The C-terminal tripeptide fragment (Lys-Pro-Val) of alpha-melanocyte stimulating hormone, retaining the anti-inflammatory activity of the parent hormone without melanocortin receptor binding. KPV inhibits NF-κB nuclear translocation, suppresses pro-inflammatory cytokine production (IL-1β, TNF-α, IL-6), and reduces neutrophil migration. Unlike full-length α-MSH, KPV does not activate MC1R — its anti-inflammatory mechanism is receptor-independent, involving direct intracellular NF-κB pathway inhibition.
Research FocusAnti-inflammation, IBD models, mucosal immunity, NF-κB biology
ReconstitutionBacteriostatic water — 1 mg/mL
Stability14 days at 2–8°C
Key distinction: Receptor-independent anti-inflammatory — inhibits NF-κB without melanocortin receptor binding, making KPV combinable with any receptor-targeted peptide without competition.
Scientific Evidence
Published Research
[1]
Brzoska T et al. Alpha-melanocyte-stimulating hormone and related tripeptides: biochemistry, antiinflammatory and protective effects. Endocr Rev 2008;29:581-602 — PubMed 18612139
[2]
Dalmasso G et al. The PepT1-transportable tripeptide KPV prevents experimental colitis. Inflamm Bowel Dis 2008;14:1514-1522 — PubMed 18626968
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