KPV is the C-terminal tripeptide (Lys-Pro-Val) of α-melanocyte-stimulating hormone (α-MSH). Studied in murine and cell-culture models of inflammatory bowel disease and colitis with PepT1-mediated intestinal-epithelial uptake and anti-inflammatory transcriptional responses as the dominant mechanistic findings.
Definition
KPV is the synthetic tripeptide Lysine-Proline-Valine, corresponding to the C-terminal three amino acids of α-melanocyte-stimulating hormone (α-MSH) — the 13-amino-acid melanocortin-1-receptor ligand. The published research literature on KPV centres on its activity in gastrointestinal inflammation models, where the tripeptide is selectively taken up by intestinal epithelial cells via the proton-coupled peptide transporter PepT1 and exerts anti-inflammatory effects on the surrounding tissue.
The PepT1-mediated-uptake framework was established by Dalmasso and colleagues in the original characterisation (PMID 18061177), with parallel publication from the Kannengiesser group documenting anti-inflammatory potential in murine inflammatory bowel disease models (PMID 18092346). The compound is not currently approved for therapeutic use in humans by any major regulator. Research-grade KPV is supplied as a lyophilised peptide for laboratory research applications only.
How KPV is studied in peptide research
The published research literature on KPV is densely focused on gastrointestinal inflammation, with extension into colitis-associated cancer contexts and into formulation-research investigating delivery vehicles for the intestinal-targeted activity profile. The Viennois work documented critical PepT1 involvement in colitis-associated cancer and the therapeutic benefits of PepT1-mediated KPV anti-inflammatory delivery in a murine model (PMID 27458604). The Xiao formulation work examined orally-targeted delivery via hyaluronic acid-functionalised nanoparticles in ulcerative colitis models (PMID 28143741). Structural-modification research investigated lysine-residue modifications and their effect on activity (PMID 29953505).
Mechanistically, the anti-inflammatory activity is distinct from the parent α-MSH compound’s broader melanocortin-receptor pharmacology — KPV acts without engaging the melanocortin-1 receptor and the published mechanism centres on downstream NF-κB-pathway modulation in intestinal epithelial cells following PepT1-mediated uptake. The compound is operationally distinct from melanocortin-receptor agonists that engage the full receptor pharmacology.
Related terms
- α-melanocyte-stimulating hormone (α-MSH)
- Melanocortin receptor
- PepT1 / SLC15A1 proton-coupled peptide transporter
- Intestinal epithelial cell
- NF-κB pathway
- Tripeptide
Where KPV appears in the Ronin catalog
- KPV 10mg — single-compound vial, lyophilized white powder under inert gas
References
- Dalmasso G et al. PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation. Gastroenterology 2008;134(1):166-178. [PMID 18061177]
- Kannengiesser K et al. Melanocortin-derived tripeptide KPV has anti-inflammatory potential in murine models of inflammatory bowel disease. Inflamm Bowel Dis 2008;14(3):324-331. [PMID 18092346]
- Viennois E et al. Critical role of PepT1 in promoting colitis-associated cancer and therapeutic benefits of the anti-inflammatory PepT1-mediated tripeptide KPV in a murine model. Cell Mol Gastroenterol Hepatol 2016;2(3):340-357. [PMID 27458604]
- Xiao B et al. Orally Targeted Delivery of Tripeptide KPV via Hyaluronic Acid-Functionalized Nanoparticles Efficiently Alleviates Ulcerative Colitis. Mol Ther 2017;25(7):1628-1640. [PMID 28143741]
- Songok AC et al. Structural modification of the tripeptide KPV by reductive “glycoalkylation” of the lysine residue. PLoS One 2018;13(2):e0192405. [PMID 29953505]
Glossary entries describe research-context use of peptide-research terminology. They do not constitute medical, veterinary, or clinical advice. KPV is sold strictly as a research-grade reagent for laboratory and bench research applications.