KPV
A C-terminal alpha-MSH tripeptide fragment that binds MC1R and MC3R receptors to suppress NF-κB-driven inflammation — offering targeted modulation of intestinal, skin, and systemic inflammatory signaling.
A C-terminal alpha-MSH tripeptide fragment that binds MC1R and MC3R receptors to suppress NF-κB-driven inflammation — offering targeted modulation of intestinal, skin, and systemic inflammatory signaling.
KPV binds melanocortin receptors MC1R and MC3R on immune cells, suppressing NF-κB nuclear translocation and reducing pro-inflammatory cytokine production (TNF-α, IL-6, IL-1β). In the gut, it translocates directly into epithelial cells via PepT1 transporters, modulating inflammasome activation and restoring mucosal barrier integrity. It also inhibits mast cell degranulation in the skin, offering multi-tissue anti-inflammatory coverage.
- [1]Kannengiesser K, et al. (2008). Melanocortin-derived tripeptide KPV has anti-inflammatory potential in murine models of bowel disease. Inflammatory Bowel Diseases, 14(3):324-331.
- [2]Brzoska T, et al. (2008). Alpha-melanocyte-stimulating hormone and related tripeptides: biochemistry, anti-inflammatory and protective effects in vitro and in vivo, and future perspectives for the treatment of immune-mediated inflammatory diseases. Endocrine Reviews, 29(5):581-602.
- [3]Catania A, et al. (2004). The melanocortin system as a tool for novel therapies in critical illness. Current Drug Targets - Inflammation and Allergy, 3(2):177-183.
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