae architecture, enhance ATP production, and reduce mitochondrial reactive oxygen species (ROS) under conditions of metabolic or oxidative stress. Due to these properties, it is widely utilized in preclinical studies examining mitochondrial resilience and bioenergetic regulation.\u003c\/p\u003e\n\u003cp data-end=\"1144\" data-start=\"882\"\u003eSS-31 is commonly applied in research models of ischemia–reperfusion injury, cardiac and renal dysfunction, and neuroinflammation, as well as in assays evaluating oxidative phosphorylation efficiency, membrane potential, and mitochondrial ultrastructure.\u003c\/p\u003e","brand":"PureX Labs","offers":[{"title":"10mg","offer_id":47548304457972,"sku":null,"price":50.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0804\/5802\/3156\/files\/Render_Mockup_1920_1920_2026-01-31_12.png?v=1769804832"},{"product_id":"klow","title":"KLOW","description":"\u003cp data-end=\"496\" data-start=\"141\"\u003eKLOW is a research-grade multi-peptide blend formulated to support investigation into regenerative biology, tissue recovery, and cellular health. This formulation combines four complementary peptides, each studied for distinct yet overlapping roles in repair signaling, immune balance, and protective mechanisms across multiple tissue systems.\u003c\/p\u003e\n\u003cul data-end=\"1101\" data-start=\"498\"\u003e\n\u003cli data-end=\"648\" data-start=\"498\"\u003e\n\u003cp data-end=\"648\" data-start=\"500\"\u003eBPC-157 (10 mg): A gastric-derived peptide fragment researched for its role in angiogenesis, wound recovery, and gastrointestinal integrity.\u003c\/p\u003e\n\u003c\/li\u003e\n\u003cli data-end=\"806\" data-start=\"649\"\u003e\n\u003cp data-end=\"806\" data-start=\"651\"\u003eGHK-Cu (50 mg): A naturally occurring copper-binding peptide complex studied for collagen signaling, skin regeneration, and cellular communication.\u003c\/p\u003e\n\u003c\/li\u003e\n\u003cli data-end=\"959\" data-start=\"807\"\u003e\n\u003cp data-end=\"959\" data-start=\"809\"\u003eTB-500 (10 mg): A synthetic thymosin beta-4 fragment investigated for cell migration, tissue repair acceleration, and cytoprotective activity.\u003c\/p\u003e\n\u003c\/li\u003e\n\u003cli data-end=\"1101\" data-start=\"960\"\u003e\n\u003cp data-end=\"1101\" data-start=\"962\"\u003eKPV (10 mg): A tripeptide fragment of α-MSH studied for anti-inflammatory signaling, antimicrobial activity, and immune modulation.\u003c\/p\u003e\n\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003cp data-end=\"1279\" data-start=\"1103\"\u003eTogether, these peptides allow researchers to examine synergistic regenerative pathways, inflammatory regulation, and recovery processes across diverse experimental models.\u003c\/p\u003e\n\u003cp data-end=\"1369\" data-start=\"1281\"\u003eTotal peptide content: 80 mg\u003c\/p\u003e","brand":"PureX Labs","offers":[{"title":"80mg","offer_id":47548307964148,"sku":null,"price":120.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0804\/5802\/3156\/files\/Render_Mockup_1920_1920_2026-01-31_13.png?v=1769804833"},{"product_id":"glow","title":"GLOW","description":"\u003cp dir=\"ltr\"\u003eBPC-157 appears to be a distinct synthetic peptide composed of fifteen amino acids and is thought to originate from a fragment of a gastric protein. However, the specific protein has not yet been established. Research models indicate that BPC-157 may interact with intracellular signaling systems relevant to vascular growth via angiogenic signaling and inflammatory regulation via attenuation of pro-inflammatory pathways.\u003cspan\u003e \u003c\/span\u003e\u003csup dir=\"ltr\"\u003e(1)\u003c\/sup\u003e\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eTB-500 is a synthetic peptide identical to the 43 amino acid structure of the endogenous thymosin beta-4, studied for its involvement in cellular migration, cytoskeletal organization, and inflammatory signaling. In vitro studies suggest that exposure to TB-500 may support cell movement and structural coordination, and may also participate in signaling pathways linked to angiogenesis and modulation of inflammatory mediators.