Immunology · KPV
KPV: an α-MSH-derived tripeptide in intestinal inflammation models
October 8, 2026 · 1 min read · Models: Mouse, Cell culture
KPV (Lys-Pro-Val) is the C-terminal tripeptide of α-melanocyte-stimulating hormone. Mouse colitis studies show it is taken up by intestinal epithelial cells through the PepT1 transporter and reduces NF-κB-driven inflammatory signaling.
A summary of published research for scientific reference. It is not medical advice and does not describe or endorse use in humans or animals. Findings from cell culture and animal models often do not carry over to other systems.
Background
α-MSH has anti-inflammatory activity through melanocortin receptors. Its C-terminal tripeptide, KPV, keeps much of that anti-inflammatory activity. In some systems it appears to work largely independently of melanocortin receptor activation.
Findings
Dalmasso and colleagues (Gastroenterology, 2008) showed that the di/tripeptide transporter PepT1 carries KPV into intestinal epithelial and immune cells. Once inside, it inhibited NF-κB and MAPK pathways and reduced pro-inflammatory cytokine expression. Mouse models of chemically induced colitis (DSS and TNBS) were used to score body-weight change, histological inflammation and myeloperoxidase activity as disease-activity readouts.
Later work used nanoparticle and hydrogel formulations as delivery tools in mouse colitis models.
Open questions
How KPV inhibits NF-κB once it is inside the cell is not fully defined. Its activity outside PepT1-expressing tissues also needs clarification.
References
- Dalmasso G, Charrier-Hisamuddin L, Nguyen HTT, et al. PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation. Gastroenterology. 2008;134(1):166–178.