KPV peptide is the anti-inflammatory tripeptide of alpha-MSH, studied across colitis and wound-repair models.

The short version

KPV peptide is a tiny molecule — just three amino acids, lysine-proline-valine — clipped from the tail end of a natural body hormone called alpha-MSH (alpha-melanocyte-stimulating hormone, a signaling molecule best known for affecting skin pigment). The remarkable part is that this fragment keeps the parent hormone's calming, anti-inflammatory effect while losing its pigment-changing one. In lab dishes and in mice, KPV quiets the cell machinery that drives inflammation, and in the gut it slips directly into the cells lining the intestine. Everything known about KPV today comes from cell and animal studies. No human clinical trial of KPV has been published, so it is sold only as a research chemical for laboratory use. This page is a plain-English map of that record, and every number on it points to a published study.

KPV at a Glance

KPV is a linear tripeptide, L-lysyl-L-prolyl-L-valine (sequence H-Lys-Pro-Val-OH), with the molecular formula C16H30N4O4 and a molecular weight of 342.44 Da ^[1][15]. It corresponds to residues 11-13 — the C-terminal tail — of alpha-MSH, the melanocortin neuropeptide ^[4]. Its registry identifiers are CAS 67727-97-3 and PubChem CID 125672 ^[15]. The defining feature throughout the literature is simple: KPV retains the broad anti-inflammatory activity of the full hormone while lacking its melanogenic (pigment-producing) action ^[4].

The research record is concentrated and consistent. In human intestinal epithelial cells, nanomolar KPV suppresses NF-kB (nuclear factor kappa B, a master switch for pro-inflammatory genes) and MAP-kinase signaling ^[1]. In mouse colitis, oral KPV produces earlier recovery, lower inflammatory infiltrate, and reduced myeloperoxidase — and that effect survives in mice lacking the MC1R melanocortin receptor, meaning it does not depend on the classic receptor route ^[2]. In rabbits, topical KPV re-epithelialized 8 of 8 corneas by 60 hours against none of the placebo-treated eyes ^[6]. These are preclinical findings, summarized here and cited to source — not demonstrated human outcomes.

Two limits frame everything else. First, the entire efficacy literature is in vitro and animal work, chiefly murine colitis, so human dosing, efficacy, and safety are unestablished ^[1][2]. Second, free KPV is a small, peptidase-labile tripeptide with no validated human pharmacokinetics — which is why much of the recent field is formulation work to keep it intact long enough to act ^[5][12]. Read the findings below as a vivid preclinical deck, not a clinical verdict, and see research-only status for where access actually stands. Common reader questions are gathered in the frequently asked questions.

What Is KPV Peptide?

What is KPV peptide?

KPV peptide (Lys-Pro-Val) is the C-terminal tripeptide corresponding to residues 11-13 of alpha-melanocyte-stimulating hormone, studied as a melanocortin-derived anti-inflammatory peptide ^[4]. It is not an independently circulating hormone; it is the active tail fragment of the parent neuropeptide ^[1].

What is KPV?

KPV stands for the tripeptide lysine-proline-valine, the C-terminal fragment of alpha-MSH studied for anti-inflammatory and gut/epithelial signaling ^[4]. The three single-letter amino-acid codes — K (lysine), P (proline), V (valine) — give the molecule its name.

What does KPV peptide do?

KPV is the C-terminal tripeptide of alpha-MSH that retains the parent hormone's anti-inflammatory activity while lacking its pigmentary action ^[4]. In research models it suppresses NF-kB and MAP-kinase signaling and reduces pro-inflammatory cytokine production ^[1]. It does this largely without the melanocortin receptors that the full hormone uses, an effect retained in MC1R-deficient models ^[2]. For the full pathway picture, see the KPV anti-inflammatory mechanism.

A quick orientation to the family helps. Alpha-MSH is an endogenous neuropeptide with both anti-inflammatory and pigmentary actions; KPV is its three-residue C-terminal fragment, and a tripeptide is simply a peptide of three amino acids joined together ^[4]. The literature also studies close relatives — KdPT (lysine-D-proline-threonine) is a KPV analog explored for intestinal anti-inflammatory and barrier-protective effects ^[4] — but KPV itself, residues 11-13 of alpha-MSH, is the molecule this site documents ^[1].

What the Research Says KPV Peptide May Do

The reported KPV peptide benefits in the published literature are research findings in cells and animals, not demonstrated human benefits. The most reproducible is anti-inflammatory action in the gut: in mouse models of inflammatory bowel disease, oral KPV reduced colonic inflammation, with earlier recovery and lower myeloperoxidase activity ^[2], and nanomolar KPV lowered NF-kB and MAPK activation in human intestinal epithelial cells ^[1].

Beyond the gut, topical KPV accelerated corneal wound healing in rabbits, completely re-epithelializing 8 of 8 corneas by 60 hours ^[6], and KPV inhibited inflammatory signaling in human bronchial epithelial cells ^[8]. A broad review places KPV within a family of alpha-MSH-related tripeptides showing protective effects across ocular, gastrointestinal, dermatologic, and other inflammatory models ^[4]. KPV's C-terminal alpha-MSH sequence has also shown direct antimicrobial activity against S. aureus and C. albicans in vitro ^[9].

A word of calibration belongs next to that list. These are encouraging preclinical signals, and none has been tested in a human trial — marketing of KPV for gut health, skin, or general anti-inflammatory use runs ahead of evidence that is mechanistic and animal-based rather than clinical ^[16]. KPV should also be kept distinct from the melanocortin agonists used for pigmentation or tanning: its signature in the literature is anti-inflammatory action without the pigmentary effect of the full hormone ^[4]. See the KPV colitis research for the gut work and doses used in research for how it was administered.