\u003cspan\u003e \u003c\/span\u003e\u003csup dir=\"ltr\"\u003e(2)\u003c\/sup\u003e\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eGHK-Cu is a peptide complex consisting of the tripeptide GHK (glycine, histidine, and lysine),  bound to a divalent copper ion (Cu²⁺). Researchers suggest that the GHK sequence may occur endogenously, specifically being released by cells, including fibroblasts, macrophages, and lymphocytes, during damage, as a result of collagen breakdown.\u003cspan\u003e \u003c\/span\u003e\u003csup dir=\"ltr\"\u003e(3)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eThus, GHK-Cu is posited to act as a repair signal, capable of interacting with enzymes, ion channels, and cell-surface receptors, with reported downstream potential on gene expression. The presence of copper may be central to these observations, including collagen synthesis, modulation of inflammatory signaling, and antioxidant potential.\u003c\/p\u003e\n\u003cp\u003eThese peptides may have partially overlapping but also complementary actions, supporting the hypothesis that combined exposure may positively affect inflammatory signaling. In addition, the peptides may all play some role in the regeneration of different cells, possibly supporting factors like vascular formation and cellular behavior.\u003c\/p\u003e\n\u003ch3\u003eChemical Makeup\u003c\/h3\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cem\u003eOther Known Titles\u003c\/em\u003e\u003c\/strong\u003e\u003c\/p\u003e\n\u003cul\u003e\n\u003cli\u003e\n\u003cstrong dir=\"ltr\"\u003e\u003cem dir=\"ltr\"\u003eBPC-157:\u003c\/em\u003e\u003c\/strong\u003e\u003cem dir=\"ltr\"\u003e\u003cspan\u003e \u003c\/span\u003eC\u003csub dir=\"ltr\"\u003e62\u003c\/sub\u003eH\u003csub dir=\"ltr\"\u003e98\u003c\/sub\u003eN\u003csub dir=\"ltr\"\u003e16\u003c\/sub\u003eO\u003csub dir=\"ltr\"\u003e22\u003c\/sub\u003e\u003c\/em\u003e\n\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong dir=\"ltr\"\u003e\u003cem dir=\"ltr\"\u003eTB-500:\u003cspan\u003e \u003c\/span\u003e\u003c\/em\u003e\u003c\/strong\u003e\u003cem dir=\"ltr\"\u003eC\u003csub dir=\"ltr\"\u003e212\u003c\/sub\u003eH\u003csub dir=\"ltr\"\u003e350\u003c\/sub\u003eN\u003csub dir=\"ltr\"\u003e56\u003c\/sub\u003eO\u003csub dir=\"ltr\"\u003e78\u003c\/sub\u003eS\u003c\/em\u003e\n\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong dir=\"ltr\"\u003e\u003cem dir=\"ltr\"\u003eGHK-Cu:\u003cspan\u003e \u003c\/span\u003e\u003c\/em\u003e\u003c\/strong\u003e\u003cem dir=\"ltr\"\u003eC\u003csub dir=\"ltr\"\u003e14\u003c\/sub\u003eH\u003csub dir=\"ltr\"\u003e23\u003c\/sub\u003eCuN\u003csub dir=\"ltr\"\u003e6\u003c\/sub\u003eO\u003csub dir=\"ltr\"\u003e4\u003c\/sub\u003e\u003c\/em\u003e\n\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cem\u003eMolecular Weight:\u003c\/em\u003e\u003c\/strong\u003e\u003c\/p\u003e\n\u003ch2\u003eResearch and Clinical Studies\u003c\/h2\u003e\n\u003ch3\u003e\u003cem\u003eAnti-inflammatory Signaling Research on BPC-157 \u0026amp; TB-500 \u0026amp; GHK-Cu\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eAll three peptides appear to play some potentially complementary and partially overlapping roles in inflammatory signaling inside and in between cells. Notably, all three appear to have a positive action on toning down inflammatory processes. For example, research conducted in laboratory settings by Santra et al. suggests that TB-500 may lower inflammation-related signaling inside cell cultures of developing brain support cells called oligodendrocyte progenitor cells.\u003cspan\u003e \u003c\/span\u003e\u003csup dir=\"ltr\"\u003e(4)\u003cspan\u003e \u003c\/span\u003e\u003c\/sup\u003eAfter cell stress or injury, these cells are posited to activate innate immune pathways, especially Toll-like receptor (TLR) signaling, which may drive inflammatory responses inside the cell.\u003c\/p\u003e\n\u003cp\u003eThe authors research whether TB-500 may tone down this signaling and suggest that the peptide may increase the level of miR-146a, a small regulatory RNA molecule whose role may be to act as an internal brake on inflammatory signaling pathways. When miR-146a levels rise, two key TLR signaling proteins, IRAK1 and TRAF6, may decrease, and thus they may not transmit inflammatory signals inside the cell, including pathways linked to NF-κB activation, which would otherwise play a major role in inflammatory signaling.