{"title":"Research Catalog","description":"\u003cp\u003eReference compounds for laboratory research. Every batch independently tested (HPLC purity, LC-MS identity) with a published, lot-matched Certificate of Analysis.\u003c\/p\u003e\u003cp\u003e\u003cstrong\u003eFor research use only. Not for human or veterinary consumption.\u003c\/strong\u003e\u003c\/p\u003e","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},{"title":"20mg","offer_id":67648604274932,"sku":null,"price":75.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0804\/5802\/3156\/files\/BPC157-5mg-sq_5537564a-a051-4d63-aa30-31ecb0045c48.png?v=1787851403"},{"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\n\n\u003ch2\u003eFrequently asked questions\u003c\/h2\u003e\n\u003cdiv class=\"purex-faq\"\u003e\n\u003cdetails\u003e\n\u003csummary\u003e\u003cstrong\u003eWhat is the BPC-157\/TB-500 blend?\u003c\/strong\u003e\u003c\/summary\u003e\n\u003cp\u003eA single vial containing both BPC-157 (a 15-amino-acid pentadecapeptide derived from gastric protein) and TB-500 (a thymosin beta-4 fragment). The blend exists because the two are often studied together in tissue-repair and recovery models. Read \u003ca href=\"\/blogs\/news\/bpc-157-vs-tb-500-comparing-two-research-peptides\"\u003eBPC-157 vs TB-500\u003c\/a\u003e for how they differ.\u003c\/p\u003e\n\u003c\/details\u003e\n\u003cdetails\u003e\n\u003csummary\u003e\u003cstrong\u003eWhy buy the blend instead of the two peptides separately?\u003c\/strong\u003e\u003c\/summary\u003e\n\u003cp\u003eConvenience and consistency: one vial, one batch, one Certificate of Analysis. If your protocol needs independent dosing of each compound, use the standalone \u003ca href=\"\/products\/bpc-157\"\u003eBPC-157\u003c\/a\u003e and \u003ca href=\"\/products\/tb-500\"\u003eTB-500\u003c\/a\u003e products instead.\u003c\/p\u003e\n\u003c\/details\u003e\n\u003cdetails\u003e\n\u003csummary\u003e\u003cstrong\u003eWhat is the ratio of BPC-157 to TB-500?\u003c\/strong\u003e\u003c\/summary\u003e\n\u003cp\u003eThe exact per-compound quantity for the current lot is stated on the batch Certificate of Analysis on our \u003ca href=\"\/pages\/lab-results\"\u003eLab Results\u003c\/a\u003e page.\u003c\/p\u003e\n\u003c\/details\u003e\n\u003cdetails\u003e\n\u003csummary\u003e\u003cstrong\u003eHow is purity verified?\u003c\/strong\u003e\u003c\/summary\u003e\n\u003cp\u003eEvery batch is tested by an independent third-party lab using HPLC-MS (high-performance liquid chromatography with mass spectrometry), which confirms identity, quantity and purity. Each vial carries a batch number, and the matching Certificate of Analysis is published on our \u003ca href=\"\/pages\/lab-results\"\u003eLab Results\u003c\/a\u003e page.\u003c\/p\u003e\n\u003c\/details\u003e\n\u003cdetails\u003e\n\u003csummary\u003e\u003cstrong\u003eHow should the blend be stored and reconstituted?\u003c\/strong\u003e\u003c\/summary\u003e\n\u003cp\u003eLyophilised (freeze-dried) peptide is stable when kept sealed, cold and protected from light. Once reconstituted with bacteriostatic water, keep the vial refrigerated and use within the window appropriate to your protocol. Avoid repeated freeze-thaw cycles. Add \u003ca href=\"\/products\/bac-water\"\u003ebacteriostatic water\u003c\/a\u003e slowly down the inside wall of the vial and let the powder dissolve on its own. Do not shake. Swirl gently if needed. The volume you add determines the final concentration, so record it with the batch number. Full walkthrough: \u003ca href=\"\/blogs\/news\/how-to-reconstitute-lyophilised-peptides-a-laboratory-guide\"\u003eHow to Reconstitute Lyophilised Peptides\u003c\/a\u003e.\u003c\/p\u003e\n\u003c\/details\u003e\n\u003cdetails\u003e\n\u003csummary\u003e\u003cstrong\u003eHow does shipping work?\u003c\/strong\u003e\u003c\/summary\u003e\n\u003cp\u003eOrders are packed in sealed, tamper-evident vials. See our \u003ca href=\"\/policies\/shipping-policy\"\u003eshipping policy\u003c\/a\u003e for processing times and carriers. Lyophilised peptides do not require cold-chain shipping.\u003c\/p\u003e\n\u003c\/details\u003e\n\u003cdetails\u003e\n\u003csummary\u003e\u003cstrong\u003eIs this for human use?\u003c\/strong\u003e\u003c\/summary\u003e\n\u003cp\u003eNo. Everything we sell is supplied strictly for laboratory and analytical research. It is not a drug, supplement or therapeutic product and is not for human or veterinary use.