Reviewed on: August 27, 2026.
This page summarizes published research and official regulatory records. It does not provide medical advice or instructions for using any substance. FDA has not identified clinical studies or human exposure data for KPV by any route.
Evidence state at a glance
KPV is the three-residue sequence lysine-proline-valine. Published findings come from cell systems, excised human cadaver skin, and animal models. FDA reports no identified clinical study, human pharmacology study, case report, or other human exposure record. The evidence therefore does not establish clinical effectiveness or human safety.
| Evidence tier | Current evidence state |
|---|---|
| In vitro | Direct cell research in intestinal epithelial and immune-cell systems; one study includes null macrophage findings |
| Animal | Direct mouse inflammation and experimentally induced colitis models, including a nanoparticle formulation |
| Ex vivo | Human cadaver-skin barrier research; this is not clinical evidence |
| Observational human | No human case report or exposure record identified by FDA |
| Interventional human | No clinical study or human pharmacology study identified by FDA |
| U.S. regulatory status | KPV free base and KPV acetate are not components of FDA-approved drugs; FDA has identified major evidence and safety-data gaps |
What exactly is KPV?
KPV is one-letter shorthand for lysine-proline-valine, a three-amino-acid sequence associated with a region of alpha-melanocyte-stimulating hormone. In its 2026 chemistry review, FDA evaluates KPV free base and KPV acetate as distinct bulk drug substances.[1]
FDA’s record writes the free base as H-Lys-Pro-Val-OH, with the formula C16H30N4O4 and molecular weight 342.43 g/mol. The acetate contains the same active moiety with acetate and is reported as C16H30N4O4·CH3COOH with a molecular weight of 402.5 g/mol.[1] FDA also notes inconsistent naming and identifier practices. The shorthand KPV therefore does not, by itself, establish terminal chemistry, free base versus acetate, counterion content, formula, or molecular mass.
That identity boundary is important for interpreting research. A free-acid C terminus is not the same specification as an amidated terminus, and a study material is not automatically equivalent to a catalog material that shares only the three-letter name.
In-vitro evidence: model-dependent signals and an important null result
Dalmasso and colleagues studied KPV transport and inflammatory-signaling measurements in cultured human-derived intestinal epithelial cells, then extended the work into mouse colitis models.[4] The cell findings concern transport, NF-kappa-B-related signaling, and experimental inflammatory endpoints. They do not demonstrate an effect on disease, symptoms, wound closure, or safety in a living person.
Getting and colleagues reported anti-inflammatory observations in mouse models, but their isolated macrophage experiments were not uniformly positive. Under the conditions tested, KPV did not inhibit the measured cytokine release and did not increase cyclic AMP.[5] Those findings complicate a simple claim that KPV acts through a conventional melanocortin-receptor signaling pathway in every model.
Animal evidence: preclinical models do not establish a human outcome
Mouse studies have reported changes in tissue and inflammatory endpoints in experimentally induced colitis or inflammation models.[4–6] These models are useful for testing hypotheses, but induced mouse inflammation is not equivalent to human inflammatory bowel disease, skin disease, or wound healing.
Xiao and colleagues incorporated KPV into engineered nanoparticles and reported cell and mouse results in an ulcerative-colitis model.[8] That experiment tested a peptide together with a particular delivery system. The result cannot be assigned to plain KPV powder, another formulation, or a catalog material of undocumented identity.
Ex-vivo human tissue is not human clinical evidence
Pawar and colleagues measured KPV movement across excised human cadaver skin. Passive permeation was below the study’s detection threshold, while physical enhancement methods increased measured delivery.[7] This is a laboratory barrier experiment involving tissue outside a living body. It does not show exposure, safety, or clinical benefit in a person.
Observational- and interventional-human evidence
FDA searched the published medical literature, ClinicalTrials.gov, Drugs@FDA, DailyMed, adverse-event reporting sources, and other records. It reported no case reports of human KPV use, no identified clinical studies or human exposure data, and no human pharmacokinetic or pharmacodynamic studies for KPV free base or KPV acetate by any route.[1]
The absence of reports is not evidence of safety. Reporting systems are incomplete, and without characterized human exposure there is no clinical evidence from which to estimate effects or risks. Claims that KPV heals wounds or treats inflammatory, skin, or gastrointestinal conditions would exceed the human evidence.
