{"title":"Skin \u0026 Aesthetic","description":"","products":[{"product_id":"ghk-cu","title":"GHK-CU","description":"\u003cp dir=\"ltr\"\u003eGHK-Cu is a naturally occurring copper-binding peptide composed of 3 amino acids, i.e. glycyl-L-histidyl-L-lysine.\u003csup dir=\"ltr\"\u003e(1)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003e-Cu refers to the chemical addition of copper. GHK-Cu (Copper) is a small tripeptide found in plasma and reportedly releases at the time of injury. The concentration of GHK-Cu declines with age. At 20 years, the average concentration of GHK-Cu of 200 ng\/mL declines to 80 ng\/mL by 60 years.\u003csup dir=\"ltr\"\u003e(1)\u003c\/sup\u003e\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eStudies\u003csup dir=\"ltr\"\u003e(4)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003ehave suggested when the plasma GHK peptide is added to the cell culture in nanomolar amounts; the peptide has the potential to induce a wide range of responses from growth stimulation to toxic cell differentiation. During the isolation of the peptide, researchers suggested that it exhibited potential chelating properties and might co-isolate with almost the same amount of copper ions and a fifth of the amount of iron found in the cells. When the peptide was incubated in the isolated cells as a bound complex with copper and iron molecules, maximal potential was reported.\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eStudies\u003csup dir=\"ltr\"\u003e(5)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003ehave suggested that the peptide exhibits potential in gene expression and may to reset elements of the genome. By this potential mechanism, GHK-Cu peptide may restore impaired cells, including carcinogenic cells and COPD cells. GHK-Cu peptide has been researched for its potential across a variety of functions\u003csup dir=\"ltr\"\u003e(1)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eincluding that it may tighten and reverse the thinning of aging skin structure, supporting the extracellular matrix, that it may restore the skin barrier and moderate texture, hyperpigmentation and lesions, may support tissue repair and mitigate inflammation, may stimulate increasing hair follicle size, may exert antioxidant properties and, finally, may exhibit gene restructuring potential.\u003c\/p\u003e\n\u003ch3\u003eSpecifications\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003e\u003cstrong dir=\"ltr\"\u003eMolecular Formula:\u003c\/strong\u003e\u003cspan\u003e \u003c\/span\u003eC\u003csub dir=\"ltr\"\u003e14\u003c\/sub\u003eH\u003csub dir=\"ltr\"\u003e23\u003c\/sub\u003eCuN\u003csub dir=\"ltr\"\u003e6\u003c\/sub\u003eO\u003csub dir=\"ltr\"\u003e4\u003c\/sub\u003e\u003cbr dir=\"ltr\"\u003e\u003cstrong dir=\"ltr\"\u003eMolecular Weight:\u003c\/strong\u003e\u003cspan\u003e \u003c\/span\u003e340.38 g\/mol\u003cbr dir=\"ltr\"\u003e\u003cstrong dir=\"ltr\"\u003eOther Known Titles:\u003c\/strong\u003e\u003cspan\u003e \u003c\/span\u003eglycyl-L-histidyl-L-lysine-copper 2+\u003c\/p\u003e\n\u003ch2\u003eResearch and Clinical Studies\u003c\/h2\u003e\n\u003ch3\u003e\u003cem\u003eGHK Peptide Initial Research\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eThis 1980s study\u003csup dir=\"ltr\"\u003e(6)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003esuggested the biological potential of the naturally occurring peptide in tissue repair. GHK peptide may host copper (II) ions due to possible copper affinity and may thereby stimulate the synthesis of collagen and increase the accumulation of total proteins and DNA at the injury site. Dermal wounded rats were used for this study. At the time of injury, the release of GHK peptide was induced. ‘Emergency response molecules’ were released from the matrix at the site of injury. Once released, GHK appeared to bind with Cu ions found in the blood and then stimulate the synthesis of decorin protein. Decorin protein is responsible for the synthesis of collagen and regulation of wound healing and anti-tumor defense mechanism. Further studies in the 2000s,\u003csup dir=\"ltr\"\u003e(7)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003esuggested that the GHK-Cu peptide hosts the potential to not only stimulate the collagen synthesis but also stimulate the production of tissue inhibitors, TIMP-1 and TIMP-2.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eGHK Peptide and Tissue Repair\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eIn this study,\u003csup dir=\"ltr\"\u003e(8)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003ethe main aim was to understand the action of the GHK-Cu peptide complex when applied to the open wounds in comparison to zinc oxide. 18 New Zealand white rabbits were used for this study, divided into three groups – one group was presented with GHK-Cu, second group with zinc oxide and third group with placebo. Woulds were induced on each rabbit and the rabbits were presented with the respective compounds for 21 consecutive days. After 21 days, it was suggested by the researchers that the group delivered with the GHK-Cu peptide complex appeared to exhibit increased healing compared to the group given zinc oxide or placebo.\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eIn this study,\u003csup dir=\"ltr\"\u003e(9)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003ethe main aim was to understand the action of the GHK-Cu peptide complex as compared to helium neon laser. Laser applications were measured at 1 J cm2 and 3 J cm2. 24 New Zealand white rabbits were used for this study, divided into three groups and presented with respective concentrations of the GHK-Cu peptide complex and helium neon laser application. Experimental wounds were created on all the rabbits and all rabbits were studied for 28 consecutive days with the respective compounds. After the study, it was suggested by the researchers that rabbits studied with GHK-Cu peptide and higher concentration of the laser application appeared more receptive toward wound healing than the other group. The rabbits presented with GHK-Cu peptide exhibited an apparent decline in neutrophil counts and increase in neovascularization.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eGHK Peptide and Metastasis\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eIn this 1983 study,\u003csup dir=\"ltr\"\u003e(1)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003ethe actions of the mixture of GHK-Cu complex and ascorbic acid (Vitamin C) on the growth of the sarcoma (tumor) cells was observed. 180 mice with cancerous growths were exposed to this mixture. Researchers suggested the mixture had the potential to induce a decline in the growth of carcinogenic cells in the subject mice. It was later reported by the researchers that GHK-Cu peptide complex exhibited some potential in increasing the expression of caspase and the associated genes, as well as gene expression associated with DNA repair. Specifically, this peptide seemed to suppress the growth of two types of cancer cells in experimental settings: SH-SY5Y neuroblastoma cells, which are a model for studying nerve cell behavior and pathology, and U937 histiocytic lymphoma cells, which are used to study the immune system's response to cancer. Additionally, the peptide might have reactivated the apoptosis pathway, a type of programmed cell death crucial for removing faulty cells, as evidenced by activity in caspases 3 and 7, which are enzymes that play key roles in apoptosis. Conversely, in a study of non-cancerous cells, GHK appeared to promote the growth of NIH-3T3 fibroblasts, which are healthy cells often used as a standard model to examine cell division and growth.