KPV (Research Overview)
KPV is the tripeptide Lys-Pro-Val, the three C-terminal residues of the 13-residue hormone alpha-melanocyte-stimulating hormone (alpha-MSH 11-13). Its average mass is about 342.4 Da. Most of the literature compares it with the parent hormone, asking which part of alpha-MSH carries which activity.
Mechanism of Action
Structure-activity work on cyclic melanotropin analogues found that Lys11 and Pro12, and to a lesser extent Val13, of the C-terminal tripeptide contribute to the potency of the analogues in melanotropin bioassays. A review of alpha-MSH and related peptides in the immune system reports that the C-terminal tripeptide, like the full hormone, was able to bind the melanocortin-1 receptor (MC-1R) and modulate the function of antigen-presenting cells.
Signalling is not simple. In human keratinocyte cells, alpha-MSH, KPV and ACTH peptides did not raise cyclic AMP; they produced intracellular calcium responses, but only in the presence of an adenosine agonist that inhibits the cyclic AMP pathway, and in MC-1R-transfected hamster ovary cells alpha-MSH and the KPV peptides raised intracellular calcium. A separate study described alpha-MSH 11-13 as having strong anti-inflammatory activity without a known cellular target and identified two tetrapeptide analogues that bound MC1 receptor and raised cyclic AMP.
In cell culture, nanomolar KPV inhibited activation of NF-kappaB and MAP kinase inflammatory signalling and reduced pro-inflammatory cytokine secretion. KPV acted through the di/tripeptide transporter PepT1, which is expressed in intestinal epithelial and immune cells.
Research Areas
Mouse colitis models are the most-cited research area. In one study, KPV given in drinking water reduced the incidence of DSS- and TNBS-induced colitis in mice, with lower pro-inflammatory cytokine mRNA expression. A separate group reported earlier recovery, fewer inflammatory infiltrates and lower myeloperoxidase activity in DSS colitis and in transfer colitis, and survival of mice with a nonfunctional MC1 receptor during DSS colitis.
In a mouse contact-hypersensitivity model, systemic or topical alpha-MSH or KPV inhibited both the sensitization and the elicitation phase, according to the immune-system review cited above.
Klow Blend contains KPV alongside GHK-Cu, BPC-157 and TB-500. The studies cited on this page examine KPV by itself, or alpha-MSH, and do not examine a combination with other peptides.
What the published literature reports
This section summarizes what published studies report. It describes study designs and results as the authors reported them. It does not describe any use of the research materials sold on this site, and it is not a recommendation, instruction or claim about any product.
Study models and endpoints
- Model Receptor-binding and signaling assays in cell lines, including human keratinocyte cells. [3][4]
- Model Mouse models of colitis and contact hypersensitivity. [2][5][6]
- Endpoint NF-κB and MAP-kinase signaling and cytokine secretion in cells. [5]
- Endpoint Body-weight recovery, histology and myeloperoxidase activity in mouse colitis. [6]
Reported findings
- A review described the α-MSH C-terminal tripeptide (KPV) as able to bind the MC-1 receptor and to modulate antigen-presenting cell function, and reported that systemic and topical α-MSH or KPV inhibited the sensitization and elicitation phases of contact hypersensitivity in mice. [2]
- A study in human keratinocyte cell lines reported no cyclic AMP elevation in response to α-MSH, KPV or ACTH peptides, and reported intracellular calcium responses to these peptides only in the presence of an adenosine agonist. [3]
- A receptor-binding study reported that two Tyr-containing analogues of the KPV sequence (HS401 and HS402) selectively bound the MC1 receptor and stimulated cyclic AMP generation, whereas other analogues tested did not. [4]
- A study reported that KPV inhibited NF-κB and MAP-kinase activation and reduced pro-inflammatory cytokine secretion in cells, acted through the PepT1 transporter, and that oral administration reduced the incidence of DSS- and TNBS-induced colitis in mice. [5]
- A study in two murine colitis models reported that KPV was associated with earlier recovery, stronger body-weight regain, reduced inflammatory infiltrates and reduced myeloperoxidase activity, and that all MC1R-deficient mice given KPV survived DSS colitis. [6]
Evidence level and limitations
Evidence level: Mostly preclinical (cell and animal) literature. Any human reports cited are described below with their limitations.
- Every study cited is in vitro or in mice; no human outcome data are cited. [3][5][6]
- The cited mechanistic studies disagree on or leave open the signaling route (for example, no cyclic AMP rise in keratinocytes versus MC1 receptor binding by analogues). [3][4]
Regulatory status
- FDA's compounding-substances page lists KPV among bulk drug substances it evaluated (since withdrawn by the nominators) and states that FDA has not identified any human exposure data on drug products containing KPV by any route.
Sources checked on 16 October 2026: FDA, "Certain Bulk Drug Substances for Use in Compounding that May Present Significant Safety Risks" (page text). Regulatory status can change.
Not established
- Any effect in humans is not established: a PubMed search of KPV restricted to randomized or clinical-trial publication types returned no results on 16 October 2026. [6]
- The complete mechanism of action is not established by the cited reports. [3][5]
Summaries of published literature, not claims about any product sold here. For laboratory research use only.
Specification summary
Klow Blend
Vial contents: GHK-Cu 50mg, BPC-157 10mg, TB-500 10mg, KPV 10mg (80mg total peptide content). Stated purity ≥99%. For laboratory research use only.
Related materials
Laboratory background
Education for people working with this material in the laboratory: guides on handling and analysis, definitions of terms, and arithmetic tools. It describes no use of the material.
Guides
Glossary terms
References
- Cody WL, Wilkes BC, Muska BJ, Hruby VJ, Castrucci AM, Hadley ME. Cyclic melanotropins. 5. Importance of the C-terminal tripeptide (Lys-Pro-Val). J Med Chem. 1984;27(9):1186-90. PMID 6332195 · DOI
- Luger TA, Scholzen TE, Brzoska T, Böhm M. New insights into the functions of alpha-MSH and related peptides in the immune system. Ann N Y Acad Sci. 2003;994:133-40. PMID 12851308 · DOI
- 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;122(4):1010-9. PMID 15102092 · DOI
- Schiöth HB, Muceniece R, Mutule I, Wikberg JE. New melanocortin 1 receptor binding motif based on the C-terminal sequence of alpha-melanocyte-stimulating hormone. Basic Clin Pharmacol Toxicol. 2006;99(4):287-93. PMID 17040213 · DOI
- Dalmasso G, Charrier-Hisamuddin L, Nguyen HT, Yan Y, Sitaraman S, Merlin D. PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation. Gastroenterology. 2008;134(1):166-78. PMID 18061177 · DOI
- Kannengiesser K, Maaser C, Heidemann J, Luegering A, Ross M, Brzoska T, et al. Melanocortin-derived tripeptide KPV has anti-inflammatory potential in murine models of inflammatory bowel disease. Inflamm Bowel Dis. 2008;14(3):324-31. PMID 18092346 · DOI
Cited literature is provided for scientific context only and does not describe or endorse any use of these products.
For laboratory research use only. Not for human or veterinary use. Not intended to diagnose, treat, cure, or prevent any disease.