\u003c\/p\u003e\n\u003c\/details\u003e\n\u003c\/div\u003e","brand":"PureX Labs","offers":[{"title":"10mg","offer_id":48098748727540,"sku":null,"price":45.0,"currency_code":"USD","in_stock":false},{"title":"20mg","offer_id":47487346573556,"sku":null,"price":85.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0804\/5802\/3156\/files\/BPC157-TB500-10mg-sq.png?v=1787850451"},{"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\/GHKCU-50mg.png?v=1787847039"},{"product_id":"glutathione","title":"Glutathione","description":"\u003cp\u003e\u003cstrong\u003eGlutathione\u003c\/strong\u003e (CAS 70-18-8) is a naturally occurring tripeptide supplied in lyophilised form for laboratory and analytical research use only.\u003c\/p\u003e\n\n\u003ch2\u003eResearch background\u003c\/h2\u003e\n\u003cp\u003eGlutathione is composed of three amino acids — glutamate, cysteine and glycine — and is one of the most extensively documented endogenous antioxidant compounds in the scientific literature. Research applications typically focus on redox biology, oxidative stress mechanisms, cellular detoxification pathways and thiol chemistry in controlled research models.\u003c\/p\u003e\n\n\u003ch2\u003eSpecifications\u003c\/h2\u003e\n\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eCompound:\u003c\/strong\u003e Glutathione (reduced, GSH)\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eCAS number:\u003c\/strong\u003e 70-18-8\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eAppearance:\u003c\/strong\u003e Lyophilised powder\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePurity:\u003c\/strong\u003e 99%+ verified by HPLC-MS\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eAvailable size:\u003c\/strong\u003e 600mg\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePresentation:\u003c\/strong\u003e Sealed, tamper-evident vial\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003ch2\u003eTesting and verification\u003c\/h2\u003e\n\u003cp\u003eIndependently analysed by third-party laboratory with batch-specific Certificates of Analysis published on our \u003ca href=\"\/pages\/lab-results\"\u003eLab Results\u003c\/a\u003e page.\u003c\/p\u003e\n\n\u003ch2\u003eHandling and storage\u003c\/h2\u003e\n\u003cp\u003eSupplied lyophilised. Store sealed vials cold and protected from light. Glutathione is sensitive to oxidation.\u003c\/p\u003e\n\n\u003cp\u003e\u003cem\u003eResearch use only. Not a medicine, supplement or therapeutic good. Not for human or veterinary consumption.\u003c\/em\u003e\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\/Render_Mockup_1920_1920_2026-08-28_6.png?v=1787852776"},{"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},{"title":"1000mg","offer_id":67648606601460,"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_2026-08-28_8.png?v=1787852775"},{"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\n\n\u003ch2\u003eFrequently asked questions\u003c\/h2\u003e\n\u003cdiv class=\"purex-faq\"\u003e\n\u003cdetails\u003e\n\u003csummary\u003e\u003cstrong\u003eWhat is TB-500?\u003c\/strong\u003e\u003c\/summary\u003e\n\u003cp\u003eTB-500 is a synthetic peptide fragment modelled on thymosin beta-4, a 43-amino-acid protein present in nearly all cells. It is studied for its role in actin regulation, cell migration and tissue repair models.\u003c\/p\u003e\n\u003c\/details\u003e\n\u003cdetails\u003e\n\u003csummary\u003e\u003cstrong\u003eWhat is the difference between TB-500 5mg and 10mg?\u003c\/strong\u003e\u003c\/summary\u003e\n\u003cp\u003eSame compound and purity; the 10mg vial simply contains twice the quantity, which is more economical for labs running larger or repeated experiments.\u003c\/p\u003e\n\u003c\/details\u003e\n\u003cdetails\u003e\n\u003csummary\u003e\u003cstrong\u003eHow is purity verified?\u003c\/strong\u003e\u003c\/summary\u003e\n\u003cp\u003eEvery batch is tested by an independent third-party lab using HPLC-MS (high-performance liquid chromatography with mass spectrometry), which confirms identity, quantity and purity. Each vial carries a batch number, and the matching Certificate of Analysis is published on our \u003ca href=\"\/pages\/lab-results\"\u003eLab Results\u003c\/a\u003e page.