KPV
KPV (lysine-proline-valine, alpha-MSH fragment)
A small anti-inflammatory tripeptide derived from alpha-MSH studied for gut inflammation and skin, mostly in preclinical models.
Overview
KPV is the C-terminal tripeptide of the hormone alpha-MSH and carries much of its anti-inflammatory activity without pigmentation effects. Preclinical research has explored it for inflammatory bowel conditions and skin inflammation, where it appears to calm inflammatory signaling inside cells. Human clinical evidence is limited and it is not approved. Regulatory update, September 2026: the FDA removed this peptide from Category 2 of the 503A bulk-drug list in April 2026, and on July 23 to 24, 2026 the Pharmacy Compounding Advisory Committee voted to recommend it for compounding against the advice of FDA scientists, who found no adequate human data. The vote is advisory; nothing changes until FDA rulemaking, and vials sold 'for research' remain unapproved drugs.
Mechanism of action
Enters cells and suppresses pro-inflammatory NF-kB signaling, reducing inflammatory cytokine production.
Key studies & citations
- Animal2008
PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation
Nanomolar KPV inhibited NF-kappaB and MAP kinase signaling in intestinal epithelial and T cells, and oral KPV reduced DSS- and TNBS-induced colitis in mice via the PepT1 transporter.
Gastroenterology - Animal2017
Orally targeted delivery of tripeptide KPV via hyaluronic acid-functionalized nanoparticles efficiently alleviates ulcerative colitis
Nanoparticle-delivered KPV accelerated mucosal healing and lowered TNF-alpha in a mouse colitis model.
Molecular Therapy - Review2026
July 23-24, 2026 meeting of the Pharmacy Compounding Advisory Committee
Official record of the meeting at which KPV was considered for the 503A bulks list; the committee's 8 to 6 vote to recommend it went against FDA reviewers' position and is advisory only.
U.S. FDA (Advisory Committee Calendar)
Frequently asked questions
Is KPV proven for gut health in humans?
No. The anti-inflammatory findings are largely from animal and cell studies. Human evidence is limited, so it is preliminary.