KPV

Also known as: Lysine-Proline-Valine, α-MSH (11-13)

**Mechanism of Action** KPV (Lysine-Proline-Valine) is the C-terminal tripeptide fragment of α-melanocyte-stimulating hormone (α-MSH 11–13). It exerts anti-inflammatory effects primarily through PepT1 (oligopeptide transporter 1)-mediated cellular uptake, which facilitates intracellular inhibition of nuclear factor-κB (NF-κB) activation. This reduces pro-inflammatory cytokine production (e.g., TNF-α, IL-1β, IL-6) and oxidative stress, without requiring melanocortin receptor binding. The peptide’s small size and stability enhance its bioavailability in gastrointestinal tissues. **Key Research Findings** Preclinical studies in murine models of inflammatory bowel disease (IBD), including dextran sulfate sodium (DSS)-induced colitis, demonstrate that KPV significantly attenuates colonic inflammation, reduces mucosal damage, and lowers myeloperoxidase activity. PepT1 knockout mice show diminished KPV efficacy, confirming transporter dependency. In vitro, KPV suppresses lipopolysaccharide (LPS)-induced NF-κB activation in intestinal epithelial cells and macrophages. Notably, KPV exhibits synergistic effects when combined with other anti-inflammatory agents (e.g., 5-aminosalicylic acid) in colitis models. **Clinical Relevance** KPV remains in preclinical development, with no completed human trials. Its potential application targets IBD (Crohn’s disease, ulcerative colitis) and other inflammatory gastrointestinal disorders, leveraging localized PepT1 expression in inflamed colonic epithelium. Challenges include optimizing oral delivery to bypass gastric degradation and ensuring sustained mucosal targeting. Further validation of safety, pharmacokinetics, and efficacy in human subjects is required before clinical translation. For research purposes only — not medical advice.

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