Negative and null findings
- FDA identified no clinical study, human exposure data, human pharmacology study, or human case report for KPV.[1]
- In isolated macrophages, KPV did not inhibit the measured cytokine release and did not increase cyclic AMP under the study conditions.[5]
- Passive movement across excised human cadaver skin was below the detection threshold in the ex-vivo study.[7]
- Nanoparticle findings test KPV plus a delivery system and cannot be generalized to an unformulated material.[8]
- FDA did not identify an adequate nonclinical safety package for the reviewed KPV materials, including major repeat-exposure, genetic-toxicity, reproductive-developmental, and carcinogenicity domains.[1]
- The names KPV, KPV free base, KPV acetate, and possible terminal variants may be used inconsistently.
- No study establishes the identity or biological equivalence of a Serum Research lot.
Current U.S. FDA status
Status checked August 27, 2026: FDA states that neither KPV free base nor KPV acetate is a component of an FDA-approved drug and that neither has an applicable USP or National Formulary drug-substance monograph.[1] In its July 2026 briefing, FDA concluded that the statutory evaluation criteria weighed against adding either material to the section 503A Bulks List.[1]
That briefing supported a Pharmacy Compounding Advisory Committee discussion. FDA explains that advisory-committee recommendations are nonbinding.[2] The staff briefing and committee process should not be described as a final rule unless a later final FDA action is identified. FDA’s current compounding safety page lists KPV among withdrawn nominations and states that the agency has not identified human exposure data and lacks important information needed to know whether KPV would cause harm in humans.[3]
What the evidence cannot establish
Cell and animal studies can generate mechanisms and hypotheses, but they cannot establish clinical effectiveness, human safety, long-term outcomes, or a suitable human-use form. The lack of human exposure data is not a minor gap; it is the central evidence conclusion.
Chemistry is another limitation. FDA found inconsistent naming and insufficient characterization across submitted records. Free base, acetate, derivatives, and terminal variants can share the shorthand KPV. A purity percentage alone would not resolve identity, counterion, impurities, aggregation, or equivalence to a study material.
Frequently asked questions
What does KPV stand for?
KPV is one-letter shorthand for lysine-proline-valine, a three-residue peptide sequence.
Are KPV free base and KPV acetate the same material?
No. They share the KPV active moiety but are distinct bulk drug substances. A research record should state the exact form, terminal chemistry, and counterion.
Has KPV been tested in people?
FDA reported that it did not identify clinical studies or human exposure data for KPV by any route. Excised human cadaver skin is an ex-vivo laboratory model, not a clinical study.
Does KPV act through a melanocortin receptor?
The mechanism is not settled across models. Some preclinical findings involve inflammatory signaling, while one primary study reported no cyclic-AMP increase and no inhibition of the measured macrophage cytokine release under its in-vitro conditions.
Is KPV FDA approved?
No FDA-approved drug contains KPV free base or KPV acetate according to FDA’s 2026 review.[1]
Does this page explain how to use KPV?
No. It is a preclinical evidence and identity summary and intentionally provides no preparation, administration, or self-use instructions.
Primary and official sources
- U.S. Food and Drug Administration. KPV-related bulk drug substances: FDA briefing document, July 2026. FDA media 193346
- U.S. Food and Drug Administration. July 23–24, 2026 Pharmacy Compounding Advisory Committee meeting. Official meeting page
- U.S. Food and Drug Administration. Certain Bulk Drug Substances for Use in Compounding that May Present Significant Safety Risks. FDA compounding safety page
- Dalmasso G, et al. KPV in intestinal epithelial cells and mouse colitis models, 2008. PMID 18061177 · PMCID PMC2431115 · DOI 10.1053/j.gastro.2007.10.026
- Getting SJ, et al. KPV in cellular and animal inflammation models, 2003. PMID 12750433 · DOI 10.1124/jpet.103.051623
- Kannengiesser K, et al. KPV in mouse colitis models, 2008. PMID 18092346 · DOI 10.1002/ibd.20334
- Pawar VK, et al. KPV movement across human cadaver skin ex vivo, 2017. PMID 28343991 · DOI 10.1016/j.xphs.2017.03.017
- Xiao B, et al. KPV nanoparticle study in cells and mice, 2017. PMID 28143741 · PMCID PMC5498804 · DOI 10.1016/j.ymthe.2016.11.020