KPV (Lys-Pro-Val) is the C-terminal tripeptide of alpha-melanocyte stimulating hormone (alpha-MSH) that retains the full anti-inflammatory activity of the parent peptide while lacking its melanogenic activity profile. Alpha-MSH exerts potent anti-inflammatory effects through MC1R and MC3R — but at 13 amino acids it requires larger synthesis scale. KPV isolates the anti-inflammatory active fragment at just 3 amino acids, making it the most parsimonious tool for studying MC1R/MC3R-mediated anti-inflammatory biology. Primary research application is inflammatory bowel disease (IBD) — specifically colitis models — where KPV reduces NF-kB activation, pro-inflammatory cytokine production, and mucosal damage.
NFkB inhibition: KPV directly suppresses IkBa degradation and NFkB p65 activation in macrophages — reducing TNF-a, IL-6, IL-1b production
Gut mucosal action: KPV reduces epithelial permeability in colitis models, decreases myeloperoxidase (MPO) activity, and attenuates macrophage infiltration
Intracellular MC1R: Evidence for intracellular MC1R in intestinal epithelium — KPV may access cytoplasmic MC1R after cellular uptake
KPV vs full alpha-MSH — why the tripeptide?
Alpha-MSH (13 aa) activates all five melanocortin receptors including MC4R (appetite/libido) and MC2R (adrenal). KPV retains MC1R/MC3R anti-inflammatory activity with minimal MC4R/MC5R activity — cleaner mechanistic tool for studying melanocortin-mediated gut inflammation without metabolic or appetite confounds.
KPV (Lys-Pro-Val) is the C-terminal tripeptide of alpha-MSH that retains full anti-inflammatory activity through MC1R/MC3R agonism and NFkB inhibition. Primary research tool for melanocortin-mediated gut inflammation, particularly colitis models.
How does KPV reduce gut inflammation?
KPV activates MC1R and MC3R → cAMP/PKA → suppresses NFkB p65 activation → reduces TNF-a, IL-6, IL-1b in macrophages and epithelial cells. Also preserves mucosal barrier function in colitis models.
Why use KPV instead of full alpha-MSH?
Alpha-MSH activates all melanocortin receptors including MC4R (appetite, libido). KPV provides selective MC1R/MC3R anti-inflammatory activity without these off-target effects.
What colitis models work best with KPV?
DSS colitis (chemical disruption of mucosal barrier) and TNBS colitis (hapten-induced Th1 inflammation) are the primary models. Both show consistent KPV efficacy on DAI scores, MPO activity, and cytokine levels.
What formats does QSC supply KPV in?
QSC supplies KPV as lyophilised research vials, ≥99% purity HPLC verified with Janoshik COA. Ships from domestic warehouses in USA, EU, UK, Canada, and Australia.
