Peptides›Healing, Immune›KPV (Lys-Pro-Val)

KPV (Lys-Pro-Val)

/ Synthetic tripeptide — C-terminal fragment of α-MSH (residues 11-13)

TIER 3 · PreclinicalN = 0 · TESTING PENDINGMW 342.40 g·mol⁻¹

ALIAS · α-MSH(11-13) · Lysine-Proline-Valine tripeptide · α-MSH C-terminal tripeptide

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Research use onlyAny dose figures below describe what specific cited studies used, reported factually. Nothing on this page is guidance for human use.READ FIRST →

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§ A · Identity

Primary sequenceKPV (Lys-Pro-Val)

MW · 342.40CLASS · Synthetic tripeptide — C-terminal fragment of α-MSH (residues 11-13)CATEGORY · Healing, Immune

Tier 3. Three-residue C-terminal fragment of α-MSH retaining anti-inflammatory activity without the pigmentary effects of full-length α-MSH. Solid rodent literature in IBD models (Kannengiesser 2008 and others); no human clinical trial.

§ B · Mechanism of action

KPV reproduces the anti-inflammatory pharmacology of α-MSH without significant melanocortin receptor pigmentary signalling. Evidence supports both melanocortin-1 receptor (MC1R) -dependent and -independent mechanisms, including direct intracellular effects on NF-κB activation. In gut models, oral KPV administration ameliorates DSS-induced colitis and TNF-α-driven inflammation.

§ C · Human clinical evidence

Tier 3. Rodent IBD models (DSS colitis, TNBS colitis), allergic contact dermatitis models, and in-vitro epithelial barrier studies. No human Phase 1 or later trials of KPV as a therapeutic.

§ D · Primary literature

PubMed18092346Kannengiesser K et al. — Melanocortin-derived tripeptide KPV has anti-inflammatory potential in murine models of inflammatory bowel disease · Inflammatory Bowel Diseases · rodentOral and parenteral KPV reduced DSS-induced colitis severity and mucosal inflammatory cytokines in mice; effect persisted in MC1R-deficient mice, suggesting MC1R-independent mechanism.Limitations: Rodent model only; oral bioavailability in humans not established.2008

§ F · Safety signal

No human safety database. Class-level α-MSH derivative concerns about melanocortin signalling are mostly absent for KPV due to its lack of pigmentary effect; oral bioavailability and gut absorption profile are not well-characterised.

§ H · Regulatory status

Regulatory status

FDA status:: Not FDA-approved

§ I · Notable gaps and controversies

The 'oral KPV' rodent model results have not been replicated in human IBD trials despite a clear regulatory pathway for IBD therapeutics. The lack of clinical translation a decade after promising preclinical data warrants caution about marketing claims of efficacy.