What it is
KPV is a tripeptide: lysine, proline, valine. It is the last three residues of alpha-melanocyte stimulating hormone, a thirteen amino acid hormone, so it also appears in the literature as α-MSH(11–13). Unlike the parent hormone it carries no pigment-inducing activity.
A caution for anyone reading the literature. Several published papers headed “KPV” studied different molecules. A C-terminal amide (H-KPV-NH2), a D-amino-acid analogue used in rat burn work, and a disulfide-linked dimer called (CKPV)2 or CZEN-002 all appear under that name. The dimer is a distinct compound with its own separate human exposure record. Findings from those papers are not KPV findings, and they are routinely cited as though they were.
How it works
Two mechanisms are reasonably well supported in laboratory work, and one widely repeated claim is not.
It suppresses NF-κB
In human intestinal and bronchial epithelial cell lines, nanomolar KPV inhibited NF-κB and MAPK activation and reduced pro-inflammatory cytokine output (Dalmasso 2008). In bronchial epithelium it appeared to enter the nucleus and block p65RelA translocation by competing at the importin-α3 binding site, an action requiring no cell-surface receptor at all (Land 2012).
It enters cells through PepT1
KPV is a substrate of the di/tripeptide transporter PepT1 (SLC15A1), which is low in healthy colon and rises in inflammatory bowel disease. This produced the strongest causal evidence in the whole KPV literature: in PepT1-knockout mice, KPV’s protective effect disappeared entirely (Viennois 2016). That is a genuine mechanistic result. It is also in mice.
The receptor question is unsettled
KPV protected mice with non-functional MC1R from chemically induced colitis, which argues against melanocortin receptor dependence (Kannengiesser 2008). In human keratinocytes it produced no cAMP rise, unlike classic MC1R agonism, though it did mobilise intracellular calcium (Elliott 2004). Reviews commonly state that KPV binds MC1R. No published binding affinity for any melanocortin receptor was located during this source pass.
Research evidence
Human evidence: none
No human trial of KPV has been published. None is registered on ClinicalTrials.gov. Searches covered KPV, Lys-Pro-Val, lysine-proline-valine and CZEN-002 as interventions, and PubMed filtered to clinical trial and randomised controlled trial publication types, returning nothing in every case.
The FDA reached the same conclusion in its own 2026 review, stating there were “no published clinical studies in humans” and “a lack of any human data on drug products containing these substances.” The agency also reported that outsourcing facilities recorded no KPV-containing products between 2017 and 2025, so there is not even an observational compounding record.
One adjacent human study is often cited as if it were KPV. It is not. An open-label phase I/II of CZEN-002, the (CKPV)2 dimer, enrolled twenty women with vulvovaginal candidiasis, seventeen completing. Uncontrolled, company-reported, and a different molecule.
Preclinical evidence
- Mouse colitis. Reduced colitis incidence and cytokine mRNA in DSS and TNBS models (Dalmasso 2008).
- Mouse colitis, MC1R-nonfunctional. Faster recovery and reduced histologic infiltrate, retained without working MC1R (Kannengiesser 2008).
- Mouse colitis-associated cancer. Prevented carcinogenesis in wild-type animals; effect abolished in PepT1-knockouts (Viennois 2016).
- Rabbit corneal abrasion, topical. Eight of eight corneas re-epithelialised at 60 hours against zero of eight on vehicle, and the effect was blocked by a nitric oxide synthase inhibitor (Bonfiglio 2006). Very small n, acute mechanical injury.
- Human keratinocytes, in vitro. Restored viability and reduced IL-1β after particulate-matter injury (Sung 2025). Cell culture only.
Every colitis model here is chemically induced. None reproduces how human ulcerative colitis or Crohn’s disease actually arises.
The delivery problem
A large share of the encouraging KPV literature is really evidence that an engineered delivery system works, which most sources covering this compound do not mention.
Nanoparticle-formulated KPV achieved equivalent protection in mice at a concentration twelve thousand times lower than free KPV (Laroui 2009). Across human skin tested outside the body, passive transdermal permeation of KPV fell below the limit of detection and required microneedles or iontophoresis to move at all (Pawar 2017). A 2026 prodrug paper exists specifically because free KPV reaches the colon poorly (Cheng 2026).
Read plainly, that body of work says free KPV is inefficient, and the formulation is doing much of the lifting.
Safety
There is no human safety data of any kind. No pharmacokinetics, no acute or repeat-dose toxicity, no genotoxicity, no developmental or carcinogenicity studies. The FDA specifically flagged immunogenicity and peptide aggregation as unaddressed risks.
Animal and cell studies reported no overt toxicity at the concentrations used, but none of them was designed as a toxicology study.
One signal is worth stating directly. PepT1 overexpression increased tumour burden in the same colitis-associated cancer model in which KPV reduced it (Viennois 2016). KPV went the protective direction, but the transporter it depends on is the same one implicated in tumour promotion.
KPV degrades under acid, alkali and peroxide to lys-pro-diketopiperazine. The biology of that degradation product is uncharacterised.
Regulatory status
Not approved as a drug in any jurisdiction.
In the United States, KPV was nominated for the 503A Bulk Drug Substances list for topical compounding. The FDA’s own reviewers recommended against adding it, citing the absent human data and finding the substance “not well-characterized,” with no impurity, aggregate or microbiological data available. On 23 July 2026 the Pharmacy Compounding Advisory Committee voted eight to six, with one abstention, in favour of adding it, alongside BPC-157 and TB-500.
That vote is advisory and non-binding. Actual listing requires notice-and-comment rulemaking, which has not concluded.
KPV is not named on the WADA 2026 Prohibited List. Its position under the S0 non-approved substances category is unresolved rather than confirmed permitted, and an athlete should treat it that way.
Handling and identity
Worth knowing before anything else: the FDA found that material sold as KPV is not well-characterised, and that the naming used commercially does not follow INN, IUPAC or USAN conventions. The identity of what is being sold under this name is itself uncertain, separately from any question about whether the molecule does anything.