KPV (Lys-Pro-Val)

KPV is the C-terminal tripeptide of α-MSH that retains potent anti-inflammatory activity via NF-κB inhibition — without melanocortin receptor-mediated pigmentation. Studied in IBD and mucosal immunity models.

KPV (Lysine-Proline-Valine) is the C-terminal tripeptide fragment corresponding to residues 11-13 of alpha-melanocyte stimulating hormone (α-MSH), a 13-amino acid neuropeptide processed from pro-opiomelanocortin (POMC) in the pituitary and hypothalamus. The remarkable finding that drove research interest in KPV is that this tiny three-amino acid fragment retains anti-inflammatory bioactivity comparable to the full-length 13-amino acid parent peptide in multiple experimental systems — making it one of the smallest known bioactive peptides in mammalian biology.

The primary anti-inflammatory mechanism of KPV involves inhibition of NF-κB nuclear translocation. KPV prevents IκB phosphorylation and degradation, thereby retaining the NF-κB p65/p50 heterodimer in the cytoplasm and suppressing transcription of pro-inflammatory target genes including IL-1β, IL-6, IL-8, TNF-α, and COX-2. Importantly, this anti-inflammatory activity occurs at concentrations where KPV does not significantly engage melanocortin receptors (MC1R-MC5R), distinguishing it from full-length α-MSH which produces pigmentation-related effects through MC1R activation on melanocytes. This receptor-independent anti-inflammatory mechanism makes KPV uniquely valuable for studying inflammatory pathways without melanocortin confounding variables.

Published research has extensively studied KPV in gastrointestinal inflammation models. The peptide is transported across intestinal epithelial cell monolayers via the PepT1 (SLC15A1) oligopeptide transporter, achieving intracellular accumulation in colonocytes and immune cells within the lamina propria. In colitis models (DSS-induced and TNBS-induced), KPV administration reduces inflammatory scores, suppresses mucosal cytokine levels, and preserves epithelial barrier integrity. Additional research encompasses skin inflammation models (UV-induced, contact dermatitis), neuroinflammation, and macrophage polarization studies. KPV promotes anti-inflammatory M2 macrophage phenotype while suppressing pro-inflammatory M1 activation.

Supplied as a lyophilized powder with ≥99% purity. Store at -20°C desiccated. For immunology and inflammation research only.

Product Specifications

Certificate of Analysis

Every batch ships with a Janoshik-verified COA covering HPLC purity, mass spectrometry confirmation, and batch traceability.

Shipping & Lead Times

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• HK warehouse: ships within 2–3 business days · estimated 7–14 day international delivery
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