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eGHK Peptide and Ulcers\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eThis clinical study\u003csup dir=\"ltr\"\u003e(10)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003ewas carried out in diabetic subjects with neuropathic ulcers. All subjects were enrolled in a standard wound care protocol, where only the subjects with sharp ulcer wound or debridement were entered into this randomized, placebo controlled clinical trial. The study was carried out using GHK-Cu peptide complex gel. All subjects were divided into different groups, where one group was presented with the peptide gel, whereas others were given standard care with a placebo application. Following the study, researchers suggested that the subjects given the gel exhibited apparently elevated healing at 98%+. The gel complex appeared to have the potential to induce closure of 98.5% of plantar ulcers whereas the control only reportedly induced 60.8% of ulcer healing.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eGHK Peptide and Behavioral Properties\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eIn this study,\u003csup dir=\"ltr\"\u003e(1)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eGHK-Cu was delivered to mice to measure pain mitigation. Mice were placed on a moderately hot plate. Due to heat and the pain, it would usually take longer for mice to lick their paws; however, upon delivery the peptide, the time taken to lick their paws reduced compared to control environments. Researchers suggested the mice got ‘comfortable’ and their pain was eased faster with the presence of GHK-Cu.\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eIn this study,\u003csup dir=\"ltr\"\u003e(11)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003emale rats were deposited into a maze, which was intended to induce anxiety and cause behavioral changes. If anxious, rats were observed to restrict arm movement, keeping \"close arms\"; whereas \"open arm\" behavior was shown in rats with lessened levels of anxiety. As a part of the study, once the peptide was delivered, the time spent by the rats in \"open arms\" state in the maze was monitored. After the study, it was reported by the researchers that the peptide exhibited some potential in increasing \"open arms\" states in the subjects.\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eIn an additional study,\u003csup dir=\"ltr\"\u003e(12)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003etwo rats were placed in a small cage and were then given minor electric shocks. As a result of these shocks, the rat would become agitated and attack the second rat. Twelve minutes before this experiment, GHK-Cu peptide was delivered to both rats. It was noted by the researchers that the number of attacks, after the electric shocks, reduced by 5 times than usual.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eGHK-Cu and Antioxidative potential\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eA study has investigated the potential of Glycyl-L-histidyl-L-lysine (GHK) to regulate the presence of reactive oxygen species (ROS) within laboratory cells, with a focus on its ability to mitigate oxidative stress through interactions with various ROS types.\u003csup dir=\"ltr\"\u003e(13)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eGHK is proposed to act as an endogenous antioxidant, potentially due to its selective targeting and neutralization of certain radicals, specifically hydroxyl (·OH) and peroxyl (ROO·) radicals. The antioxidant properties of GHK were assessed using two primary techniques: flow cytometry, a method for analyzing various cellular characteristics, and electron spin resonance (ESR) spin-trapping, which is employed to detect free radicals. Throughout these evaluations, GHK appeared to lower ROS levels induced by tert-butyl hydroperoxide (t-BOPD), a chemical known to promote oxidative stress within cells. The ESR data revealed that GHK was notably positive in reducing the concentrations of ·OH and ROO· radicals, although it had a seemingly modest action on superoxide (O2 -·) radicals. Additional examinations utilizing ESR assessed the relative potential of GHK in neutralizing ·OH radicals compared to other antioxidants like carnosine and reduced glutathione (GSH), both recognized for their antioxidant capabilities. Preliminary results suggest that GHK could be more proficient at neutralizing ·OH radicals compared to these alternatives.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eGHK-Cu and Antioxidative potential\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eA study has investigated the possible mechanisms through which the peptide complex GHK-Cu could influence anti-inflammatory actions, particularly against lung tissue inflammation induced by cigarette smoke (CS).\u003csup dir=\"ltr\"\u003e(14)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eIt is hypothesized that GHK-Cu may influence various biochemical pathways and molecular markers related to inflammation and oxidative stress, although the specific mechanisms remain somewhat uncertain. In experiments involving mouse models exposed to CS, exposure to GHK-Cu was linked to a potential decrease in the production of pro-inflammatory cytokines, including interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α), found in bronchoalveolar lavage fluid—fluid used to capture cells and soluble factors from the airways and lung tissues. These results tentatively suggest that GHK-Cu might help mitigate the inflammatory responses triggered by cigarette smoke. Additionally, there was a noted possible reduction in the activity of myeloperoxidase (MPO), an enzyme that serves as a marker for neutrophil-driven inflammation and oxidative stress, in lung tissues that received GHK-Cu exposure. This observation could indicate a potential role of GHK-Cu in limiting the activation or mobilization of neutrophils, possibly curtailing the oxidative bursts and consequent inflammation. At the molecular level, the research proposes that GHK-Cu may interact with the nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) signaling pathway. NF-κB plays a critical role in the initiation and perpetuation of inflammation. The peptide complex is thought to possibly inhibit NF-κB activation by affecting the phosphorylation of IκBα, a protein that inhibits NF-κB. This interaction could hypothetically result in lower expression of genes that promote inflammation, controlled by NF-κB. Furthermore, the study suggests that GHK-Cu could potentially influence the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway. Nrf2 is integral to cellular defenses against oxidative damage. GHK-Cu is posited to possibly boost the expression and nuclear translocation of Nrf2 in lung tissues, thereby promoting the transcription of genes that combat oxidative stress and possibly enhancing the cellular resilience against oxidative damage. The investigation further examines how GHK-Cu interacts with markers of oxidative stress, such as malondialdehyde (MDA) and glutathione (GSH). MDA is a product of lipid peroxidation and an indicator of oxidative stress, while GSH is a vital antioxidant that plays a crucial role in cellular defense mechanisms. The experimentation with GHK-Cu is associated with a tentative reduction in MDA levels and a possible restoration of GSH levels, suggesting a potential ameliorative action on oxidative stress.