KPV
The anti-inflammatory C-terminal tripeptide of α-MSH.
Research peptidePreclinical
Identity
- Class
- Tripeptide (Lys-Pro-Val) — α-MSH(11-13)
- Source
- Synthetic; the C-terminal fragment of α-MSH
- Receptor
- Anti-inflammatory action largely receptor-independent; gut uptake via the PepT1 transporter
Key properties
Molecular weight
~342.4 Da
Approximate values for the native hormone. Engineered analogs are often deliberately larger and far longer-acting.
Mechanism
KPV is the C-terminal tripeptide of α-MSH (residues 11-13) and carries much of α-MSH's anti-inflammatory activity without its pigmentation or appetite effects. In cell and animal models it dampens NF-κB signaling and pro-inflammatory cytokines, and in the gut it is taken up intact via the PepT1 transporter — an effect that appears largely independent of the classical melanocortin receptors.
Reference notes
- It reproduces α-MSH's anti-inflammatory effect while dropping the pigment- and appetite-related actions of the parent peptide.
- Much of its activity is receptor-independent and, in the intestine, mediated by the PepT1 peptide transporter.
- Evidence is preclinical — cell and rodent models, notably colitis; controlled human data are absent.
Selected literature
Curated peer-reviewed reviews, sourced from PubMed. Selected for relevance, not exhaustive — open any entry on PubMed for the full record and its primary citations.
- 1.Melanocortin-derived tripeptide KPV has anti-inflammatory potential in murine models of inflammatory bowel disease · Inflammatory bowel diseases, 2008 · PMID 18092346
- 2.PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation · Gastroenterology, 2008 · PMID 18061177
- 3.Effects of the COOH-terminal tripeptide alpha-MSH(11-13) on corneal epithelial wound healing: role of nitric oxide · Experimental eye research, 2006 · PMID 16965771