Not medical advice. KPV is a research compound. This guide does not provide dosing, diagnosis, therapy recommendations, or claims about effects in humans.
KPV is the three-amino-acid tail of α-melanocyte stimulating hormone that retains the full anti-inflammatory punch of the parent hormone without touching melanocortin receptors.
One-paragraph overview from our research datasheet — still scientific, but faster to read than the full mechanism list below.
KPV anti-inflammatory tripeptide from α-MSH C-terminus inhibits NF-κB via importin-α3 competitive blockade, independent of melanocortin receptor signaling.
Peer-reviewed literature typically discusses KPV in specific experimental settings. The points below reflect how the scientific community frames this compound—not as health claims, but as the research questions being asked.
Research vs. personal use: Literature describes experiments in controlled lab and animal models. This is distinct from any real-world use; our products are for laboratory research only.
Compounds in this family are frequently studied in models of tissue injury, wound closure, and how cells reorganise after damage. Research looks at cell movement, blood-vessel support, and inflammatory balance -not at replacing medical care.
Our datasheet lists mechanistic themes observed in preclinical work. These are research endpoints, not health claims. They help scientists understand and compare pathways.
Storage requirements: Lyophilised powder: store in freezer (−20 °C). Reconstituted: refrigerate 1–6 °C, away from sunlight. Use within the validated stability window for the specific batch and formulation. · Learn best practices in our detailed storage guide.
Research dosing context: Literature typically discusses 200-500 μg per day · Once or twice daily, subcutaneous injection or oral administration · MW 342.43 Da, extremely small peptide with favorable oral absorption profile. PepT1 transporter-mediated uptake in intestinal epithelium. Non-MCR mechanism confirmed: does not bind MC1,3,5R and does not compete with α-MSH. Minimal systemic immunosuppressive risk compared to broad-spectrum anti-inflammatory agents.
Preparation steps: Follow our detailed reconstitution guide, use the calculator tool for volume confirmation, and always verify purity with the COA reading guide.
KPV is the C-terminal tripeptide (Lys-Pro-Val) of α-melanocyte stimulating hormone. It works by entering cells through the PepT1 di/tripeptide transporter, translocating to the nucleus, and competitively blocking the import of the NF-κB p65 subunit — shutting down the master switch for inflammatory gene expression. Crucially it does this without activating melanocortin receptors, so it carries α-MSH's anti-inflammatory activity in isolation.
α-MSH produces pigmentation through melanocortin receptor activation at its N-terminal core (around His-Phe-Arg-Trp). KPV is just the C-terminal tail, which has no melanocortin receptor affinity but carries the non-MCR anti-inflammatory activity mediated by NF-κB blockade. Splitting the activities apart is the whole point of using the fragment.
In the landmark Dalmasso et al. study (Gastroenterology, 2008), oral KPV was transported into colonic cells via PepT1 and reduced both DSS- and TNBS-induced colitis in mice, lowering disease-activity and histological inflammation scores. Mechanistically it inhibited NF-κB and MAP-kinase signalling and reduced pro-inflammatory cytokine secretion in epithelial cells and macrophages. These are preclinical animal-model findings, not demonstrated human effects.
Not exclusively, but the PepT1 transporter is most abundant in the small intestine and colon, which gives KPV a natural bias toward gut-targeted effects. It has also been studied in cutaneous, ocular, respiratory, and joint inflammation models, so its anti-inflammatory mechanism is broadly relevant — gut targeting is just its most distinctive feature.
Its small size and PepT1 uptake give KPV unusually favourable oral absorption characteristics for a peptide, and oral administration has been used in preclinical IBD models with measurable anti-inflammatory effect. Formal human oral pharmacokinetic data is limited, so published protocols also use parenteral delivery for consistency. KPV is supplied for laboratory research only.
Both are studied for gut protection but through different mechanisms. KPV is a direct anti-inflammatory: it blocks NF-κB to dampen the cytokine cascade and homes to inflamed tissue via PepT1. BPC-157 is a broader tissue-repair and cytoprotective peptide acting through VEGFR2/eNOS angiogenesis and growth-hormone-receptor pathways. Researchers studying inflammation specifically often choose KPV; those studying mucosal repair often choose BPC-157.
Keep the lyophilised powder frozen at −20 °C. After reconstitution with bacteriostatic water, refrigerate at 1–6 °C and protect from light. The tripeptide is one of the smaller and more robust research peptides and tolerates standard handling, but avoid repeated freeze-thaw cycles of the reconstituted solution.
No, and no. This article is educational only. We do not provide dosing, medical recommendations, or health claims. Our products are sold strictly for laboratory research, not for personal use of any kind.
Open the shop listing via “View product details.” There you will see batch specs, the Certificate of Analysis (COA), concentration, purity grade, and available SKUs with current pricing.
Other compounds researchers often read about alongside KPV.
Primary literature and registries for KPV, plus mainstream coverage of the peptide category. Research use only - not medical advice.
Databases & literature:
Peptides in the news:
Access concentration, batch info, variants, and current pricing on our shop.
Also known as: KPV Tripeptide, α-MSH(11-13), Alpha-MSH C-Terminal Fragment, Lys-Pro-Val, Anti-Inflammatory Tripeptide, α-Melanocyte-Stimulating Hormone Fragment