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eGHK-Cu and Lipid Peroxidation\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eA theoretical model posits that GHK could play a role in mitigating the discharge of iron from ferritin.\u003csup dir=\"ltr\"\u003e(15)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eFerritin, a protein complex that stores iron, releases it in a form that can facilitate lipid peroxidation, a process where free radicals attack lipids, leading to cell damage. It is suggested that GHK might inhibit the assembly of iron complexes within injured tissues, which could, in turn, decrease inflammation. Further exploration of GHK's role reveals that it may interact with specific biological pathways that govern the release of iron from ferritin. This interaction might restrict the release of iron by up to 87%, although this is a provisional estimate. Such a significant reduction in iron release could conceivably diminish both inflammation and oxidative stress, the latter being a condition where damaging oxidative processes occur more rapidly than the body's ability to counteract them, in the affected tissues.\u003c\/p\u003e\n\u003cp\u003e\u003cem\u003e\u003cstrong dir=\"ltr\"\u003eGHK-Cu peptide is available for research and laboratory purposes only.\u003c\/strong\u003e\u003c\/em\u003e\u003c\/p\u003e\n\u003ch3\u003eReferences:\u003c\/h3\u003e\n\u003col\u003e\n\u003cli\u003ePickart, Loren, and Anna Margolina. “Regenerative and Protective Actions of the GHK-Cu Peptide in the Light of the New Gene Data.” International journal of molecular sciences vol. 19,7 1987. 7 Jul. 2018, doi:10.3390\/ijms19071987.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC6073405\/\"\u003ehttps:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC6073405\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003ePickart L, Freedman JH, Loker WJ, Peisach J, Perkins CM, Stenkamp RE, Weinstein B. Growth-modulating plasma tripeptide may function by facilitating copper uptake into cells. Nature. 1980 Dec 25;288(5792):715-7. doi: 10.1038\/288715a0. PMID: 7453802.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/7453802\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/7453802\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eL.O. Pilgeram, L.R. Pickart, Control of fibrinogen biosynthesis: The role of free fatty acid, Journal of Atherosclerosis Research, Volume 8, Issue 1, 1968, Pages 155-166, ISSN 0368-1319,\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/doi.org\/10.1016\/S0368-1319(68)80089-4\"\u003ehttps:\/\/doi.org\/10.1016\/S0368-1319(68)80089-4\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003ePickart L, Freedman JH, Loker WJ, Peisach J, Perkins CM, Stenkamp RE, Weinstein B. Growth-modulating plasma tripeptide may function by facilitating copper uptake into cells. Nature. 1980 Dec 25;288(5792):715-7. doi: 10.1038\/288715a0. PMID: 7453802.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/7453802\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/7453802\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003ePickart L, Vasquez-Soltero JM, Margolina A. GHK and DNA: resetting the human genome to health. Biomed Res Int. 2014;2014:151479. doi: 10.1155\/2014\/151479. Epub 2014 Sep 11. PMID: 25302294; PMCID: PMC4180391.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/25302294\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/25302294\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eMaquart FX, Pickart L, Laurent M, Gillery P, Monboisse JC, Borel JP. Stimulation of collagen synthesis in fibroblast cultures by the tripeptide-copper complex glycyl-L-histidyl-L-lysine-Cu2+. FEBS Lett. 1988 Oct 10;238(2):343-6. doi: 10.1016\/0014-5793(88)80509-x. PMID: 3169264.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/3169264\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/3169264\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eSiméon A, Emonard H, Hornebeck W, Maquart FX. The tripeptide-copper complex glycyl-L-histidyl-L-lysine-Cu2+ stimulates matrix metalloproteinase-2 expression by fibroblast cultures. Life Sci. 2000 Sep 22;67(18):2257-65. doi: 10.1016\/s0024-3205(00)00803-1. PMID: 11045606.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/11045606\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/11045606\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eCangul IT, Gul NY, Topal A, Yilmaz R. Evaluation of the effects of tripeptide-copper complex and zinc oxide on open-wound healing in rabbits. Vet Dermatol. 2006 Dec;17(6):417-23. doi: 10.1111\/j.1365-3164.2006.00551.x. PMID: 17083573.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/17083573\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/17083573\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eGul NY, Topal A, Cangul IT, Yanik K. The effects of tripeptide copper complex and helium-neon laser on wound healing in rabbits. Vet Dermatol. 2008 Feb;19(1):7-14. doi: 10.1111\/j.1365-3164.2007.00647.x. PMID: 18177285.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/18177285\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/18177285\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eMulder GD, Patt LM, Sanders L, Rosenstock J, Altman MI, Hanley ME, Duncan GW. Enhanced healing of ulcers in patients with diabetes by treatment with glycyl-l-histidyl-l-lysine copper. Wound Repair Regen. 1994 Oct;2(4):259-69. doi: 10.1046\/j.1524-475X.1994.20406.x. PMID: 17147644.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/17147644\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/17147644\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eBobyntsev II, Chernysheva OI, Dolgintsev ME, Smakhtin MY, Belykh AE. Anxiolytic effects of Gly-His-Lys peptide and its analogs. Bull Exp Biol Med. 2015 Apr;158(6):726-8. doi: 10.1007\/s10517-015-2847-3. Epub 2015 Apr 23. PMID: 25900608.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/25900608\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/25900608\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eSever'yanova LА, Dolgintsev ME. Effects of Tripeptide Gly-His-Lys in Pain-Induced Aggressive-Defensive Behavior in Rats. Bull Exp Biol Med. 2017 Dec;164(2):140-143. doi: 10.1007\/s10517-017-3943-3. Epub 2017 Nov 27. PMID: 29181666.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/29181666\/\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/29181666\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eSakuma, S., Ishimura, M., Yuba, Y., Itoh, Y., \u0026amp; Fujimoto, Y. (2018). The peptide glycyl-ʟ-histidyl-ʟ-lysine is an endogenous antioxidant in living organisms, possibly by diminishing hydroxyl and peroxyl radicals. International journal of physiology, pathophysiology and pharmacology, 10(3), 132–138.\u003c\/li\u003e\n\u003cli\u003eZhang, Q., Yan, L., Lu, J., \u0026amp; Zhou, X. (2022). Glycyl-L-histidyl-L-lysine-Cu2+ attenuates cigarette smoke-induced pulmonary emphysema and inflammation by reducing oxidative stress pathway. Frontiers in molecular biosciences, 9, 925700.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/doi.org\/10.3389\/fmolb.2022.925700\"\u003ehttps:\/\/doi.org\/10.3389\/fmolb.2022.925700\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eMiller, D. M., DeSilva, D., Pickart, L., \u0026amp; Aust, S. D. (1990). Effects of glycyl-histidyl-lysyl chelated Cu(II) on ferritin dependent lipid peroxidation. Advances in experimental medicine and biology, 264, 79–84.