KPV

KPV is a naturally occurring tripeptide consisting of the amino acids lysine, proline, and valine. It corresponds to the C-terminal fragment (residues 11-13) of alpha-melanocyte stimulating hormone (alpha-MSH) and retains the potent anti-inflammatory properties of the parent hormone without its pigmentation effects. KPV has gained significant attention for its ability to suppress inflammatory pathways, particularly through the inhibition of NF-kB and reduction of pro-inflammatory cytokines.

Research has demonstrated that KPV can be absorbed through the intestinal epithelium via the PepT1 transporter, making it one of the few peptides with demonstrated oral bioavailability for targeting gut inflammation. Studies in colitis models have shown that orally administered KPV significantly reduces intestinal inflammation, suggesting potential applications for inflammatory bowel conditions. Unlike many melanocortin peptides, KPV appears to exert its anti-inflammatory effects independently of melanocortin receptors, likely acting through direct inhibition of IL-1 beta signaling.

KPV also exhibits antimicrobial properties against common pathogens including Staphylococcus aureus and Candida albicans. Its favorable safety profile, small molecular size, and oral bioavailability make it a peptide of growing interest for managing chronic inflammatory conditions, though human clinical trials are still needed to establish efficacy and optimal dosing protocols.

KPV is the C-terminal tripeptide fragment (residues 11-13) of alpha-melanocyte stimulating hormone (alpha-MSH), a 13-amino-acid neuropeptide. Alpha-MSH itself was first characterized in the 1950s for its role in skin pigmentation regulation. The anti-inflammatory properties of the C-terminal fragment KPV were identified in the early 2000s by researchers studying the structure-activity relationships of alpha-MSH.

Key work by Getting et al. (2003) demonstrated that KPV retains potent anti-inflammatory activity independent of melanocortin receptors, establishing that this small tripeptide fragment operates through a distinct mechanism likely involving direct inhibition of IL-1 beta functions. The discovery of its oral bioavailability via the PepT1 intestinal peptide transporter by Dalmasso et al. (2008) significantly increased interest in KPV for gut inflammatory conditions, as most peptides require injection for systemic delivery. This unique combination of oral bioavailability, anti-inflammatory potency, and a favorable safety profile has positioned KPV as one of the more accessible peptides for research into inflammatory bowel conditions.