\u003c\/p\u003e\n\u003c\/details\u003e\n\u003cdetails\u003e\n\u003csummary\u003e\u003cstrong\u003eWhat is the difference between TB-500 and BPC-157?\u003c\/strong\u003e\u003c\/summary\u003e\n\u003cp\u003eBoth are studied in tissue-repair research but act through different mechanisms: TB-500 is associated with actin binding and cell migration, while BPC-157 is a gastric-derived pentadecapeptide studied for angiogenesis and tendon\/ligament models. See \u003ca href=\"\/blogs\/news\/bpc-157-vs-tb-500-comparing-two-research-peptides\"\u003eBPC-157 vs TB-500\u003c\/a\u003e for a full comparison. We also offer them as a combined \u003ca href=\"\/products\/bpc-157-tb500\"\u003eBPC-157\/TB-500 blend\u003c\/a\u003e.\u003c\/p\u003e\n\u003c\/details\u003e\n\u003cdetails\u003e\n\u003csummary\u003e\u003cstrong\u003eHow should TB-500 be stored and reconstituted?\u003c\/strong\u003e\u003c\/summary\u003e\n\u003cp\u003eLyophilised (freeze-dried) peptide is stable when kept sealed, cold and protected from light. Once reconstituted with bacteriostatic water, keep the vial refrigerated and use within the window appropriate to your protocol. Avoid repeated freeze-thaw cycles. Add \u003ca href=\"\/products\/bac-water\"\u003ebacteriostatic water\u003c\/a\u003e slowly down the inside wall of the vial and let the powder dissolve on its own. Do not shake. Swirl gently if needed. The volume you add determines the final concentration, so record it with the batch number. Full walkthrough: \u003ca href=\"\/blogs\/news\/how-to-reconstitute-lyophilised-peptides-a-laboratory-guide\"\u003eHow to Reconstitute Lyophilised Peptides\u003c\/a\u003e.\u003c\/p\u003e\n\u003c\/details\u003e\n\u003cdetails\u003e\n\u003csummary\u003e\u003cstrong\u003eHow does shipping work?\u003c\/strong\u003e\u003c\/summary\u003e\n\u003cp\u003eOrders are packed in sealed, tamper-evident vials. See our \u003ca href=\"\/policies\/shipping-policy\"\u003eshipping policy\u003c\/a\u003e for processing times and carriers. Lyophilised peptides do not require cold-chain shipping.\u003c\/p\u003e\n\u003c\/details\u003e\n\u003cdetails\u003e\n\u003csummary\u003e\u003cstrong\u003eIs this for human use?\u003c\/strong\u003e\u003c\/summary\u003e\n\u003cp\u003eNo. Everything we sell is supplied strictly for laboratory and analytical research. It is not a drug, supplement or therapeutic product and is not for human or veterinary use.\u003c\/p\u003e\n\u003c\/details\u003e\n\u003c\/div\u003e","brand":"PureX Labs","offers":[{"title":"5mg","offer_id":47548294758644,"sku":null,"price":45.0,"currency_code":"USD","in_stock":true},{"title":"10mg","offer_id":48527160312052,"sku":null,"price":90.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0804\/5802\/3156\/files\/TB500-5mg-sq.png?v=1787850452"},{"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\n\n\u003ch2\u003eFrequently asked questions\u003c\/h2\u003e\n\u003cdiv class=\"purex-faq\"\u003e\n\u003cdetails\u003e\n\u003csummary\u003e\u003cstrong\u003eWhat is MOTS-c?\u003c\/strong\u003e\u003c\/summary\u003e\n\u003cp\u003eMOTS-c is a 16-amino-acid peptide encoded within the mitochondrial genome (the 12S rRNA region), one of a small family of mitochondria-derived peptides. It is used in laboratory research on AMPK signalling, mitochondrial–nuclear communication and cellular metabolism. Our overview \u003ca href=\"\/blogs\/news\/mots-c-a-research-overview-of-the-mitochondrial-peptide\"\u003eMOTS-c: A Research Overview of the Mitochondrial Peptide\u003c\/a\u003e covers the published literature in more depth.\u003c\/p\u003e\n\u003c\/details\u003e\n\u003cdetails\u003e\n\u003csummary\u003e\u003cstrong\u003eWhat vial sizes are available?\u003c\/strong\u003e\u003c\/summary\u003e\n\u003cp\u003eMOTS-c is available in 10mg and 40mg vials of lyophilised (freeze-dried) powder. Each vial is labelled with its batch number.\u003c\/p\u003e\n\u003c\/details\u003e\n\u003cdetails\u003e\n\u003csummary\u003e\u003cstrong\u003eHow is purity verified?\u003c\/strong\u003e\u003c\/summary\u003e\n\u003cp\u003eEvery batch is tested by an independent third-party lab using HPLC-MS (high-performance liquid chromatography with mass spectrometry), which confirms identity, quantity and purity. The expected molecular weight for MOTS-c is approximately 2,174.6 g\/mol. The matching Certificate of Analysis for each batch is published on our \u003ca href=\"\/pages\/lab-results\"\u003eLab Results\u003c\/a\u003e page.