\u003cspan\u003e \u003c\/span\u003e\u003ca dir=\"ltr\" rel=\"noopener\" href=\"https:\/\/doi.org\/10.1007\/978-1-4684-5730-8_11\"\u003ehttps:\/\/doi.org\/10.1007\/978-1-4684-5730-8_11\u003c\/a\u003e\n\u003c\/li\u003e\n\u003c\/ol\u003e","brand":"PureX Labs","offers":[{"title":"50mg","offer_id":47487353553140,"sku":null,"price":25.0,"currency_code":"USD","in_stock":true},{"title":"100mg","offer_id":47487358173428,"sku":null,"price":50.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0804\/5802\/3156\/files\/GHK-CU_50MG.png?v=1769106141"},{"product_id":"mt-2-melanotan-ii","title":"MT-2 (Melanotan II)","description":"\u003cdiv class=\"wp-block-woocommerce-product-details alignwide is-style-minimal\" data-hide-tab-title=\"true\" data-block-name=\"woocommerce\/product-details\"\u003e\n\u003cdiv\u003e\n\u003cdiv class=\"woocommerce-tabs wc-tabs-wrapper\"\u003e\n\u003cdiv aria-labelledby=\"tab-title-description\" role=\"tabpanel\" id=\"tab-description\" class=\"woocommerce-Tabs-panel woocommerce-Tabs-panel--description panel entry-content wc-tab\"\u003e\n\u003cp\u003eMelanotan II (MT-2) is a synthetic peptide analog of the naturally occurring hormone α-MSH (alpha-melanocyte-stimulating hormone). Research has explored MT-2 for its ability to bind to melanocortin receptors, which play a role in skin pigmentation and tanning responses. Studies have also investigated its potential influence on appetite and sexual function through these receptor pathways. MT-2 is commonly evaluated in laboratory settings for its possible applications in photoprotection, tanning, and metabolic research. It is intended strictly for scientific study and is not approved for human consumption or cosmetic use.\u003c\/p\u003e\n\u003c\/div\u003e\n\u003c\/div\u003e\n\u003c\/div\u003e\n\u003c\/div\u003e\n\u003cdiv class=\"wp-block-woocommerce-product-collection alignwide is-layout-flow wp-block-woocommerce-product-collection-is-layout-flow\" data-tag-name=\"div\" data-query='{\"perPage\":3,\"pages\":1,\"offset\":0,\"postType\":\"product\",\"order\":\"asc\",\"orderBy\":\"title\",\"search\":\"\",\"exclude\":[],\"inherit\":false,\"taxQuery\":[],\"isProductCollectionBlock\":true,\"featured\":false,\"woocommerceOnSale\":false,\"woocommerceStockStatus\":[\"instock\"],\"woocommerceAttributes\":[],\"woocommerceHandPickedProducts\":[],\"filterable\":true,\"relatedBy\":{\"categories\":true,\"tags\":true}}' data-query-id=\"2\" data-query-context-includes='[\"collection\"]' data-hide-controls='[\"inherit\"]' data-display-layout='{\"type\":\"flex\",\"columns\":3,\"shrinkColumns\":false}' data-dimensions='{\"widthType\":\"fill\"}' data-collection=\"woocommerce\/product-collection\/related\" data-block-name=\"woocommerce\/product-collection\" data-__private-preview-state='{\"isPreview\":true,\"previewMessage\":\"Actual products will vary depending on the product being viewed.\"}' data-wp-router-region=\"wc-product-collection-2\" data-wp-interactive=\"woocommerce\/product-collection\" data-wp-init=\"callbacks.onRender\" data-wp-context='{\"notices\":[],\"hideNextPreviousButtons\":false,\"isDisabledPrevious\":true,\"isDisabledNext\":false,\"ariaLabelPrevious\":\"Previous products\",\"ariaLabelNext\":\"Next products\",\"collection\":\"woocommerce\\\/product-collection\\\/related\"}'\u003e\n\u003cdiv class=\"wc-block-components-notices alignwide\" data-wp-interactive=\"woocommerce\/store-notices\"\u003e\u003cbr\u003e\u003c\/div\u003e\n\u003c\/div\u003e\n\u003cp dir=\"ltr\"\u003e\u003cmeta charset=\"utf-8\"\u003eMelanotan II (MT-2) likely serves as a non-selective agonist with the potential to bind with four out of the five different subtypes of melanocortin receptors (MC-R).\u003csup dir=\"ltr\"\u003e(3)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eDepending on the localization, the receptor-Melanotan 2 bond may induce different actions. Namely, the four receptors that Melanotan 2 may interact with include:\u003c\/p\u003e\n\u003cul\u003e\n\u003cli\u003eThe melanocortin 1 receptor (MC1R) may be expressed in melanocytes, which are cells found in tissues such as dermal tissues, hair, and possibly cells and tissues found in the eye.\u003c\/li\u003e\n\u003cli\u003eThe melanocortin 3 receptor (MC3R) might be found in a range of tissues, potentially including the brain and the placenta. Initial observations suggest that MC3R might be involved in modulating appetite under certain experimental conditions.\u003c\/li\u003e\n\u003cli\u003eThe melanocortin 4 receptor (MC4R) may be localized within the central nervous system, perhaps in the hypothalamus. Some early indications suggest that this receptor may impact neurons that are believed to have some influence over mating behaviors and general arousal.\u003c\/li\u003e\n\u003cli\u003eThe melanocortin 5 receptor (MC5R) appears to be distributed across multiple tissues, although what role it might serve remains unclear.\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003cp dir=\"ltr\"\u003eFor example, the potential interaction between Melanotan 2 and the MC1Rs may lead to increased production of eumelanin, which causes darkening of the epidermal layer’s pigment.\u003csup dir=\"ltr\"\u003e(4)\u003c\/sup\u003e\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eOn the other hand, when Melanotan 2 binds with the MC4R, it may induce supraspinal centers in the brain, which may lead to increased libido. These signals may then be carried to the sympathetic and parasympathetic centers in the spinal cord and thoracolumbar region.\u003csup dir=\"ltr\"\u003e(3)\u003c\/sup\u003e\u003c\/p\u003e\n\u003ch2\u003eChemical Makeup\u003c\/h2\u003e\n\u003cp dir=\"ltr\"\u003e\u003cstrong dir=\"ltr\"\u003eOther Known Titles:\u003c\/strong\u003e\u003cspan\u003e \u003c\/span\u003eMT-II\u003cbr dir=\"ltr\"\u003e\u003cstrong dir=\"ltr\"\u003eMolecular Weight:\u003c\/strong\u003e\u003cspan\u003e \u003c\/span\u003e1024.19 g\/mol\u003cbr dir=\"ltr\"\u003e\u003cstrong dir=\"ltr\"\u003eMolecular Formula:\u003c\/strong\u003e\u003cspan\u003e \u003c\/span\u003eC\u003csub dir=\"ltr\"\u003e50\u003c\/sub\u003eH\u003csub dir=\"ltr\"\u003e69\u003c\/sub\u003eN\u003csub dir=\"ltr\"\u003e15\u003c\/sub\u003eO\u003csub dir=\"ltr\"\u003e9\u003c\/sub\u003e\u003c\/p\u003e\n\u003ch2\u003eResearch and Clinical Studies\u003c\/h2\u003e\n\u003ch3\u003e\u003cem\u003eMelanotan 2 Peptide and Nerve Cell Regeneration\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eResearch\u003csup dir=\"ltr\"\u003e(5)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003ein a murine model of an induced peripheral nerve injury has been employed to investigate the neurotrophic potential of Melanotan 2. 48 hours after half of the murine models were presented with the peptide, it was noted that the Melanotan 2 research models appeared to indicate a recovery in their sensory function. Furthermore, when the murine models were presented with a chemotherapeutic compound, Melanotan 2 appeared to exhibit neuroprotective properties, which protected the nerves from the compound's induced neurotoxicity to a certain extent. This potential is posited to be mediated via the MC4 receptors, which might even promote neurite outgrowth and possibly support the intrinsic capacity of neuronal tissue to recover after injury.