KPV
C-terminal tripeptide of α-melanocyte-stimulating hormone; has been reported to attenuate NF-κB-driven cytokine production and reduce inflammatory infiltrate in colitis and skin models.
KPV is the C-terminal tripeptide of α-melanocyte-stimulating hormone (α-MSH). Although the parent peptide is best known for its pigmentation effects via MC1R, the KPV fragment retains the anti-inflammatory portion of α-MSH’s activity without significant melanocortin receptor agonism, making it a focus of inflammation research independent of the broader melanocortin axis.
Across in vitro and rodent models, KPV administration has been associated with attenuated NF-κB nuclear translocation, reduced cytokine output (TNF-α, IL-1β, IL-6), and decreased neutrophilic infiltrate in models of inflammatory bowel disease, atopic dermatitis, and oral mucositis. The mechanism appears to involve direct inhibition of inflammatory transcription rather than receptor-mediated signaling, although intracellular targets remain incompletely characterized.
Oral, topical, and injectable formulations have been investigated, with the oral route attracting interest because of KPV’s small size and relative protease stability. The peptide is investigational and is not approved for therapeutic use.