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KPV peptides are Synthesized and Lyophilized in the USA.
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What is the KPV peptide?
KPV, the C-terminal peptide stretch of alpha-melanocyte-stimulating hormone (alpha-MSH), has been explored for its potential photoprotective properties, possible effects against ischemia, sexual influences, and other possible benefits on feeding behavior, anti-inflammatory properties, and energy homeostasis. It has been studied via oral, intravenous, and transdermal routes of administration.
Synonyms: MSH(11-13), ACTH(11-13), alpha-MSH(11-13)
Molecular Formula: C16H30N4O4
Molecular Weight: 342.43 g/mol
PubChem: CID 125672
CAS Number: 67727-97-3
KPV Peptide and Intestinal Inflammation
The primary subject of KPV research has been focused on its potential for reducing intestinal inflammation. In mouse models of inflammatory bowel disease (IBD), it appeared to reduce inflammatory infiltrates, MPO activity, and overall histological evidence of inflammation. KPV appeared to help mice to recover faster and gain weight. Delivery of KPV using nanoparticles functionalized with hyaluronic acid appeared to help direct inflammation to targeted intestinal locations. Thus the suppression of TNF-alpha may reduce inflammation and cause mucosal healing in mice. Modifying KPV has the potential to improve the peptide’s oral bioavailability, potency, and total dose. The researchers note that “These results collectively demonstrate that our HA-KPV-NP/hydrogel system has the capacity to release HA-KPV-NPs in the colonic lumen and that these NPs subsequently penetrate into colitis tissues and enable KPV to be internalized into target cells, thereby alleviating ulcerative colitis.” Studies have suggested that the peptide also may reduce NF-kappaB and mitogen-activated protein kinase (MAPK) activity. TNF-alpha, NF-kappaB, and MAPK inhibition together ameliorate the inflammatory changes in the intestine. Mice administered with KPV appeared to exhibit less colonic infiltration and average colon lengths than the control group.
KPV Peptide and General Inflammation
Studies in rabbits dating back to 1984 posited that KPV may have potent anti-inflammatory and fever reducer (antipyretic) properties. However, the peptide exhibited lower potency in these trials than the total length alpha-MSH molecule, suggesting that KPV lacked crucial sequences of alpha-MSH necessary for complete antipyretic activity. Researchers explored various analogs of alpha-MSH to reduce inflammation in a broad spectrum of diseases such as fever, irritant, allergic contact dermatitis, vasculitis, fibrosis, arthritis, and inflammation of the eyes, brain, lungs, and gastrointestinal tract. The scientists reported that “This study indicates that KPV is transported into cells by PepT1 and might be a new therapeutic agent for IBD.” However, one major drawback has been skin pigmentation which the peptide appears to overcome. The apparent anti-inflammatory effects of KPV may differ from alpha-MSH only marginally. The parent molecule is likely better at suppressing late inflammatory responses, indicating that it might be influencing immune modulation, which is separate from immediate inflammatory responses only marginally. Wound healing is a complex process that involves three general phases in the wound healing process: inflammatory, proliferative, and remodeling. Most of these cells involved in wound healing express a Melanocortin 1 receptor (MC1R) that binds alpha-melanocyte-stimulating hormone and analogs like KPV and KdPT. KVP peptide researchers found that the peptide appeared to reduce the inflammatory properties without inducing the pigmentation associated with natural scar formation in the study setting. KPV may have both anti-inflammatory and anti-microbial activities. It appears to inhibit the growth of both Candida albicans and Staphylococcus aureus and may prevent infection in the setting of severe wounds like burns. This possible benefit of the peptide is in contrast to other anti-inflammatory medications that inhibit the ability of the body to fight off infection.