\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eFurthermore, research by Sikiric et al. suggests that BPC-157 may also interact with inflammatory signaling, specifically by attenuating inflammatory cell infiltration in research models.\u003cspan\u003e \u003c\/span\u003e\u003csup dir=\"ltr\"\u003e(5)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eApparently, the researchers observed lower levels of biochemical markers linked to inflammation, including markers of neutrophil accumulation, leukotriene B4, and thromboxane B2 in inflamed cellular cultures.\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eThis peptide also appeared to modulate immune cell behavior, with reports of increased macrophage activity, which may support resolution rather than persistence of inflammation. Importantly, these implications were observed without direct immunosuppression of specific cytokines such as TNF, implying a more regulatory mode of action. BPC-157 may “\u003cem dir=\"ltr\"\u003einteract with the NO-system\u003cspan\u003e \u003c\/span\u003e\u003c\/em\u003e[nitric oxide system]\u003cem dir=\"ltr\"\u003e, providing endothelium protection”\u003c\/em\u003e, which may indirectly limit inflammatory amplification by preserving microvascular integrity.\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eLast but not least, experiments by Park et al. suggest that GHK-Cu may also tone down inflammatory signaling in macrophages activated by pro-inflammatory triggers and in lung cell injury models.\u003cspan\u003e \u003c\/span\u003e\u003csup dir=\"ltr\"\u003e(6)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eIn activated macrophages, GHK-Cu apparently lowered intracellular reactive oxygen species and restored superoxide dismutase activity toward control values. The pro-inflammatory triggers apparently increased TNF-α and IL-6 release, while GHK-Cu apparently reduced both cytokines.\u003c\/p\u003e\n\u003cp\u003eMechanistically, the authors suggest that GHK-Cu may have suppressed NF-κB activation by reducing the activation of key regulators. The researchers did not notice significant action on ERK1\/2, JNK1\/2, or NO secretion. In the lung cell cultures, the peptide complex apparently reduced edema, inflammatory cell infiltration, and overall histologic injury scores. The researchers also observed reductions in TNF-α, IL-6, total cell counts, neutrophils, MPO activity, and markers of alveolar permeability.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eCellular Regeneration Potential of BPC-157 \u0026amp; TB-500 \u0026amp; GHK-Cu\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp\u003eIn addition to their potentially positive actions on toning down inflammatory signaling, all three peptides have been posited to also support cellular regeneration via different mechanisms that ultimately support vascularity and nutrient delivery to the cellular structure. Notably, TB-500 has been posited to exert positive actions on cellular regeneration by interacting with cellular mobility and thus supporting angiogenesis.\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eResearch by Lv et al. suggests that TB-500 may interact with cell movement as it binds globular actin (G-actin) and may modulate how actin filaments assemble to plausibly make endothelial cells more able to change shape, migrate, and form multicellular structures.\u003cspan\u003e \u003c\/span\u003e\u003csup dir=\"ltr\"\u003e(7)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eThat type of motility is a basic requirement for sprouting angiogenesis, where endothelial cells need to move into hypoxic tissue and organize into new tubes.\u003c\/p\u003e\n\u003cp\u003eThe researchers suggest that during evaluation, the peptide increased cell viability and migration and increased tube formation on matrices, which is commonly exposed to research models as a lab proxy for angiogenic behavior. In parallel, TB-500 appeared to increase expression of angiogenesis-linked factors, including VEGFA, angiopoietin-2 (Ang2), and the Tie2 receptor. Mechanistically, the study posits that TB-500 may push angiogenesis through a Notch to NF-κB signaling axis. Thus, TB-500 may be hypothesized to support angiogenesis by combining a cytoskeleton-linked increase in endothelial motility with signaling changes that raise pro-angiogenic programs (VEGF-A and Ang2\/Tie2) via Notch\/NF-κB coupling in damaged cellular structure.