Abstract
KPV (Lys-Pro-Val) is a C-terminal tripeptide fragment derived from alpha-melanocyte-stimulating hormone (α-MSH). Unlike full-length α-MSH, KPV does not bind melanocortin receptors but has been studied for anti-inflammatory properties through NF-κB pathway modulation.
Molecular Background
- Sequence: Lysine-Proline-Valine (KPV)
- Origin: C-terminal fragment of α-MSH
- Receptor binding: Does not activate melanocortin receptors
- Molecular Weight: Small tripeptide
Research Applications
- Inflammatory Studies: NF-κB pathway research
- Gut Research: Intestinal inflammation models
- Skin Studies: Dermal inflammation investigations
- Inflammasome Research: NLRP3 modulation studies
Proposed Mechanisms
- NF-κB Inhibition: Suppression of nuclear translocation
- NLRP3 Modulation: Inflammasome pathway effects
- Cytokine Reduction: IL-1β, TNF-α, IL-6 suppression
- PGE2 Effects: Prostaglandin pathway modulation
Preclinical Research
Studies have examined KPV in:
- Colitis and IBD models
- Skin inflammation models
- Macrophage activation assays
- Epithelial barrier studies
Technical Specifications
- Purity: ≥99% (HPLC verified)
- Storage: Store lyophilized at -20°C
- Solubility: Water soluble
Current Research Status
KPV represents one of the shorter anti-inflammatory peptides studied in preclinical research. Its small size and lack of melanocortin receptor activity distinguish it from full-length α-MSH. Human clinical data remain limited.