\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eAlthough the exact signaling pathways are not fully understood, it is often suggested that the pro-opiomelanocortin (POMC)-derived melanocortin peptides, including compounds analogous to a-melanocyte-stimulating hormone (a-MSH), may influence neuronal structures by increasing the number and length of neurites and potentially promoting nerve sprouting in damaged regions. Since Melanotan 2 is considered a potent melanocortin receptor agonist, it may trigger a cascade of intracellular events that theoretically lead to a better-supported ability of nerve fibers to regenerate after various forms of insult, as well as a partial protective response against toxic neuropathic conditions. Therefore, the researchers concluded that they “\u003cem dir=\"ltr\"\u003eobserved that Melanotan-II also possesses neuroprotective properties, as it partially protected the nerve from a toxic neuropathy induced by cisplatin.\u003c\/em\u003e”\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eMelanotan 2 Peptide and Arousal Neurosignaling\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eIn a clinical study,\u003csup dir=\"ltr\"\u003e(6)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eMelanotan 2 has been suggested to induce increased arousal neuron signaling in more than 80% of cases, compared to only 20% success with a placebo. This research peptide may act via the MC4 receptors and downstream of established neuromodulators, including dopaminergic and oxytocinergic signals, possibly integrating their actions within discrete hypothalamic centers. These regions are thought to coordinate various homeostatic and motivational behaviors, and the introduction of an agonist like Melanotan 2 may potentially reframe the balance of neuronal activity. These researchers also posit that the involvement of MC5 receptors in certain peripheral glands may potentially provide a parallel route that links central neuro signaling with peripheral modulatory factors. However, this remains an area where mechanisms are only hypothesized.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eMelanotan 2 Peptide and Neurodevelopmental Modulation\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eResearchers have said that Melanotan 2 may potentially influence aberrant neural mechanisms by possibly stimulating populations of neurons that may govern social cognition through endogenous oxytocinergic signaling.\u003csup dir=\"ltr\"\u003e(7)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eThese MC4R-sensitive circuits, potentially located in regions such as the paraventricular nucleus of the hypothalamus, might release endogenous oxytocin in response to Melanotan 2, possibly recalibrating imbalanced neurochemical activity thought to underlie key aspects of social impairment. This oxytocin release may, in turn, modulate neurotransmission involving serotonin, glutamate, dopamine, and GABA, all of which are implicated in shaping social adaptation.\u003c\/p\u003e\n\u003cp\u003eBy engaging these systems, Melanotan 2 may alter the functional connectivity of cortical and subcortical networks—regions including, for instance, the anterior cingulate cortex—where oxytocin receptor distribution may differ in atypical neurodevelopmental contexts. In doing so, researchers have been able to hypothesize that Melanotan 2 might restore or modify synaptic communication and synaptic plasticity, which may go so far as to reshape the underlying neuroarchitecture.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eMelanotan 2 Peptide and Models of Sunless Tanning\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eMelanotan 2 may increase melanin production and thereby induce darker pigmentation without the need for ultraviolet irradiation by engaging the MC1R on melanocytes.\u003csup dir=\"ltr\"\u003e(8)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eMoreover, the peptide's cyclic structure supports a more prolonged metabotropic activity compared to other MSH analogs.\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eAlthough the precise intracellular signaling cascades remain incompletely understood, current data suggest that receptor interactions might lead to the elevated synthesis of eumelanin. This might offer a potential pathway for the development of sunless tanning models in a controlled research environment. Specifically, researchers have made comments about their observation of outcomes in research models, such as “\u003cem dir=\"ltr\"\u003eincreased [darkened] pigmentation in the face, upper body, and buttock\u003c\/em\u003e” in experimental settings.\u003c\/p\u003e\n\u003cp\u003e\u003cem\u003e\u003cstrong dir=\"ltr\"\u003eMelanotan 2 peptide is available for research and laboratory purposes only. \u003c\/strong\u003e\u003c\/em\u003e\u003c\/p\u003e\n\u003ch3\u003eReferences:\u003c\/h3\u003e\n\u003col\u003e\n\u003cli\u003eRyakhovsky, Vladimir V et al. “The first preparative solution phase synthesis of Melanotan II.” Beilstein Journal of Organic Chemistry vol. 4 (2008): 39. doi:10.3762\/bjoc.4.39.\u003cspan\u003e \u003c\/span\u003e\u003ca href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/19043625\/\" rel=\"noopener\" dir=\"ltr\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/19043625\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eMac E. Hadley, Discovery that a melanocortin regulates sexual functions in male and female humans, Peptides, Volume 26, Issue 10, 2005, Pages 1687-1689, ISSN 0196-9781,\u003cspan\u003e \u003c\/span\u003e\u003ca href=\"https:\/\/doi.org\/10.1016\/j.peptides.2005.01.023\" rel=\"noopener\" dir=\"ltr\"\u003ehttps:\/\/doi.org\/10.1016\/j.peptides.2005.01.023\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eKing, Stephen H et al. “Melanocortin receptors, melanotropic peptides and penile erection.” Current topics in medicinal chemistry vol. 7,11 (2007): 1098-1106.\u003cspan\u003e \u003c\/span\u003e\u003ca href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC2694735\/\" rel=\"noopener\" dir=\"ltr\"\u003ehttps:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC2694735\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003ePeters, Björn, et al. “Melanotan II: a possible cause of renal infarction: review of the literature and case report.” CEN case reports vol. 9,2 (2020): 159-161. doi:10.1007\/s13730-020-00447-z.\u003cspan\u003e \u003c\/span\u003e\u003ca href=\"https:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC7148395\/\" dir=\"ltr\"\u003ehttps:\/\/www.ncbi.nlm.nih.gov\/pmc\/articles\/PMC7148395\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eTer Laak, Mariël P, et al. “The potent melanocortin receptor agonist melanotan-II promotes peripheral nerve regeneration and has neuroprotective properties in the rat.” European Journal of Pharmacology vol. 462,1-3 (2003): 179-83. doi:10.1016\/s0014-2999(02)02945-x.\u003cspan\u003e \u003c\/span\u003e\u003ca href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/12591111\" rel=\"noopener\" dir=\"ltr\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/12591111\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eWessells, H et al. “Melanocortin receptor agonists, penile erection, and sexual motivation: human studies with Melanotan II.” International journal of impotence research vol. 12 Suppl 4 (2000): S74-9. doi:10.1038\/sj.ijir.3900582.\u003cspan\u003e \u003c\/span\u003e\u003ca href=\"https:\/\/pubmed.ncbi.nlm.nih.gov\/11035391\/\" rel=\"noopener\" dir=\"ltr\"\u003ehttps:\/\/pubmed.ncbi.nlm.nih.gov\/11035391\/\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eMinakova E, Lang J, Medel-Matus JS, Gould GG, Reynolds A, Shin D, Mazarati A, Sankar R. Melanotan-II reverses autistic features in a maternal immune activation mouse model of autism. PLoS One. 2019 Jan 10;14(1):e0210389. Doi: 10.1371\/journal.pone.0210389. PMID: 30629642; PMCID: PMC6328175.