Research Peptide · For laboratory research use only
Also known as Lysine-Proline-Valine
KPV is the tripeptide Lys-Pro-Val, the C-terminal sequence (residues 11 to 13) of alpha-melanocyte-stimulating hormone (alpha-MSH)2. It has been studied as a small melanocortin-derived peptide with anti-inflammatory activity in cell and rodent models1,2.
Most published work concerns intestinal inflammation: uptake by the di/tripeptide transporter PepT1 in intestinal epithelial and immune cells, and murine colitis models1,2,3. More recent in vitro and mouse studies have examined lipid accumulation in hepatocyte and adipocyte models4,5.
As described in the research literature
As described in the research literature, KPV is taken up into intestinal epithelial cells and T cells by PepT1, a transporter normally expressed in small intestine and induced in colon during inflammation. In Caco2-BBE, HT29-Cl.19A and Jurkat cells stimulated with pro-inflammatory cytokines, nanomolar KPV inhibited activation of NF-kappaB and MAP kinase signalling and reduced pro-inflammatory cytokine secretion1.
Because full-length alpha-MSH acts through melanocortin receptors, the role of MC1R was tested directly: KPV was studied in mice expressing a non-functional MC1R (MC1Re/e), and the authors concluded that its effects in colitis were at least partially independent of MC1R signalling2. In HepG2 and 3T3-L1 cells, KPV was reported to reduce reactive oxygen species and to modulate AKT, mTORC1 and PPAR-gamma signalling4,5.
What published studies have examined
Uptake kinetics of radiolabelled KPV and competition with a PepT1 substrate were measured in human intestinal epithelial and T cell lines, together with NF-kappaB reporter activity, MAP kinase signalling and cytokine secretion1.
Sources [1]
KPV was examined in DSS and TNBS-induced colitis1, and in DSS colitis and CD45RBhi transfer colitis, including MC1Re/e mice, with body-weight change, histology and myeloperoxidase activity as measures2. A delivery study loaded KPV into hyaluronic acid-functionalised nanoparticles targeting colonic epithelial cells and macrophages, and assessed mucosal damage and TNF-alpha in a mouse colitis model3.
In oleic acid-treated HepG2 cells, studies examined lipid deposition, fatty acid synthase expression, ROS generation and ERK, AKT, mTORC1 and PPAR-gamma phosphorylation4. A study in 3T3-L1 preadipocytes examined adipocyte differentiation, and a high-fat diet mouse model examined body weight, white adipose tissue and plasma lipids5.
PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation.
Dalmasso G, Charrier-Hisamuddin L, Nguyen HT, et al. Gastroenterology, 2008.
Melanocortin-derived tripeptide KPV has anti-inflammatory potential in murine models of inflammatory bowel disease.
Kannengiesser K, Maaser C, Heidemann J, et al. Inflammatory Bowel Diseases, 2008.
Orally Targeted Delivery of Tripeptide KPV via Hyaluronic Acid-Functionalized Nanoparticles Efficiently Alleviates Ulcerative Colitis.
Xiao B, Xu Z, Viennois E, et al. Molecular Therapy, 2017.
Lysine-proline-valine peptide attenuates hepatic lipid accumulation through ROS-dependent regulation of the PPARγ pathway in HepG2 cells.
Lee JY, Lee J, Jung WK, et al. Cytotechnology, 2026.
KPV attenuates adipogenesis and lipid metabolism through modulation of ROS-mediated AKT/mTORC1/PPARγ signaling.
An SH, Park JY, Lee SJ Tissue & Cell, 2026.
This page is provided for research and educational reference only. It does not constitute medical advice, dosing guidance, or a recommendation for use. All compounds are strictly for laboratory and in-vitro research purposes.