\u003c\/p\u003e\n\u003c\/details\u003e\n\u003cdetails\u003e\n\u003csummary\u003e\u003cstrong\u003eWhich related compounds are studied alongside MOTS-c?\u003c\/strong\u003e\u003c\/summary\u003e\n\u003cp\u003eMOTS-c is often examined in the same research areas as other compounds involved in mitochondrial function and NAD+ metabolism, such as \u003ca href=\"\/products\/nad\"\u003eNAD+\u003c\/a\u003e, \u003ca href=\"\/products\/ss-31\"\u003eSS-31\u003c\/a\u003e and \u003ca href=\"\/products\/5-amino-1mq\"\u003e5-Amino-1MQ\u003c\/a\u003e. The full range is in our \u003ca href=\"\/collections\/longevity-cellular\"\u003eLongevity \u0026amp; Cellular\u003c\/a\u003e collection.\u003c\/p\u003e\n\u003c\/details\u003e\n\u003cdetails\u003e\n\u003csummary\u003e\u003cstrong\u003eHow should it be stored and reconstituted?\u003c\/strong\u003e\u003c\/summary\u003e\n\u003cp\u003eLyophilised (freeze-dried) peptide is stable when kept sealed, cold and protected from light. Once reconstituted with bacteriostatic water, keep the vial refrigerated and use within the window appropriate to your protocol. Avoid repeated freeze-thaw cycles. Add \u003ca href=\"\/products\/bac-water\"\u003ebacteriostatic water\u003c\/a\u003e slowly down the inside wall of the vial and let the powder dissolve on its own. Do not shake. Swirl gently if needed. The volume you add determines the final concentration, so record it with the batch number. Full walkthrough: \u003ca href=\"\/blogs\/news\/how-to-reconstitute-lyophilised-peptides-a-laboratory-guide\"\u003eHow to Reconstitute Lyophilised Peptides\u003c\/a\u003e.\u003c\/p\u003e\n\u003c\/details\u003e\n\u003cdetails\u003e\n\u003csummary\u003e\u003cstrong\u003eHow does shipping work?\u003c\/strong\u003e\u003c\/summary\u003e\n\u003cp\u003eOrders are packed in sealed, tamper-evident vials. See our \u003ca href=\"\/policies\/shipping-policy\"\u003eshipping policy\u003c\/a\u003e for processing times and carriers. Lyophilised peptides do not require cold-chain shipping.\u003c\/p\u003e\n\u003c\/details\u003e\n\u003cdetails\u003e\n\u003csummary\u003e\u003cstrong\u003eIs this for human use?\u003c\/strong\u003e\u003c\/summary\u003e\n\u003cp\u003eNo. Everything we sell is supplied strictly for laboratory and analytical research. It is not a drug, supplement or therapeutic product and is not for human or veterinary use.\u003c\/p\u003e\n\u003c\/details\u003e\n\u003c\/div\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\/MOTSc-10mg.png?v=1787847038"},{"product_id":"5-amino-1mq","title":"5-Amino-1MQ","description":"\u003cp\u003e\u003cstrong\u003e5-Amino-1MQ\u003c\/strong\u003e (CAS 1881738-10-8) is a small-molecule research compound supplied for laboratory and analytical research use only.\u003c\/p\u003e\n\n\u003ch2\u003eResearch background\u003c\/h2\u003e\n\u003cp\u003e5-Amino-1MQ is studied in the literature as an inhibitor of nicotinamide N-methyltransferase (NNMT), an enzyme involved in nicotinamide and NAD+ metabolic pathways. This mechanism has made it a subject of interest in cellular metabolism research, where investigators examine enzyme inhibition characteristics and downstream metabolic signalling in controlled research models. Unlike the peptides in our catalogue, 5-Amino-1MQ is a small molecule rather than a peptide chain.\u003c\/p\u003e\n\n\u003ch2\u003eSpecifications\u003c\/h2\u003e\n\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eCompound:\u003c\/strong\u003e 5-Amino-1MQ\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eCAS number:\u003c\/strong\u003e 1881738-10-8\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eAppearance:\u003c\/strong\u003e Lyophilised powder\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePurity:\u003c\/strong\u003e 99%+ verified by HPLC-MS\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eAvailable sizes:\u003c\/strong\u003e 5mg, 10mg\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePresentation:\u003c\/strong\u003e Sealed, tamper-evident vial\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003ch2\u003eTesting and verification\u003c\/h2\u003e\n\u003cp\u003eIndependently analysed by third-party laboratory using HPLC-MS, with batch-specific Certificates of Analysis published on our \u003ca href=\"\/pages\/lab-results\"\u003eLab Results\u003c\/a\u003e page.