\u003c\/li\u003e\n\u003cli\u003eDorr RT, Lines R, Levine N, Brooks C, Xiang L, Hruby VJ, Hadley ME. Evaluation of melanotan-II, a superpotent cyclic melanotropic peptide in a pilot phase-I clinical study. Life Sci. 1996;58(20):1777-84. doi: 10.1016\/0024-3205(96)00160-9. PMID: 8637402.\u003c\/li\u003e\n\u003c\/ol\u003e","brand":"PureX Labs","offers":[{"title":"10mg","offer_id":47548289220852,"sku":null,"price":25.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0804\/5802\/3156\/files\/Render_Mockup_1920_1920_2026-01-31_3.png?v=1769802134"},{"product_id":"klow","title":"KLOW","description":"\u003cp data-end=\"496\" data-start=\"141\"\u003eKLOW is a research-grade multi-peptide blend formulated to support investigation into regenerative biology, tissue recovery, and cellular health. This formulation combines four complementary peptides, each studied for distinct yet overlapping roles in repair signaling, immune balance, and protective mechanisms across multiple tissue systems.\u003c\/p\u003e\n\u003cul data-end=\"1101\" data-start=\"498\"\u003e\n\u003cli data-end=\"648\" data-start=\"498\"\u003e\n\u003cp data-end=\"648\" data-start=\"500\"\u003eBPC-157 (10 mg): A gastric-derived peptide fragment researched for its role in angiogenesis, wound recovery, and gastrointestinal integrity.\u003c\/p\u003e\n\u003c\/li\u003e\n\u003cli data-end=\"806\" data-start=\"649\"\u003e\n\u003cp data-end=\"806\" data-start=\"651\"\u003eGHK-Cu (50 mg): A naturally occurring copper-binding peptide complex studied for collagen signaling, skin regeneration, and cellular communication.\u003c\/p\u003e\n\u003c\/li\u003e\n\u003cli data-end=\"959\" data-start=\"807\"\u003e\n\u003cp data-end=\"959\" data-start=\"809\"\u003eTB-500 (10 mg): A synthetic thymosin beta-4 fragment investigated for cell migration, tissue repair acceleration, and cytoprotective activity.\u003c\/p\u003e\n\u003c\/li\u003e\n\u003cli data-end=\"1101\" data-start=\"960\"\u003e\n\u003cp data-end=\"1101\" data-start=\"962\"\u003eKPV (10 mg): A tripeptide fragment of α-MSH studied for anti-inflammatory signaling, antimicrobial activity, and immune modulation.\u003c\/p\u003e\n\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003cp data-end=\"1279\" data-start=\"1103\"\u003eTogether, these peptides allow researchers to examine synergistic regenerative pathways, inflammatory regulation, and recovery processes across diverse experimental models.\u003c\/p\u003e\n\u003cp data-end=\"1369\" data-start=\"1281\"\u003eTotal peptide content: 80 mg\u003c\/p\u003e","brand":"PureX Labs","offers":[{"title":"80mg","offer_id":47548307964148,"sku":null,"price":120.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0804\/5802\/3156\/files\/Render_Mockup_1920_1920_2026-01-31_13.png?v=1769804833"},{"product_id":"glow","title":"GLOW","description":"\u003cp dir=\"ltr\"\u003eBPC-157 appears to be a distinct synthetic peptide composed of fifteen amino acids and is thought to originate from a fragment of a gastric protein. However, the specific protein has not yet been established. Research models indicate that BPC-157 may interact with intracellular signaling systems relevant to vascular growth via angiogenic signaling and inflammatory regulation via attenuation of pro-inflammatory pathways.\u003cspan\u003e \u003c\/span\u003e\u003csup dir=\"ltr\"\u003e(1)\u003c\/sup\u003e\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eTB-500 is a synthetic peptide identical to the 43 amino acid structure of the endogenous thymosin beta-4, studied for its involvement in cellular migration, cytoskeletal organization, and inflammatory signaling. In vitro studies suggest that exposure to TB-500 may support cell movement and structural coordination, and may also participate in signaling pathways linked to angiogenesis and modulation of inflammatory mediators.\u003cspan\u003e \u003c\/span\u003e\u003csup dir=\"ltr\"\u003e(2)\u003c\/sup\u003e\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eGHK-Cu is a peptide complex consisting of the tripeptide GHK (glycine, histidine, and lysine),  bound to a divalent copper ion (Cu²⁺). Researchers suggest that the GHK sequence may occur endogenously, specifically being released by cells, including fibroblasts, macrophages, and lymphocytes, during damage, as a result of collagen breakdown.\u003cspan\u003e \u003c\/span\u003e\u003csup dir=\"ltr\"\u003e(3)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eThus, GHK-Cu is posited to act as a repair signal, capable of interacting with enzymes, ion channels, and cell-surface receptors, with reported downstream potential on gene expression. The presence of copper may be central to these observations, including collagen synthesis, modulation of inflammatory signaling, and antioxidant potential.\u003c\/p\u003e\n\u003cp\u003eThese peptides may have partially overlapping but also complementary actions, supporting the hypothesis that combined exposure may positively affect inflammatory signaling. In addition, the peptides may all play some role in the regeneration of different cells, possibly supporting factors like vascular formation and cellular behavior.\u003c\/p\u003e\n\u003ch3\u003eChemical Makeup\u003c\/h3\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cem\u003eOther Known Titles\u003c\/em\u003e\u003c\/strong\u003e\u003c\/p\u003e\n\u003cul\u003e\n\u003cli\u003e\n\u003cstrong dir=\"ltr\"\u003e\u003cem dir=\"ltr\"\u003eBPC-157:\u003c\/em\u003e\u003c\/strong\u003e\u003cem dir=\"ltr\"\u003e\u003cspan\u003e \u003c\/span\u003eC\u003csub dir=\"ltr\"\u003e62\u003c\/sub\u003eH\u003csub dir=\"ltr\"\u003e98\u003c\/sub\u003eN\u003csub dir=\"ltr\"\u003e16\u003c\/sub\u003eO\u003csub dir=\"ltr\"\u003e22\u003c\/sub\u003e\u003c\/em\u003e\n\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong dir=\"ltr\"\u003e\u003cem dir=\"ltr\"\u003eTB-500:\u003cspan\u003e \u003c\/span\u003e\u003c\/em\u003e\u003c\/strong\u003e\u003cem dir=\"ltr\"\u003eC\u003csub dir=\"ltr\"\u003e212\u003c\/sub\u003eH\u003csub dir=\"ltr\"\u003e350\u003c\/sub\u003eN\u003csub dir=\"ltr\"\u003e56\u003c\/sub\u003eO\u003csub dir=\"ltr\"\u003e78\u003c\/sub\u003eS\u003c\/em\u003e\n\u003c\/li\u003e\n\u003cli\u003e\n\u003cstrong dir=\"ltr\"\u003e\u003cem dir=\"ltr\"\u003eGHK-Cu:\u003cspan\u003e \u003c\/span\u003e\u003c\/em\u003e\u003c\/strong\u003e\u003cem dir=\"ltr\"\u003eC\u003csub dir=\"ltr\"\u003e14\u003c\/sub\u003eH\u003csub dir=\"ltr\"\u003e23\u003c\/sub\u003eCuN\u003csub dir=\"ltr\"\u003e6\u003c\/sub\u003eO\u003csub dir=\"ltr\"\u003e4\u003c\/sub\u003e\u003c\/em\u003e\n\u003c\/li\u003e\n\u003c\/ul\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cem\u003eMolecular Weight:\u003c\/em\u003e\u003c\/strong\u003e\u003c\/p\u003e\n\u003ch2\u003eResearch and Clinical Studies\u003c\/h2\u003e\n\u003ch3\u003e\u003cem\u003eAnti-inflammatory Signaling Research on BPC-157 \u0026amp; TB-500 \u0026amp; GHK-Cu\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eAll three peptides appear to play some potentially complementary and partially overlapping roles in inflammatory signaling inside and in between cells. Notably, all three appear to have a positive action on toning down inflammatory processes. For example, research conducted in laboratory settings by Santra et al. suggests that TB-500 may lower inflammation-related signaling inside cell cultures of developing brain support cells called oligodendrocyte progenitor cells.