\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eResearch by Sikiric et al. also suggests that BPC-157 may also support angiogenesis and thus cellular regeneration.\u003cspan\u003e \u003c\/span\u003e\u003csup dir=\"ltr\"\u003e(8)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eMore specifically, this peptide may act indirectly by stabilizing the vascular environment needed for new vessel growth. Across multiple injury models, the researchers have observed that the peptide may work by protecting endothelial cells and preserving vessel patency. Such endothelium protection creates conditions in which endothelial sprouting and maturation may occur.\u003c\/p\u003e\n\u003cp\u003eAt the cellular level, BPC-157 has been linked to activation of repair-associated signaling pathways, including Egr-1 with its regulator NAB2, and FAK–paxillin signaling, which are potentially involved in cell adhesion and migration. These processes are essential for endothelial movement through the extracellular matrix during capillary sprouting. The peptide has also been associated with normalised NO signaling under both excessive and suppressed NO states, counteracting the implications of NOS blockade and NO overproduction. Because NO regulates vasodilation, endothelial survival, and angiogenic signaling, this balancing may support perfusion of injured cellular structures and facilitate endothelial activation and vessel remodeling during repair.\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eMechanistically, research on GHK-Cu by Mulder et al. also suggests that the peptide may upregulate VEGF, increase endothelial cell proliferation, and promote endothelial migration and tube formation.\u003cspan\u003e \u003c\/span\u003e\u003csup dir=\"ltr\"\u003e(9)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eThese actions are consistent with stimulation of angiogenesis. At the same time, copper itself is a required cofactor for several angiogenic enzymes and transcriptional programs, and the GHK peptide appears to deliver copper in a biologically functional form at sites of cellular injury.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eCollagen Repair Potential of BPC-157 \u0026amp; TB-500 \u0026amp; GHK-Cu\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eMultiple experiments with each of the three peptides also suggest that they may support the regeneration and repair of collagen and other supporting structures in cell cultures such as tendon fibroblasts. For example, research on TB-500 by Xu et al. may support the structural organization in models of recovering tendon fibroblasts.\u003cspan\u003e \u003c\/span\u003e\u003csup dir=\"ltr\"\u003e(10)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eApparently, the researchers observed collagen fibers that were more uniformly aligned along the ligament axis and more evenly spaced than in controls. Electron microscopy suggested larger collagen fibril diameters, a feature linked to better-supported mechanical properties. These structural changes apparently were accompanied by higher tensile strength and stiffness of the recovered tendon structures.\u003c\/p\u003e\n\u003cp\u003eBased on this data, the researchers posit that TB-500 may support how ligament fibroblasts organize and deposit collagen during repair, improving tissue quality. BPC-157 may also support repair by supporting tendon fibroblasts, as the research by Chang reports accelerated fibroblast migration and spreading in laboratory studies, both of which are essential for repopulating an injury site. Apparently, the peptide may also have better supported fibroblast survival under oxidative stress, a condition commonly present in injured tendon cell cultures.