KPV
Also known as lysine-proline-valine, alpha-MSH (11-13), Lys-Pro-Val
Anti-inflammatory tripeptide from alpha-MSH; the evidence is entirely preclinical, with no human studies.
At a glance
- Category
- Recovery & tissue
- Status
- research chemical
- Route
- oral, subcutaneous or topical in practice; in animal research orally via drinking water
- Half-life
- Not known; there is no validated human or animal pharmacokinetics. Half-lives quoted by suppliers cannot be traced to a source
- Onset
- unknown
- Molecular weight
- approximately 342 g/mol
- Sequence
- KPV (Lys-Pro-Val)
Not approved as a medicine anywhere, and not established as a cosmetic ingredient or supplement. The FDA lists KPV by name among bulk drug substances that may present significant safety risks, stating that it "has not identified any human exposure data on drug products containing KPV administered via any route of administration"; as of the agency's April 2026 update KPV sits in the "nominated but withdrawn" table, having previously been in category 2 of the interim 503A/503B policies 5. Sold as a 'research chemical', as a capsule or as a compounded cream.
Doping status: Not listed by name on the WADA list; as a non-approved substance it could fall under S0. Verification with the anti-doping authority is advisable.
Checked against the WADA 2026 Prohibited List. For a specific product and country, Global DRO is the lookup athletes are expected to use — the List names substances, not brand names.
Mechanism of action
KPV is the C-terminal tripeptide of alpha-melanocyte-stimulating hormone (residues 11-13). It retains the anti-inflammatory action of alpha-MSH without the effects on pigmentation or appetite.
The mechanism of action is remarkably well worked out for an otherwise preclinical compound: KPV is taken up via the peptide transporter PepT1 into intestinal epithelial cells (Km approximately 160 microMolar) and into colonic immune cells (Km approximately 700 microMolar), and then acts intracellularly 1.
Within the cell, nanomolar concentrations inhibit the NF-kB and MAP kinase pathways: activation of NF-kB is delayed and the recovery of IkB-alpha accelerated, resulting in less release of pro-inflammatory cytokines.
That the action does not run via melanocortin receptors has been shown by the fact that KPV also protected mice with a non-functional MC1R against mortality in a colitis model 2.
What the research shows
After roughly two decades of research, KPV is still entirely preclinical. The mechanism is soundly worked out in cell culture and mouse models, but there is not a single human study, no human pharmacokinetics and no human safety data. Anyone offering KPV for gut or skin complaints is selling a result from an animal model.
Research in humans
No published human clinical studies. A targeted search of clinicaltrials.gov returned not a single registered KPV study. There is no validated human pharmacokinetics and no human efficacy or safety outcome.
Animal and lab research
Two mouse models of colitis (DSS-induced and transfer colitis) showed faster recovery, better weight recovery, less inflammatory infiltrate and lower myeloperoxidase activity. Oral KPV reduced both DSS- and TNBS-induced colitis. More recent research focuses on delivery systems: hyaluronic acid-functionalised nanoparticles and a PepT1-targeted nanomedicine in which KPV is combined with FK506.
Caveats. Rodent models of colitis translate poorly to human inflammatory bowel disease. Much recent work relies on engineered nanoparticles rather than the free peptide, so the results do not automatically apply to the loose peptide that is on the market. The dosing in animal research (100 microMolar in drinking water) does not readily convert to a human dose in milligrams.
What it is used for
Dosing
- These doses come exclusively from peptide vendors. There is not a single clinical study from which a dose can be derived; the FDA states it has identified no human exposure data for KPV by any route 5.
- In animal research the oral route via the intestinal lumen was used, consistent with uptake by the intestinal peptide transporter PepT1 14. Subcutaneous administration bypasses that very route and has never been studied.
- Material sold as a 'research chemical' carries no guarantee of identity, purity or sterility.
These figures describe what the literature and published protocols report. They are not advice and not a dosing instruction.
Protocols
Subcutaneous course
user protocol — not validatedSource: Peptide vendor protocols
This is not a validated schedule. It is a pattern that circulates among users and sellers, reproduced because it is what people actually follow — not because it has been tested. No trial established these doses, this interval or this duration, and nobody is checking what is in the vial. Treat every number below as an assertion, not a finding.
| Week 1 | 200 mcg per day subcutaneously |
|---|---|
| Weeks 2-8 | increased to 500 mcg per day if tolerated |
The step up after a week is a tolerance convention rather than titration to any measured effect. More importantly, this route bypasses PepT1 in the intestinal epithelium, the transporter on which KPV's entire gut rationale rests — so a subcutaneous schedule is not a smaller version of the animal experiments, it is a different exposure altogether.
Schedules are reproduced as their source states them. Units, IU and milligrams explains why the figures are not interchangeable between products.
Reconstitution
- Vial sizes
- 10 mg
- Solvent
- bacteriostatic water (0.9% benzyl alcohol)
- Storage
- Reconstituted 2-8 °C, protected from light. Powder in the freezer. Common shelf-life periods are convention, not a stability finding.
Worked example
10 mg vial + 2 ml bacteriostatic water = 5 mg/ml. 500 mcg = 0.1 ml, that is 10 units on a U100 insulin syringe.
Do not shake; let the water run down the wall of the vial.
Work it out for KPV
Safety
Side effects
- Injection site reactions
- Gastrointestinal complaints with oral administration
- Otherwise not characterised in humans. The absence of documented side effects reflects the absence of research, not demonstrated safety: the FDA records no human exposure data for KPV by any route and says it "lacks important information regarding any safety issues raised by KPV, including whether it would cause harm if administered to humans" 5
Do not use if
- Active infection: KPV suppresses NF-kB signalling 1, which may theoretically dampen the immune response
- Immunosuppression or use of immunosuppressants, for the same reason
- Pregnancy and breastfeeding: no data
- Children and adolescents: no data
Interactions
Not systematically studied; there are no interaction studies. Theoretically, additive immunosuppression is conceivable with concurrent use of corticosteroids or other immunosuppressants. Because KPV is taken up via PepT1, competitive interactions with other PepT1 substrates (such as beta-lactam antibiotics and ACE inhibitors) are theoretically possible, but have not been studied.
Sources
- PepT1-Mediated Tripeptide KPV Uptake Reduces Intestinal InflammationGastroenterology, 2008
- Melanocortin-derived tripeptide KPV has anti-inflammatory potential in murine models of inflammatory bowel diseaseInflammatory Bowel Diseases, 2008
- Orally Targeted Delivery of Tripeptide KPV via Hyaluronic Acid-Functionalized Nanoparticles Efficiently Alleviates Ulcerative ColitisPubMed Central
- The role and pathophysiological relevance of membrane transporter PepT1 in intestinal inflammation and inflammatory bowel diseasePubMed Central
- Certain Bulk Drug Substances for Use in Compounding that May Present Significant Safety RisksUS Food and Drug Administration, page current as of 22 April 2026 - KPV appears under substances nominated but withdrawn, previously category 2