\u003cspan\u003e \u003c\/span\u003e\u003csup dir=\"ltr\"\u003e(4)\u003cspan\u003e \u003c\/span\u003e\u003c\/sup\u003eAfter cell stress or injury, these cells are posited to activate innate immune pathways, especially Toll-like receptor (TLR) signaling, which may drive inflammatory responses inside the cell.\u003c\/p\u003e\n\u003cp\u003eThe authors research whether TB-500 may tone down this signaling and suggest that the peptide may increase the level of miR-146a, a small regulatory RNA molecule whose role may be to act as an internal brake on inflammatory signaling pathways. When miR-146a levels rise, two key TLR signaling proteins, IRAK1 and TRAF6, may decrease, and thus they may not transmit inflammatory signals inside the cell, including pathways linked to NF-κB activation, which would otherwise play a major role in inflammatory signaling.\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eFurthermore, research by Sikiric et al. suggests that BPC-157 may also interact with inflammatory signaling, specifically by attenuating inflammatory cell infiltration in research models.\u003cspan\u003e \u003c\/span\u003e\u003csup dir=\"ltr\"\u003e(5)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eApparently, the researchers observed lower levels of biochemical markers linked to inflammation, including markers of neutrophil accumulation, leukotriene B4, and thromboxane B2 in inflamed cellular cultures.\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eThis peptide also appeared to modulate immune cell behavior, with reports of increased macrophage activity, which may support resolution rather than persistence of inflammation. Importantly, these implications were observed without direct immunosuppression of specific cytokines such as TNF, implying a more regulatory mode of action. BPC-157 may “\u003cem dir=\"ltr\"\u003einteract with the NO-system\u003cspan\u003e \u003c\/span\u003e\u003c\/em\u003e[nitric oxide system]\u003cem dir=\"ltr\"\u003e, providing endothelium protection”\u003c\/em\u003e, which may indirectly limit inflammatory amplification by preserving microvascular integrity.\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eLast but not least, experiments by Park et al. suggest that GHK-Cu may also tone down inflammatory signaling in macrophages activated by pro-inflammatory triggers and in lung cell injury models.\u003cspan\u003e \u003c\/span\u003e\u003csup dir=\"ltr\"\u003e(6)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eIn activated macrophages, GHK-Cu apparently lowered intracellular reactive oxygen species and restored superoxide dismutase activity toward control values. The pro-inflammatory triggers apparently increased TNF-α and IL-6 release, while GHK-Cu apparently reduced both cytokines.\u003c\/p\u003e\n\u003cp\u003eMechanistically, the authors suggest that GHK-Cu may have suppressed NF-κB activation by reducing the activation of key regulators. The researchers did not notice significant action on ERK1\/2, JNK1\/2, or NO secretion. In the lung cell cultures, the peptide complex apparently reduced edema, inflammatory cell infiltration, and overall histologic injury scores. The researchers also observed reductions in TNF-α, IL-6, total cell counts, neutrophils, MPO activity, and markers of alveolar permeability.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eCellular Regeneration Potential of BPC-157 \u0026amp; TB-500 \u0026amp; GHK-Cu\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp\u003eIn addition to their potentially positive actions on toning down inflammatory signaling, all three peptides have been posited to also support cellular regeneration via different mechanisms that ultimately support vascularity and nutrient delivery to the cellular structure. Notably, TB-500 has been posited to exert positive actions on cellular regeneration by interacting with cellular mobility and thus supporting angiogenesis.\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eResearch by Lv et al. suggests that TB-500 may interact with cell movement as it binds globular actin (G-actin) and may modulate how actin filaments assemble to plausibly make endothelial cells more able to change shape, migrate, and form multicellular structures.\u003cspan\u003e \u003c\/span\u003e\u003csup dir=\"ltr\"\u003e(7)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eThat type of motility is a basic requirement for sprouting angiogenesis, where endothelial cells need to move into hypoxic tissue and organize into new tubes.\u003c\/p\u003e\n\u003cp\u003eThe researchers suggest that during evaluation, the peptide increased cell viability and migration and increased tube formation on matrices, which is commonly exposed to research models as a lab proxy for angiogenic behavior. In parallel, TB-500 appeared to increase expression of angiogenesis-linked factors, including VEGFA, angiopoietin-2 (Ang2), and the Tie2 receptor. Mechanistically, the study posits that TB-500 may push angiogenesis through a Notch to NF-κB signaling axis. Thus, TB-500 may be hypothesized to support angiogenesis by combining a cytoskeleton-linked increase in endothelial motility with signaling changes that raise pro-angiogenic programs (VEGF-A and Ang2\/Tie2) via Notch\/NF-κB coupling in damaged cellular structure.\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eResearch by Sikiric et al. also suggests that BPC-157 may also support angiogenesis and thus cellular regeneration.\u003cspan\u003e \u003c\/span\u003e\u003csup dir=\"ltr\"\u003e(8)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eMore specifically, this peptide may act indirectly by stabilizing the vascular environment needed for new vessel growth. Across multiple injury models, the researchers have observed that the peptide may work by protecting endothelial cells and preserving vessel patency. Such endothelium protection creates conditions in which endothelial sprouting and maturation may occur.\u003c\/p\u003e\n\u003cp\u003eAt the cellular level, BPC-157 has been linked to activation of repair-associated signaling pathways, including Egr-1 with its regulator NAB2, and FAK–paxillin signaling, which are potentially involved in cell adhesion and migration. These processes are essential for endothelial movement through the extracellular matrix during capillary sprouting. The peptide has also been associated with normalised NO signaling under both excessive and suppressed NO states, counteracting the implications of NOS blockade and NO overproduction. Because NO regulates vasodilation, endothelial survival, and angiogenic signaling, this balancing may support perfusion of injured cellular structures and facilitate endothelial activation and vessel remodeling during repair.\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eMechanistically, research on GHK-Cu by Mulder et al. also suggests that the peptide may upregulate VEGF, increase endothelial cell proliferation, and promote endothelial migration and tube formation.\u003cspan\u003e \u003c\/span\u003e\u003csup dir=\"ltr\"\u003e(9)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eThese actions are consistent with stimulation of angiogenesis. At the same time, copper itself is a required cofactor for several angiogenic enzymes and transcriptional programs, and the GHK peptide appears to deliver copper in a biologically functional form at sites of cellular injury.