\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eAt the cellular level, these implications were posited to be related to the upregulation of actin fiber formation, as the researchers commented that “\u003cem dir=\"ltr\"\u003eF-actin formation as detected by FITC-phalloidin staining was induced in BPC 157\u003c\/em\u003e” exposed cells. Moreover, the activation of focal adhesion signaling through phosphorylation of FAK and paxillin is also posited to aid cell attachment and movement within the extracellular matrix, thus ultimately facilitating repair.\u003c\/p\u003e\n\u003cp\u003eGHK-Cu may also promote collagen synthesis, particularly in the binding between tendon cells and bone cells. Research by Fu et al. suggests that research models exposed to the peptide complex may have better bone formation around tendon cell grafts and a trend toward higher cell presence within the graft structure itself. Overall, all three peptides appear to exert potential positive actions linked to cellular repair and integrity, including anti-inflammatory signaling, angiogenesis, collagen synthesis, and more. Unfortunately, research investigating the simultaneous experimentation with all three compounds has yet to be conducted.\u003c\/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cem dir=\"ltr\"\u003eBPC-157 \u0026amp; TB-500 \u0026amp; GHK-Cu (GLOW) blend is available for research and laboratory purposes only.\u003c\/em\u003e\u003c\/strong\u003e\u003c\/p\u003e\n\u003ch3\u003eReferences:\u003c\/h3\u003e\n\u003col\u003e\n\u003cli\u003eSeiwerth S, Milavic M, Vukojevic J, Gojkovic S, Krezic I, Vuletic LB, Pavlov KH, Petrovic A, Sikiric S, Vranes H, Prtoric A, Zizek H, Durasin T, Dobric I, Staresinic M, Strbe S, Knezevic M, Sola M, Kokot A, Sever M, Lovric E, Skrtic A, Blagaic AB, Sikiric P. Stable Gastric Pentadecapeptide BPC 157 and Wound Healing. Front Pharmacol. 2021 Jun 29;12:627533. doi: 10.3389\/fphar.2021.627533. PMID: 34267654; PMCID: PMC8275860.\u003c\/li\u003e\n\u003cli\u003eMaar, K., Hetenyi, R., Maar, S., Faskerti, G., Hanna, D., Lippai, B., Takatsy, A., \u0026amp; Bock-Marquette, I. (2021). Utilizing Developmentally Essential Secreted Peptides Such as Thymosin Beta-4 to Remind the Adult Organs of Their Embryonic State-New Directions in Anti-Aging Regenerative Therapies. Cells, 10(6), 1343.\u003cspan\u003e \u003c\/span\u003e\u003ca href=\"https:\/\/doi.org\/10.3390\/cells10061343\" rel=\"noopener\" dir=\"ltr\"\u003ehttps:\/\/doi.org\/10.3390\/cells10061343\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eMaquart FX, Pickart L, Laurent M, Gillery P, Monboisse JC, Borel JP. Stimulation of collagen synthesis in fibroblast cultures by the tripeptide-copper complex glycyl-L-histidyl-L-lysine-Cu2+. FEBS Lett. 1988 Oct 10;238(2):343-6. doi: 10.1016\/0014-5793(88)80509-x. PMID: 3169264.\u003c\/li\u003e\n\u003cli\u003eSantra M, Zhang ZG, Yang J, Santra S, Santra S, Chopp M, Morris DC. Thymosin β4 up-regulation of microRNA-146a promotes oligodendrocyte differentiation and suppression of the Toll-like proinflammatory pathway. J Biol Chem. 2014 Jul 11;289(28):19508-18. doi: 10.1074\/jbc.M113.529966. Epub 2014 May 14. PMID: 24828499; PMCID: PMC4094061.\u003c\/li\u003e\n\u003cli\u003eSikiric P, Seiwerth S, Rucman R, Turkovic B, Rokotov DS, Brcic L, Sever M, Klicek R, Radic B, Drmic D, Ilic S, Kolenc D, Stambolija V, Zoricic Z, Vrcic H, Sebecic B. Focus on ulcerative colitis: stable gastric pentadecapeptide BPC 157. Curr Med Chem. 2012;19(1):126-32. doi: 10.2174\/092986712803414015. PMID: 22300085.\u003c\/li\u003e\n\u003cli\u003ePark JR, Lee H, Kim SI, Yang SR. The tripeptide GHK-Cu complex ameliorates lipopolysaccharide-induced acute lung injury in mice. Oncotarget. 2016 Sep 6;7(36):58405-58417. doi: 10.18632\/oncotarget.11168. PMID: 27517151; PMCID: PMC5295439.\u003c\/li\u003e\n\u003cli\u003eLv S, Cai H, Xu Y, Dai J, Rong X, Zheng L. Thymosin‑β 4 induces angiogenesis in critical limb ischemia mice via regulating Notch\/NF‑κB pathway. Int J Mol Med. 2020 Oct;46(4):1347-1358. doi: 10.3892\/ijmm.2020.4701. Epub 2020 Aug 11. PMID: 32945357; PMCID: PMC7447324.\u003c\/li\u003e\n\u003cli\u003eSikiric P, Seiwerth S, Rucman R, Kolenc D, Vuletic LB, Drmic D, Grgic T, Strbe S, Zukanovic G, Crvenkovic D, Madzarac G, Rukavina I, Sucic M, Baric M, Starcevic N, Krstonijevic Z, Bencic ML, Filipcic I, Rokotov DS, Vlainic J. Brain-gut Axis and Pentadecapeptide BPC 157: Theoretical and Practical Implications. Curr Neuropharmacol. 