KPV
The three-residue tail of α-MSH — anti-inflammatory without the pigmentation.
Repair & recovery · 6 min read · updated 13 Aug 2026
Research use only. The ranges below are what published studies and community protocols report. They are reference material for laboratory research, not medical advice or a recommendation for human or veterinary use.
The compound
KPV
View- Type
- Anti-Inflammatory Tripeptide
- CAS
- 67727-97-3
- Formula
- C₁₆H₃₀N₄O₄
- Mass
- 342.44 g/mol
At a glance
- Class
- Anti-inflammatory tripeptide
- Sequence
- Lys-Pro-Val — α-MSH residues 11–13
- Molecular weight
- 342.44 Da
- CAS
- 67727-97-3
- Distinguishing feature
- Acts intracellularly, not through melanocortin receptors
- Vial size stocked
- 10 mg
KPV is the C-terminal tripeptide of α-melanocyte-stimulating hormone. α-MSH is a potent endogenous anti-inflammatory peptide, but it is also the hormone that drives melanogenesis, which makes it unattractive as a research tool for inflammation specifically. KPV retains most of the anti-inflammatory activity and essentially none of the pigmentation activity.
The reason for that separation is that KPV does not work through the melanocortin receptors at all. It is taken up into cells — in intestinal epithelium via the PepT1 di/tripeptide transporter — and acts intracellularly on inflammatory signalling. This is unusual: most peptides in this catalogue are receptor ligands operating from outside the cell.
Its size is also unusual. At 342 Da it is barely a peptide by mass — smaller than many small-molecule drugs — which contributes to good tissue penetration and to genuine topical activity.
Mechanism in detail
- NF-κB inhibition: KPV interferes with NF-κB nuclear translocation and activation, reducing transcription of pro-inflammatory cytokines including IL-1β, IL-6 and TNF-α.
- PepT1-mediated uptake: in intestinal and colonic epithelium the PepT1 transporter carries KPV into the cell. PepT1 expression rises in inflamed intestinal tissue, which means uptake concentrates where inflammation is — an elegant targeting mechanism that occurs by accident of biology.
- Independence from melanocortin receptors: demonstrated in MC1R-deficient models where anti-inflammatory activity persists. This is what separates it from α-MSH.
- Antimicrobial activity: α-MSH and its C-terminal fragments show activity against Candida albicans and Staphylococcus aureus in vitro, an effect that carries over to KPV.
Where it is studied
- Inflammatory bowel disease models — the largest body of work, mostly DSS- and TNBS-induced colitis in mice, delivered orally or by nanoparticle.
- Dermatological inflammation, including topical application in dermatitis models, where the small size supports genuine skin penetration.
- General inflammation-resolution research as a comparator to α-MSH without the confound of pigmentation.
Route matters more than usual here
For gut-focused research questions, oral administration is mechanistically correct rather than a convenience — PepT1 is expressed in intestinal epithelium and that is where the uptake happens. For dermal questions, topical formulation reaches the target directly. Subcutaneous administration is the general-purpose systemic route and the one most reported protocols use when the target is not the gut or skin.
Storage
- Lyophilised: 2–8 °C or −20 °C. More tolerant of handling than the large peptides.
- Reconstituted: 2–8 °C, used within about 28 days.
- Short peptides are less fragile but not immune to degradation. The usual rules apply.
Cautions
- No controlled human trials. The evidence base is rodent and in-vitro.
- Suppressing NF-κB suppresses a defensive pathway as well as a damaging one. Concurrent infection is the obvious concern in any model.
- Topical formulations are the least standardised route — concentration, base and penetration all vary, and results across studies are correspondingly hard to compare.
- Its antimicrobial activity is real but modest; it is not a substitute for anything designed for that purpose.
References & credit
- 1Dalmasso G et al., Gastroenterology 2008 — PepT1-mediated transport of KPV and attenuation of colitis in mouse models.
- 2Kannengiesser K et al., Inflamm Bowel Dis 2008 — Melanocortin-derived tripeptide KPV and intestinal inflammation.
- 3Cutuli M et al., J Leukoc Biol 2000 — Antimicrobial effects of α-MSH peptides.
This article was written in-house. Where a dose range reflects community practice rather than a published trial, the community references we consulted are credited above and the article says which is which.