The Minimal Anti-Inflammatory Peptide Fragment
KPV is the C-terminal tripeptide (Lys-Pro-Val) of α-melanocyte-stimulating hormone. Despite being only three amino acids long, it retains the core anti-inflammatory activity of the parent hormone-without acting through melanocortin receptors.
Key Research Highlights
Mechanistic distinctiveness. Unlike full-length α-MSH, KPV operates independently of MC1R/MC3R signaling. Research demonstrates that KPV suppresses NF-κB activation, stabilizes I-κBα, and blocks p65 nuclear translocation through interaction with importin-α3 binding sites . This receptor-independent pathway makes KPV a valuable tool for dissecting melanocortin biology.
Broad research applications. Published preclinical studies span multiple biological systems:
Hepatic lipid regulation - Attenuates oleic acid-induced lipid accumulation and suppresses FAS expression via ROS-dependent PPARγ modulation in HepG2 cells
Skin protection - Mitigates PM10-induced keratinocyte apoptosis and inflammation by inhibiting the ERK/p38 MAPK/NF-κB axis
Intestinal inflammation - Well-characterized in DSS and T-cell transfer colitis models; uptake mediated by PepT1 transporter
Airway epithelium - Inhibits TNF-α-evoked NF-κB activation and IL-8 secretion in bronchial epithelial cells
PepT1 substrate. KPV is actively transported by the di/tripeptide transporter PepT1 (SLC15A1), which is upregulated in inflamed intestinal tissue-suggesting a natural targeting mechanism for inflammatory sites .
Available Forms
Free acid (H-Lys-Pro-Val-OH)
Acetylated, amidated (Ac-KPV-NH₂) - enhanced stability for research applications
Research Use Statement
This product is supplied for laboratory research purposes only. It is not intended for human or veterinary use, diagnostic applications, or therapeutic administration.
For bulk inquiries, custom synthesis, or COA requests, please contact our sales team.(miley@joybiotech.com)