2016;14(8):857-865. doi: 10.2174\/1570159x13666160502153022. PMID: 27138887; PMCID: PMC5333585.\u003c\/li\u003e\n\u003cli\u003eMulder GD, Patt LM, Sanders L, Rosenstock J, Altman MI, Hanley ME, Duncan GW. Enhanced healing of ulcers in patients with diabetes by topical treatment with glycyl-l-histidyl-l-lysine copper. Wound Repair Regen. 1994 Oct;2(4):259-69. doi: 10.1046\/j.1524-475X.1994.20406.x. PMID: 17147644.\u003c\/li\u003e\n\u003cli\u003eXu B, Yang M, Li Z, Zhang Y, Jiang Z, Guan S, Jiang D. Thymosin β4 enhances the healing of medial collateral ligament injury in rats. Regul Pept. 2013 Jun 10;184:1-5. doi: 10.1016\/j.regpep.2013.03.026. Epub 2013 Mar 21. PMID: 23523891.\u003c\/li\u003e\n\u003cli\u003eChang CH, Tsai WC, Lin MS, Hsu YH, Pang JH. The promoting effect of pentadecapeptide BPC 157 on tendon healing involves tendon outgrowth, cell survival, and cell migration. J Appl Physiol (1985). 2011 Mar;110(3):774-80. doi: 10.1152\/japplphysiol.00945.2010. Epub 2010 Oct 28. PMID: 21030672.\u003c\/li\u003e\n\u003cli\u003eFu SC, Cheuk YC, Chiu WY, Yung SH, Rolf CG, Chan KM. Tripeptide-copper complex GHK-Cu (II) transiently improved healing outcome in a rat model of ACL reconstruction. J Orthop Res. 2015 Jul;33(7):1024-33. doi: 10.1002\/jor.22831. Epub 2015 Apr 10. PMID: 25731775.\u003c\/li\u003e\n\u003c\/ol\u003e","brand":"PureX Labs","offers":[{"title":"70mg","offer_id":47548311208180,"sku":null,"price":100.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0804\/5802\/3156\/files\/Render_Mockup_1920_1920_2026-01-31_14.png?v=1769804832"},{"product_id":"semiglutide","title":"Semaglutide","description":"\u003cdiv class=\"flex max-w-full flex-col gap-4 grow\"\u003e\n\u003cdiv data-message-author-role=\"assistant\" data-message-id=\"2040b58a-303c-4f7a-a5b5-50c64427701e\" dir=\"auto\" data-message-model-slug=\"gpt-5-5-thinking\" class=\"min-h-8 text-message relative flex w-full flex-col items-end gap-2 text-start break-words whitespace-normal outline-none keyboard-focused:focus-ring [.text-message+\u0026amp;]:mt-1\" data-turn-start-message=\"true\" tabindex=\"0\"\u003e\n\u003cdiv class=\"flex w-full flex-col gap-1 empty:hidden\"\u003e\n\u003cdiv class=\"markdown prose dark:prose-invert w-full wrap-break-word dark markdown-new-styling\"\u003e\n\u003cp data-start=\"0\" data-end=\"391\"\u003e\u003cstrong data-start=\"0\" data-end=\"15\"\u003eSemaglutide\u003c\/strong\u003e is a research-grade GLP-1 receptor agonist analog studied for its interaction with glucagon-like peptide-1 receptors involved in metabolic signaling, glucose regulation pathways, and appetite-related neuroendocrine activity. Its extended half-life and receptor-binding profile make it a widely used compound in preclinical and laboratory research focused on incretin biology.\u003c\/p\u003e\n\u003cp data-start=\"393\" data-end=\"693\"\u003eIn research models, semaglutide has been evaluated for its role in insulin secretion pathways, glucagon regulation, gastric emptying mechanisms, and central appetite signaling. These areas of study make it a valuable tool for investigating metabolic function, energy balance, and glucose homeostasis.\u003c\/p\u003e\n\u003cp data-start=\"695\" data-end=\"897\"\u003eSemaglutide is commonly applied in research involving metabolic regulation, pancreatic beta-cell signaling, obesity-related models, insulin sensitivity, and long-duration GLP-1 receptor activity assays.\u003c\/p\u003e\n\u003cp data-start=\"899\" data-end=\"962\" data-is-last-node=\"\" data-is-only-node=\"\"\u003e\u003cstrong data-start=\"899\" data-end=\"962\" data-is-last-node=\"\"\u003eFor research use only. Not for human or animal consumption.\u003c\/strong\u003e\u003c\/p\u003e\n\u003c\/div\u003e\n\u003c\/div\u003e\n\u003c\/div\u003e\n\u003c\/div\u003e","brand":"PureX Labs","offers":[{"title":"20mg","offer_id":48045021528308,"sku":null,"price":50.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0804\/5802\/3156\/files\/Render_Mockup_1920_1920_2026-05-12.jpg?v=1778528159"}],"url":"https:\/\/purexlabs.io\/collections\/all.oembed","provider":"PureX Labs","version":"1.0","type":"link"}