KPV Peptide and Scar Formation
KPV may decrease chronic inflammation, which causes hypertrophic scarring (e.g., keloid). Hypertrophic scarring is caused by widespread macrophage infiltration, TNF immunoreactivity, and neutrophil abundance. Use of alpha-MSH in this setting may cause more minor scars and a less harsh inflammatory response. These findings suggest that KPV could be used in preventing the scarring seen with some chemotherapy agents. This process might not only decrease the side effects of cancer treatment, but could permit the use of increased concentrations of these medications with better outcomes. In comparison to related hormones, Alpha-MSH appears to be a more effective molecule than KPV but has one serious disadvantage to KPV – it may cause skin pigmentation. KPV is the preferred choice because it exhibits the most anti-inflammatory properties but has not exhibited any side effects in studies so far. The peptide is also easy to manufacture and thus has commercial and logistic benefits. The possible anti-inflammatory effects of KPV are mediated through a different pathway compared to those of alpha-MSH. Whereas alpha-MSH binds to specific melanocortin receptors, KPV does not appear to. The peptide may be administered very quickly, and animal studies have not reported any serious side effects. Diverse routes of administration may affect the way the peptide works and where its anti-inflammatory effects are targeted. The ability to alter the delivery method of KPV makes it easy for scientists to target different areas within the body for research.
KPV appears to be a potent anti-inflammatory peptide that has shown promise in different disease milieus. It has shown immense promise in research related to IBD treatment. In animal studies, the peptide has been observed to be safe and effective when administered through oral, intravenous, and subcutaneous routes. KPV and other alpha-MSH derivatives may bring benefits that enhance wound healing, reduce infection, fight inflammation, and promote improved cosmetic results. KPV and similar peptides could revolutionize wound healing and scar reduction following surgery. Experimental studies report that KPV appears to show minimal side effects and low oral and excellent subcutaneous bioavailability in mice. The dosage in mice (per kg of body weight) does not match humans.
- Elliott RJ, Szabo M, Wagner MJ, Kemp EH, MacNeil S, Haycock JW. alpha-Melanocyte-stimulating hormone, MSH 11-13 KPV and adrenocorticotropic hormone signalling in human keratinocyte cells. J Invest Dermatol. 2004 Apr;122(4):1010-9. doi: 10.1111/j.0022-202X.2004.22404.x. PMID: 15102092.
- Xiao B, Xu Z, Viennois E, Zhang Y, Zhang Z, Zhang M, Han MK, Kang Y, Merlin D. Orally Targeted Delivery of Tripeptide KPV via Hyaluronic Acid-Functionalized Nanoparticles Efficiently Alleviates Ulcerative Colitis. Mol Ther. 2017 Jul 5;25(7):1628-1640. doi: 10.1016/j.ymthe.2016.11.020. Epub 2017 Jan 28. PMID: 28143741; PMCID: PMC5498804.
- Zhu W, Ren L, Zhang L, Qiao Q, Farooq MZ, Xu Q. The Potential of Food Protein-Derived Bioactive Peptides against Chronic Intestinal Inflammation. Mediators Inflamm. 2020 Sep 9;2020:6817156. doi: 10.1155/2020/6817156. PMID: 32963495; PMCID: PMC7499337.
- Richards DB, Lipton JM. Effect of alpha-MSH 11-13 (lysine-proline-valine) on fever in the rabbit. Peptides. 1984 Jul-Aug;5(4):815-7. doi: 10.1016/0196-9781(84)90027-5. PMID: 6333677.
- Dalmasso G, Charrier-Hisamuddin L, Nguyen HT, Yan Y, Sitaraman S, Merlin D. PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation. Gastroenterology. 2008 Jan;134(1):166-78. doi: 10.1053/j.gastro.2007.10.026. Epub 2007 Oct 17. PMID: 18061177; PMCID: PMC2431115.
- Song J, Li X, Li J. Emerging evidence for the roles of peptide in hypertrophic scar. Life Sci. 2020 Jan 15;241:117174. doi: 10.1016/j.lfs.2019.117174. Epub 2019 Dec 13. PMID: 31843531.
Dr. Usman (BSc, MBBS, MaRCP) completed his studies in medicine at the Royal College of Physicians, London. He is an avid researcher with more than 30 publications in internationally recognized peer-reviewed journals. Dr. Usman has worked as a researcher and a medical consultant for reputable pharmaceutical companies such as Johnson & Johnson and Sanofi.