The anti-inflammatory C-terminal tripeptide of α-MSH. Structurally it is Tripeptide (Lys-Pro-Val) — α-MSH(11-13).

How strong is the evidence for KPV?

PeptideHormone grades KPV at the "Preclinical" evidence tier — the evidence is largely animal or in-vitro, with human data thin or absent. It is catalogued as a community research peptide outside the approved-drug system, and the tier is an editorial judgment about the public literature that can change as the science does.

What is the half-life of KPV?

The reported circulating half-life of KPV is Minutes (poorly characterized).

KPV

The anti-inflammatory C-terminal tripeptide of α-MSH.

Research peptidePreclinical

Three residues from the tail of α-MSH, still carrying the anti-inflammatory half of the message. Brevity taken to its limit.

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

Evidence floorCommunityREF1COMM1

Molecular weight

~342.4 Da

REF

Half-life (native)

Minutes (poorly characterized)

COMMHalf-life is poorly characterized in humans. The figure is indicative of order-of-magnitude, not an established value.

Approximate values for the native hormone; engineered analogs are often deliberately larger and far longer-acting. Each figure carries its own provenance tier, and the floor is the weakest of them - the Standard.

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.

Common questions

What is KPV?: The anti-inflammatory C-terminal tripeptide of α-MSH. Structurally it is Tripeptide (Lys-Pro-Val) — α-MSH(11-13).
How does KPV work?: 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.
How strong is the evidence for KPV?: PeptideHormone grades KPV at the "Preclinical" evidence tier — the evidence is largely animal or in-vitro, with human data thin or absent. It is catalogued as a community research peptide outside the approved-drug system, and the tier is an editorial judgment about the public literature that can change as the science does.
What is the half-life of KPV?: The reported circulating half-life of KPV is Minutes (poorly characterized).

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