\u003c\/p\u003e\n\n\u003ch2\u003eHandling and storage\u003c\/h2\u003e\n\u003cp\u003eStore the sealed vial cold and protected from light.\u003c\/p\u003e\n\n\u003cp\u003e\u003cem\u003eResearch use only. Not a medicine, supplement or therapeutic good. Not for human or veterinary consumption.\u003c\/em\u003e\u003c\/p\u003e","brand":"PureX Labs","offers":[{"title":"5mg","offer_id":47548302983412,"sku":null,"price":35.0,"currency_code":"USD","in_stock":true},{"title":"10mg","offer_id":67648605487348,"sku":null,"price":60.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0804\/5802\/3156\/files\/5-Amino-1MQ-5mg.png?v=1787847038"},{"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},{"title":"10mg","offer_id":67648611090676,"sku":null,"price":45.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0804\/5802\/3156\/files\/Semax-5mg.png?v=1787847038"},{"product_id":"ss-31","title":"SS-31","description":"\u003cp\u003e\u003cstrong\u003eSS-31\u003c\/strong\u003e (Elamipretide, CAS 736992-21-5) is a mitochondria-targeted tetrapeptide supplied for laboratory and analytical research use only.\u003c\/p\u003e\n\n\u003ch2\u003eResearch background\u003c\/h2\u003e\n\u003cp\u003eSS-31 is studied for its affinity for cardiolipin, a phospholipid located in the inner mitochondrial membrane. This localisation property has made it a compound of interest in mitochondrial research, where investigators examine membrane interaction, cellular bioenergetics and oxidative stress mechanisms in controlled research models.\u003c\/p\u003e\n\n\u003ch2\u003eSpecifications\u003c\/h2\u003e\n\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eCompound:\u003c\/strong\u003e SS-31 (Elamipretide)\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eCAS number:\u003c\/strong\u003e 736992-21-5\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eAppearance:\u003c\/strong\u003e Lyophilised white powder\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePurity:\u003c\/strong\u003e 99.058% verified by HPLC-MS\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eAvailable size:\u003c\/strong\u003e 10mg\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePresentation:\u003c\/strong\u003e Sealed, tamper-evident vial\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003ch2\u003eTesting and verification\u003c\/h2\u003e\n\u003cp\u003eIndependently analysed by third-party laboratory using HPLC-MS, with the batch-specific Certificate of Analysis published on our \u003ca href=\"\/pages\/lab-results\"\u003eLab Results\u003c\/a\u003e page.\u003c\/p\u003e\n\n\u003ch2\u003eHandling and storage\u003c\/h2\u003e\n\u003cp\u003eSupplied lyophilised. Store sealed vials cold and protected from light.\u003c\/p\u003e\n\n\u003cp\u003e\u003cem\u003eResearch use only. Not a medicine, supplement or therapeutic good. Not for human or veterinary consumption.\u003c\/em\u003e\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\/SS31-10mg.png?v=1787847039"},{"product_id":"klow","title":"KLOW","description":"\u003cp\u003e\u003cstrong\u003eKLOW\u003c\/strong\u003e is a four-component research blend supplied for laboratory and analytical research use only, combining GHK-Cu, BPC-157, TB-500 and KPV in a single lyophilised vial.\u003c\/p\u003e\n\n\u003ch2\u003eResearch background\u003c\/h2\u003e\n\u003cp\u003eKLOW combines four compounds that are individually well documented in tissue and dermal research literature. GHK-Cu is a copper-binding tripeptide studied in collagen and skin research; BPC-157 and TB-500 are studied in soft-tissue and structural repair models; and KPV is a tripeptide fragment studied in inflammatory signalling research. Blends of this type are used by researchers examining combined-compound activity rather than isolated single-compound effects.\u003c\/p\u003e\n\n\u003ch2\u003eSpecifications\u003c\/h2\u003e\n\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eComponents:\u003c\/strong\u003e GHK-Cu, BPC-157, TB-500, KPV\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eAppearance:\u003c\/strong\u003e Lyophilised powder\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePurity:\u003c\/strong\u003e 99.4%+ verified by HPLC-MS\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eAvailable size:\u003c\/strong\u003e 80mg total\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePresentation:\u003c\/strong\u003e Sealed, tamper-evident vial\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003ch2\u003eTesting and verification\u003c\/h2\u003e\n\u003cp\u003eEach component is independently analysed by third-party laboratory using HPLC-MS. Certificates of Analysis for the blend are published on our \u003ca href=\"\/pages\/lab-results\"\u003eLab Results\u003c\/a\u003e page.