KPV
The C-terminal tripeptide of α-MSH studied for anti-inflammatory effects in gut and skin disease.
In plain English
KPV is a short tripeptide (Lys-Pro-Val) corresponding to the C-terminal three residues of alpha-melanocyte-stimulating hormone. Unlike the parent hormone, KPV is stripped of pigmentation effects but retains anti-inflammatory activity. It has been studied in cell and animal models of inflammatory bowel disease, atopic dermatitis, and other inflammatory conditions, where it appears to reduce NF-κB signaling and pro-inflammatory cytokines. Direct human RCT data are limited, but topical formulations have entered cosmetic and dermatology research. KPV is not FDA-approved.
What it is
KPV is the synthetic tripeptide Lys-Pro-Val, the C-terminal three amino acids of α-MSH.
Mechanism (summary)
KPV reduces NF-κB-mediated inflammatory signaling and downregulates pro-inflammatory cytokines in epithelial and immune cells. It enters cells via PEPT1 transporters, supporting activity at the intestinal epithelium.
Why people research it
- Inflammatory bowel disease (UC and Crohn's)
- Atopic dermatitis and skin inflammation
- Wound healing
- General anti-inflammatory signaling
Human evidence
Human RCT data are limited. KPV has been incorporated into early-phase clinical and cosmetic research for skin and gut inflammation, but well-powered human trials are not available.
Animal / lab evidence
Mouse colitis models show reductions in disease activity and inflammation with KPV. Atopic-dermatitis-like models in mice show benefit with topical α-MSH and KPV.
Key studies
Each summary explains the design, what was found, and what it doesn't prove.
Mice with experimental colitis got better when given KPV by mouth.
KPV gets into gut cells through a known transporter and quiets a key inflammation pathway in a dish.
History
Identified as a minimally bioactive fragment of α-MSH retaining anti-inflammatory but not pigmentation effects.
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