\u003c\/p\u003e\n\u003ch3\u003e\u003cem\u003eCollagen Repair Potential of BPC-157 \u0026amp; TB-500 \u0026amp; GHK-Cu\u003c\/em\u003e\u003c\/h3\u003e\n\u003cp dir=\"ltr\"\u003eMultiple experiments with each of the three peptides also suggest that they may support the regeneration and repair of collagen and other supporting structures in cell cultures such as tendon fibroblasts. For example, research on TB-500 by Xu et al. may support the structural organization in models of recovering tendon fibroblasts.\u003cspan\u003e \u003c\/span\u003e\u003csup dir=\"ltr\"\u003e(10)\u003c\/sup\u003e\u003cspan\u003e \u003c\/span\u003eApparently, the researchers observed collagen fibers that were more uniformly aligned along the ligament axis and more evenly spaced than in controls. Electron microscopy suggested larger collagen fibril diameters, a feature linked to better-supported mechanical properties. These structural changes apparently were accompanied by higher tensile strength and stiffness of the recovered tendon structures.\u003c\/p\u003e\n\u003cp\u003eBased on this data, the researchers posit that TB-500 may support how ligament fibroblasts organize and deposit collagen during repair, improving tissue quality. BPC-157 may also support repair by supporting tendon fibroblasts, as the research by Chang reports accelerated fibroblast migration and spreading in laboratory studies, both of which are essential for repopulating an injury site. Apparently, the peptide may also have better supported fibroblast survival under oxidative stress, a condition commonly present in injured tendon cell cultures.\u003c\/p\u003e\n\u003cp dir=\"ltr\"\u003eAt the cellular level, these implications were posited to be related to the upregulation of actin fiber formation, as the researchers commented that “\u003cem dir=\"ltr\"\u003eF-actin formation as detected by FITC-phalloidin staining was induced in BPC 157\u003c\/em\u003e” exposed cells. Moreover, the activation of focal adhesion signaling through phosphorylation of FAK and paxillin is also posited to aid cell attachment and movement within the extracellular matrix, thus ultimately facilitating repair.\u003c\/p\u003e\n\u003cp\u003eGHK-Cu may also promote collagen synthesis, particularly in the binding between tendon cells and bone cells. Research by Fu et al. suggests that research models exposed to the peptide complex may have better bone formation around tendon cell grafts and a trend toward higher cell presence within the graft structure itself. Overall, all three peptides appear to exert potential positive actions linked to cellular repair and integrity, including anti-inflammatory signaling, angiogenesis, collagen synthesis, and more. Unfortunately, research investigating the simultaneous experimentation with all three compounds has yet to be conducted.\u003c\/p\u003e\n\u003cp\u003e\u003cstrong\u003e\u003cem dir=\"ltr\"\u003eBPC-157 \u0026amp; TB-500 \u0026amp; GHK-Cu (GLOW) blend is available for research and laboratory purposes only.\u003c\/em\u003e\u003c\/strong\u003e\u003c\/p\u003e\n\u003ch3\u003eReferences:\u003c\/h3\u003e\n\u003col\u003e\n\u003cli\u003eSeiwerth S, Milavic M, Vukojevic J, Gojkovic S, Krezic I, Vuletic LB, Pavlov KH, Petrovic A, Sikiric S, Vranes H, Prtoric A, Zizek H, Durasin T, Dobric I, Staresinic M, Strbe S, Knezevic M, Sola M, Kokot A, Sever M, Lovric E, Skrtic A, Blagaic AB, Sikiric P. Stable Gastric Pentadecapeptide BPC 157 and Wound Healing. Front Pharmacol. 2021 Jun 29;12:627533. doi: 10.3389\/fphar.2021.627533. PMID: 34267654; PMCID: PMC8275860.\u003c\/li\u003e\n\u003cli\u003eMaar, K., Hetenyi, R., Maar, S., Faskerti, G., Hanna, D., Lippai, B., Takatsy, A., \u0026amp; Bock-Marquette, I. (2021). Utilizing Developmentally Essential Secreted Peptides Such as Thymosin Beta-4 to Remind the Adult Organs of Their Embryonic State-New Directions in Anti-Aging Regenerative Therapies. Cells, 10(6), 1343.\u003cspan\u003e \u003c\/span\u003e\u003ca href=\"https:\/\/doi.org\/10.3390\/cells10061343\" rel=\"noopener\" dir=\"ltr\"\u003ehttps:\/\/doi.org\/10.3390\/cells10061343\u003c\/a\u003e\n\u003c\/li\u003e\n\u003cli\u003eMaquart FX, Pickart L, Laurent M, Gillery P, Monboisse JC, Borel JP. Stimulation of collagen synthesis in fibroblast cultures by the tripeptide-copper complex glycyl-L-histidyl-L-lysine-Cu2+. FEBS Lett. 1988 Oct 10;238(2):343-6. doi: 10.1016\/0014-5793(88)80509-x. PMID: 3169264.\u003c\/li\u003e\n\u003cli\u003eSantra M, Zhang ZG, Yang J, Santra S, Santra S, Chopp M, Morris DC. Thymosin β4 up-regulation of microRNA-146a promotes oligodendrocyte differentiation and suppression of the Toll-like proinflammatory pathway. J Biol Chem. 2014 Jul 11;289(28):19508-18. doi: 10.1074\/jbc.M113.529966. Epub 2014 May 14. PMID: 24828499; PMCID: PMC4094061.\u003c\/li\u003e\n\u003cli\u003eSikiric P, Seiwerth S, Rucman R, Turkovic B, Rokotov DS, Brcic L, Sever M, Klicek R, Radic B, Drmic D, Ilic S, Kolenc D, Stambolija V, Zoricic Z, Vrcic H, Sebecic B. Focus on ulcerative colitis: stable gastric pentadecapeptide BPC 157. Curr Med Chem. 2012;19(1):126-32. doi: 10.2174\/092986712803414015. PMID: 22300085.\u003c\/li\u003e\n\u003cli\u003ePark JR, Lee H, Kim SI, Yang SR. The tripeptide GHK-Cu complex ameliorates lipopolysaccharide-induced acute lung injury in mice. Oncotarget. 2016 Sep 6;7(36):58405-58417. doi: 10.18632\/oncotarget.11168. PMID: 27517151; PMCID: PMC5295439.\u003c\/li\u003e\n\u003cli\u003eLv S, Cai H, Xu Y, Dai J, Rong X, Zheng L. Thymosin‑β 4 induces angiogenesis in critical limb ischemia mice via regulating Notch\/NF‑κB pathway. Int J Mol Med. 2020 Oct;46(4):1347-1358. doi: 10.3892\/ijmm.2020.4701. Epub 2020 Aug 11. PMID: 32945357; PMCID: PMC7447324.\u003c\/li\u003e\n\u003cli\u003eSikiric P, Seiwerth S, Rucman R, Kolenc D, Vuletic LB, Drmic D, Grgic T, Strbe S, Zukanovic G, Crvenkovic D, Madzarac G, Rukavina I, Sucic M, Baric M, Starcevic N, Krstonijevic Z, Bencic ML, Filipcic I, Rokotov DS, Vlainic J. Brain-gut Axis and Pentadecapeptide BPC 157: Theoretical and Practical Implications. Curr Neuropharmacol. 2016;14(8):857-865. doi: 10.2174\/1570159x13666160502153022. PMID: 27138887; PMCID: PMC5333585.\u003c\/li\u003e\n\u003cli\u003eMulder GD, Patt LM, Sanders L, Rosenstock J, Altman MI, Hanley ME, Duncan GW. Enhanced healing of ulcers in patients with diabetes by topical treatment with glycyl-l-histidyl-l-lysine copper. Wound Repair Regen. 1994 Oct;2(4):259-69. doi: 10.1046\/j.1524-475X.1994.20406.x. PMID: 17147644.\u003c\/li\u003e\n\u003cli\u003eXu B, Yang M, Li Z, Zhang Y, Jiang Z, Guan S, Jiang D. Thymosin β4 enhances the healing of medial collateral ligament injury in rats. Regul Pept. 2013 Jun 10;184:1-5. doi: 10.1016\/j.regpep.2013.03.026. Epub 2013 Mar 21. PMID: 23523891.\u003c\/li\u003e\n\u003cli\u003eChang CH, Tsai WC, Lin MS, Hsu YH, Pang JH. The promoting effect of pentadecapeptide BPC 157 on tendon healing involves tendon outgrowth, cell survival, and cell migration. J Appl Physiol (1985). 2011 Mar;110(3):774-80. doi: 10.1152\/japplphysiol.00945.2010. Epub 2010 Oct 28. PMID: 21030672.\u003c\/li\u003e\n\u003cli\u003eFu SC, Cheuk YC, Chiu WY, Yung SH, Rolf CG, Chan KM. Tripeptide-copper complex GHK-Cu (II) transiently improved healing outcome in a rat model of ACL reconstruction. J Orthop Res. 2015 Jul;33(7):1024-33. doi: 10.1002\/jor.22831. Epub 2015 Apr 10. PMID: 25731775.\u003c\/li\u003e\n\u003c\/ol\u003e","brand":"PureX Labs","offers":[{"title":"70mg","offer_id":47548311208180,"sku":null,"price":100.0,"currency_code":"USD","in_stock":true}],"thumbnail_url":"\/\/cdn.shopify.com\/s\/files\/1\/0804\/5802\/3156\/files\/Render_Mockup_1920_1920_2026-01-31_14.png?v=1769804832"}],"url":"https:\/\/purexlabs.io\/collections\/skin-aesthetic.oembed","provider":"PureX Labs","version":"1.0","type":"link"}