\u003c\/p\u003e\n\n\u003ch2\u003eHandling and storage\u003c\/h2\u003e\n\u003cp\u003eSupplied lyophilised. Store sealed vials cold and protected from light.\u003c\/p\u003e\n\n\u003cp\u003e\u003cem\u003eResearch use only. Not a medicine, supplement or therapeutic good. Not for human or veterinary consumption.\u003c\/em\u003e\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\/KLOW-80mg.png?v=1787847038"},{"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\/GLOW-70mg.png?v=1787847038"},{"product_id":"kpv","title":"KPV","description":"\u003cp\u003e\u003cstrong\u003eKPV\u003c\/strong\u003e (Lys-Pro-Val, CAS 67727-97-3) is a synthetic tripeptide supplied for laboratory and analytical research use only. It corresponds to the C-terminal three amino acids of alpha-melanocyte-stimulating hormone (α-MSH) and is one of the smallest peptides in our catalogue.\u003c\/p\u003e\n\n\u003ch2\u003eResearch background\u003c\/h2\u003e\n\u003cp\u003eKPV is characterised in the literature as the minimal anti-inflammatory fragment of α-MSH. Reported areas of investigation include inhibition of NF-κB activation, modulation of pro-inflammatory cytokine expression and interaction with the PepT1 transporter in intestinal epithelial models. Investigators typically study it in the context of mucosal inflammation, wound-healing models and comparative melanocortin-fragment activity. It is also a component of our \u003ca href=\"\/products\/klow\"\u003eKLOW\u003c\/a\u003e research blend.\u003c\/p\u003e\n\n\u003ch2\u003eSpecifications\u003c\/h2\u003e\n\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eCompound:\u003c\/strong\u003e KPV\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eSequence:\u003c\/strong\u003e Lys-Pro-Val\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eCAS number:\u003c\/strong\u003e 67727-97-3\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eAppearance:\u003c\/strong\u003e Lyophilised white powder\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePurity:\u003c\/strong\u003e 99%+ verified by HPLC-MS\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eAvailable size:\u003c\/strong\u003e 10mg\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePresentation:\u003c\/strong\u003e Sealed, tamper-evident vial\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003ch2\u003eTesting and verification\u003c\/h2\u003e\n\u003cp\u003eEvery batch is independently analysed by a third-party laboratory using HPLC-MS to confirm identity, quantity and purity. Each lot is assigned a unique batch identifier and published with its corresponding Certificate of Analysis on our \u003ca href=\"\/pages\/lab-results\"\u003eLab Results\u003c\/a\u003e page, so the exact paperwork for the batch you receive can be reviewed before a vial is ever opened.\u003c\/p\u003e\n\n\u003ch2\u003eHandling and storage\u003c\/h2\u003e\n\u003cp\u003eSupplied lyophilised for stability in transit. Store the sealed vial cold and protected from light. Standard laboratory handling practices apply.\u003c\/p\u003e\n\n\u003cp\u003e\u003cem\u003eResearch use only. This material is intended strictly for laboratory and analytical research. It is not a medicine, supplement or therapeutic good, and is not for human or veterinary consumption.\u003c\/em\u003e\u003c\/p\u003e","brand":"PureX Labs","offers":[{"title":"10mg","offer_id":49064755396852,"sku":null,"price":50.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0804\/5802\/3156\/files\/KPV-10mg.png?v=1787847038"},{"product_id":"epithalon","title":"Epithalon","description":"\u003cp\u003e\u003cstrong\u003eEpithalon\u003c\/strong\u003e (Epitalon, CAS 307297-39-8) is a synthetic tetrapeptide (Ala-Glu-Asp-Gly) supplied for laboratory and analytical research use only. It is based on the naturally occurring pineal peptide epithalamin and is one of the most widely referenced compounds in cellular ageing research.