D tier · weak
A clean and reproducible anti-inflammatory mechanism in cell culture and rodent colitis models has never been tested in a single published human trial, and FDA has stated it lacks important safety information for the substance.
kpv
KPV is the three-residue carboxy-terminal fragment of alpha-melanocyte-stimulating hormone, studied mainly as a gut-targeted anti-inflammatory in cell culture and rodent colitis models. The mechanistic work is coherent and reproducible but no human clinical trial has been published.
// we supply this one
available as a research reagent
≥ 99% HPLC · lyophilised powder · batch certificate published. Grade D above is our own and is not adjusted because we stock it.
the explanation
KPV is the tail end of a natural hormone, cut down to just three building blocks, and it calms inflammation in lab dishes and in mice with inflamed bowels. Nobody has yet published a proper trial of it in people, so its human effects are unknown.
regulatory status
not approved for human use
No marketing approval in any jurisdiction; nominated for the FDA 503A compounding bulks list, where FDA stated it lacks important information regarding safety issues, before the nomination was withdrawn; appears in some unregulated topical cosmetic formulations. At the Pharmacy Compounding Advisory Committee meeting of 23 July 2026 the panel voted 8 to 6 with one abstention to recommend adding KPV to the section 503A bulks list, against FDA staff advice. A recommendation is non-binding, confers no approval and is not a finding of efficacy; implementation would require notice-and-comment rulemaking. FDA has not published meeting minutes and these tallies are trade-press reporting from the room.
how it works · proposed mechanism
KPV is unusual for this class in having a specific, transporter-defined route into the cells it acts on.
PepT1-mediated cellular uptake
KPV enters intestinal epithelial and immune cells through the PepT1 di/tripeptide transporter, which is upregulated in inflamed intestinal tissue. This provides a plausible mechanism for selective targeting of inflamed gut.
NF-kB pathway inhibition
At nanomolar concentrations KPV blocks NF-kB activation and MAP kinase signalling inside the cell. This is the core anti-inflammatory action reported across independent cell systems.
Melanocortin receptor binding
KPV retains binding to the MC-1 receptor inherited from its alpha-MSH parent sequence. Systemic and topical application inhibited both sensitisation and elicitation phases of contact hypersensitivity in mice.
Cytokine suppression across tissues
In human bronchial epithelial cells KPV produced dose-dependent inhibition of NF-kB, MMP-9, IL-8 and eotaxin secretion. The effect therefore is not confined to gut tissue in vitro.
what’s reported
evidence shape
5 sourcesThe composition of the cited literature by study type. This describes the shape of the evidence, not its quality — and it does not by itself set the grade.
⚠ the catch
There is no published human clinical trial of KPV for any indication, so every claim about human benefit is an extrapolation from mouse colitis and cell culture. Translation from rodent immunomodulation models to human therapy has an especially poor historical track record.
key published findings
- In vitro and mouse study (Gastroenterology, 2008) showed nanomolar KPV inhibited NF-kB and MAP kinase pathways in human intestinal epithelial and T cells, and that oral administration reduced the incidence and severity of both DSS- and TNBS-induced colitis in mice.
- In vitro study in human bronchial epithelial cells (International Journal of Physiology, Pathophysiology and Pharmacology, 2012) found dose-dependent inhibition of NF-kB activation, MMP-9, IL-8 and eotaxin secretion.
- Mouse contact-hypersensitivity work (Annals of the New York Academy of Sciences, 2003) reported that KPV binds MC-1R and that both systemic and topical application inhibited the sensitisation and elicitation phases.
- More recent cell-based work (2025) attributes skin-protective effects to regulation of oxidative stress and modulation of the MAPK/NF-kB pathway in keratinocytes exposed to environmental stressors.
- FDA's compounding review recorded that it lacks important information regarding safety issues for KPV.
limitations of the evidence
- No human efficacy or safety trial has been published for any route or indication.
- No human pharmacokinetic data exist, and oral bioavailability of a free tripeptide is a substantial open question.
- Reported molecular weight and CAS number vary widely across commercial suppliers, indicating poor material characterisation in the unregulated supply chain.
identity
| full name | Lysine-proline-valine, the C-terminal tripeptide of alpha-melanocyte-stimulating hormone (alpha-MSH 11-13) |
| category | Healing & Repair |
| modality | peptide |
| formula | C16H30N4O4 |
| molar mass | 342.4 g/mol |
| sequence | KPV |
laboratory handling
| storage | Lyophilised powder is typically stored at -20 °C protected from light and moisture; reconstituted laboratory solutions are kept refrigerated at 2-8 °C for short-term use or frozen in aliquots. |
| solubility | Highly water-soluble in laboratory settings; commonly prepared in sterile water, saline or aqueous buffer, and incorporated into aqueous topical and oral research formulations. |
| co-studied with | Most commonly co-studied with BPC-157 in gut-inflammation contexts and formulated alongside other alpha-MSH-derived melanocortin fragments in preclinical work. |
Handling information describes laboratory practice for a research reagent. It is not a preparation guide for use in humans.
the receipts
6 citedUS Food and Drug Administration · 2026 · official
Gastroenterology · 2008 · preclinical
International Journal of Physiology, Pathophysiology and Pharmacology · 2012 · preclinical
Annals of the New York Academy of Sciences · 2003 · preclinical
Regulatory Affairs Professionals Society · 2026 · trade press
Wikipedia · 2026 · tertiary
Sources marked tertiary or press release are the weakest citations on this page.
others in Healing & Repair