\u003c\/p\u003e\n\n\u003ch2\u003eResearch background\u003c\/h2\u003e\n\u003cp\u003eEpithalon is characterised in the literature for its investigated relationship with telomerase activity and telomere length in cultured cell models. Research interest centres on its potential role in cellular senescence pathways, circadian regulation and pineal gland function. Investigators typically study it in the context of telomere biology, gene-expression modulation and comparative longevity models.\u003c\/p\u003e\n\n\u003ch2\u003eSpecifications\u003c\/h2\u003e\n\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eCompound:\u003c\/strong\u003e Epithalon (Epitalon)\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eSequence:\u003c\/strong\u003e Ala-Glu-Asp-Gly\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eCAS number:\u003c\/strong\u003e 307297-39-8\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eAppearance:\u003c\/strong\u003e Lyophilised white powder\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePurity:\u003c\/strong\u003e 99%+ verified by HPLC-MS\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eAvailable sizes:\u003c\/strong\u003e 10mg, 50mg\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePresentation:\u003c\/strong\u003e Sealed, tamper-evident vial\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003ch2\u003eTesting and verification\u003c\/h2\u003e\n\u003cp\u003eEvery batch is independently analysed by a third-party laboratory using HPLC-MS to confirm identity, quantity and purity. Each lot is assigned a unique batch identifier and published with its corresponding Certificate of Analysis on our \u003ca href=\"\/pages\/lab-results\"\u003eLab Results\u003c\/a\u003e page, so the exact paperwork for the batch you receive can be reviewed before a vial is ever opened.\u003c\/p\u003e\n\n\u003ch2\u003eHandling and storage\u003c\/h2\u003e\n\u003cp\u003eSupplied lyophilised for stability in transit. Store the sealed vial cold and protected from light. Standard laboratory handling practices apply.\u003c\/p\u003e\n\n\u003cp\u003e\u003cem\u003eResearch use only. This material is intended strictly for laboratory and analytical research. It is not a medicine, supplement or therapeutic good, and is not for human or veterinary consumption.\u003c\/em\u003e\u003c\/p\u003e","brand":"PureX Labs","offers":[{"title":"10mg","offer_id":67648572326132,"sku":null,"price":35.0,"currency_code":"USD","in_stock":true},{"title":"50mg","offer_id":67648572358900,"sku":null,"price":120.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0804\/5802\/3156\/files\/Epithalon-10mg.png?v=1792092350"},{"product_id":"dsip","title":"DSIP","description":"\u003cp\u003e\u003cstrong\u003eDSIP\u003c\/strong\u003e (Delta Sleep-Inducing Peptide, CAS 62568-57-4) is a naturally occurring nonapeptide supplied in synthetic form for laboratory and analytical research use only. It was first isolated from the cerebral venous blood of rabbits and has been studied for several decades as a neuromodulatory peptide.\u003c\/p\u003e\n\n\u003ch2\u003eResearch background\u003c\/h2\u003e\n\u003cp\u003eDSIP is characterised in the literature by its reported association with slow-wave (delta) sleep patterns in early electroencephalographic studies. Subsequent research has examined its interaction with hypothalamic-pituitary signalling, stress-response pathways and oxidative-stress markers in various models. Investigators typically study it in the context of neuropeptide signalling, sleep-architecture research and neuroendocrine regulation.\u003c\/p\u003e\n\n\u003ch2\u003eSpecifications\u003c\/h2\u003e\n\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eCompound:\u003c\/strong\u003e DSIP (Delta Sleep-Inducing Peptide)\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eSequence:\u003c\/strong\u003e Trp-Ala-Gly-Gly-Asp-Ala-Ser-Gly-Glu\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eCAS number:\u003c\/strong\u003e 62568-57-4\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eAppearance:\u003c\/strong\u003e Lyophilised white powder\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePurity:\u003c\/strong\u003e 99%+ verified by HPLC-MS\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eAvailable size:\u003c\/strong\u003e 10mg\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePresentation:\u003c\/strong\u003e Sealed, tamper-evident vial\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003ch2\u003eTesting and verification\u003c\/h2\u003e\n\u003cp\u003eEvery batch is independently analysed by a third-party laboratory using HPLC-MS to confirm identity, quantity and purity. Each lot is assigned a unique batch identifier and published with its corresponding Certificate of Analysis on our \u003ca href=\"\/pages\/lab-results\"\u003eLab Results\u003c\/a\u003e page, so the exact paperwork for the batch you receive can be reviewed before a vial is ever opened.\u003c\/p\u003e\n\n\u003ch2\u003eHandling and storage\u003c\/h2\u003e\n\u003cp\u003eSupplied lyophilised for stability in transit. Store the sealed vial cold and protected from light. Standard laboratory handling practices apply.\u003c\/p\u003e\n\n\u003cp\u003e\u003cem\u003eResearch use only. This material is intended strictly for laboratory and analytical research. It is not a medicine, supplement or therapeutic good, and is not for human or veterinary consumption.\u003c\/em\u003e\u003c\/p\u003e","brand":"PureX Labs","offers":[{"title":"10mg","offer_id":67648595689716,"sku":null,"price":35.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0804\/5802\/3156\/files\/DSIP-10mg.png?v=1792092349"},{"product_id":"selank","title":"Selank","description":"\u003cp\u003e\u003cstrong\u003eSelank\u003c\/strong\u003e (CAS 129954-34-3) is a synthetic heptapeptide supplied for laboratory and analytical research use only. It is a stabilised analogue of the endogenous immunomodulatory peptide tuftsin, extended with a Pro-Gly-Pro C-terminal sequence, and is closely related to Semax in origin and research context.\u003c\/p\u003e\n\n\u003ch2\u003eResearch background\u003c\/h2\u003e\n\u003cp\u003eSelank is characterised in the literature as a nootropic and anxiolytic-class research peptide. Reported areas of investigation include modulation of GABAergic signalling, expression of brain-derived neurotrophic factor (BDNF), enkephalin degradation and immune-related gene expression. Investigators typically study it alongside Semax in the context of neuropeptide signalling, stress-response models and comparative peptide pharmacology.\u003c\/p\u003e\n\n\u003ch2\u003eSpecifications\u003c\/h2\u003e\n\u003cul\u003e\n\u003cli\u003e\n\u003cstrong\u003eCompound:\u003c\/strong\u003e Selank\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eSequence:\u003c\/strong\u003e Thr-Lys-Pro-Arg-Pro-Gly-Pro\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eCAS number:\u003c\/strong\u003e 129954-34-3\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eAppearance:\u003c\/strong\u003e Lyophilised white powder\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePurity:\u003c\/strong\u003e 99%+ verified by HPLC-MS\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003eAvailable size:\u003c\/strong\u003e 10mg\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong\u003ePresentation:\u003c\/strong\u003e Sealed, tamper-evident vial\u003c\/li\u003e\n\u003c\/ul\u003e\n\n\u003ch2\u003eTesting and verification\u003c\/h2\u003e\n\u003cp\u003eEvery batch is independently analysed by a third-party laboratory using HPLC-MS to confirm identity, quantity and purity. Each lot is assigned a unique batch identifier and published with its corresponding Certificate of Analysis on our \u003ca href=\"\/pages\/lab-results\"\u003eLab Results\u003c\/a\u003e page, so the exact paperwork for the batch you receive can be reviewed before a vial is ever opened.\u003c\/p\u003e\n\n\u003ch2\u003eHandling and storage\u003c\/h2\u003e\n\u003cp\u003eSupplied lyophilised for stability in transit. Store the sealed vial cold and protected from light. Standard laboratory handling practices apply.\u003c\/p\u003e\n\n\u003cp\u003e\u003cem\u003eResearch use only. This material is intended strictly for laboratory and analytical research. It is not a medicine, supplement or therapeutic good, and is not for human or veterinary consumption.\u003c\/em\u003e\u003c\/p\u003e","brand":"PureX Labs","offers":[{"title":"10mg","offer_id":67648600113396,"sku":null,"price":40.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0804\/5802\/3156\/files\/Selank-10mg.png?v=1792092349"}],"url":"https:\/\/purexlabs.io\/collections\/research-catalog.oembed","provider":"PureX Labs","version":"1.0","type":"link"}