Gathering the record
Relay is organizing the evidence and source boundaries.
Alpha-MSH-derived tripeptide
KPV is a three-amino-acid fragment associated with alpha-MSH. Cell and mouse studies explore inflammatory signaling, colitis, and targeted delivery, but FDA found no KPV administered to humans by any route. Human benefits, safety, dose, and route remain unknown.
60-Second Overview
Start with what it is, why it matters, what research has shown, and what remains unknown. The science follows after the orientation.
Start here. These four answers explain why the compound matters before the page introduces the deeper science.
KPV is a three-amino-acid fragment related to alpha-melanocyte-stimulating hormone. Research has focused on whether it can influence inflammatory signaling and experimental delivery across the gut or skin.
Cell and animal studies have produced signals in experimental colitis and targeted-delivery systems. Researchers want to know whether those effects can survive the much harder steps of human absorption, safety testing, and clinical outcomes.
KPV reduced inflammatory measures in several mouse colitis models, sometimes using specialized nanoparticles or hydrogels. An excised human-skin experiment found poor passive movement across skin and greater laboratory delivery after microporation or electrical assistance. No administration study in living people was identified.
Human bioavailability, pharmacokinetics, route-specific exposure, acute and repeated-use safety, immunogenicity, and any clinical benefit remain unknown. Engineered animal formulations cannot validate ordinary capsules, topical products, or injections.
The research depth, routes, studies, and primary sources below explain how Relay knows—and where the evidence stops.
Research context
Published research has investigated this compound using the following study designs.
These records explain what researchers did. They are not instructions, recommendations, or a transferable protocol.
Published research investigated KPV in intestinal cell systems and mouse models of experimental colitis. This is preclinical context, not a human administration record.
Reported study administration—not a recommendation.
Research at a glance
Evidence depth, confidence, and route context explain how Relay knows—not what anyone should do.
Cell, mouse, engineered-delivery, and ex-vivo skin studies exist, but FDA located no administration to living humans.
Research depth describes how large and mature the overall record is. It does not tell you whether the results were positive.
Human exposure, bioavailability, pharmacokinetics, effectiveness, acute safety, and repeated-use safety remain unknown.
Confidence describes how reliable and consistent the conclusions are. It can be high for one outcome and low for another.
The strongest evidence type shows what the best-supported conclusions are actually based on.
Human findings are more directly relevant than animal or laboratory results, but they still apply only to the populations and outcomes studied.
Route-specific record
These are exposures used in cited research for a specific route and population—not an instruction for an individual.
Half-life describes how long it takes the measured amount in the body to fall by half. It is not a dosing recommendation.
Evidence can change by administration method. Findings from one route should not automatically be applied to another.
Evidence boundary: No verified study administered KPV to living human participants by any route. Mouse inflammation outcomes do not establish human absorption, a clinical effect, safety, or a transferable preparation pattern. Amounts shown describe cited research exposure—not a dosage recommendation.
Detailed evidence
Start with the strongest supported conclusion and its main uncertainty. Claim-level records below show how the evidence changes by question, population, route, formulation, and study design.
None. The closest human-derived evidence is an ex-vivo cadaver-skin permeation study, which is laboratory evidence—not administration to living participants.
This is the strongest supported conclusion in the current human evidence—not a summary of every claim made about the compound.
Whether KPV produces any clinically meaningful human effect; human bioavailability, pharmacokinetics, acute and repeated-use safety, immunogenicity, dose-response, route differences, and combination effects.
Keeping the main uncertainty visible prevents an early or promising finding from looking more settled than it is.
Questions people bring to the evidence
Research questions—not promises of benefit.
The name describes three amino acids—lysine, proline, and valine. FDA separately evaluated the free base and acetate because they are distinct bulk drug substances.
FDA searched the literature, ClinicalTrials.gov, adverse-event systems, and other sources and found no products containing KPV free base or acetate administered to people.
Cell and mouse experiments support PepT1 transport and changes in inflammatory signaling, but FDA says the molecular targets underlying KPV pharmacologic effects remain unknown.
Several studies reported reduced inflammation in experimental mouse models, but no human KPV intervention study was located.
The delivery vehicles were engineered to protect KPV and target the colon, making the formulation part of the tested intervention.
Microporation and iontophoresis increased delivery, but the experiment used cadaver skin rather than living participants.
The finding was model-specific and depended on PepT1 in genetically modified mice.
The committee voted 8-6 with one abstention for both KPV free base and KPV acetate. FDA still controls the final determination and any later rulemaking.
Component studies examine different substances, formulations, routes, and models; they do not test the blend commonly called KLOW.
Mechanisms
KPV (Lys-Pro-Val) is an alpha-MSH-derived tripeptide studied in preclinical inflammatory models. Experiments report PepT1-mediated uptake in intestinal and immune-cell lines, changes in NF-kB/MAPK-related signaling, and activity in mouse colitis models. Engineered nanoparticle and hydrogel formulations also reduced experimental colitis endpoints, while passive permeation across excised human skin was poor. FDA's 2026 review found no human exposure, PK/PD, effectiveness, or clinical safety data and described the molecular targets as unresolved.
A plausible mechanism can explain why a study was attempted. It does not prove that the compound improves a human outcome.
Studies
Study arms are reported for transparency. They describe what researchers did in a defined record and do not transfer across identities, routes, formulations, or populations.
A later trial phase can ask a more mature question, but it does not guarantee a positive result, regulatory approval, or relevance outside the studied population.
Hyaluronic-acid-functionalized KPV nanoparticle experiments in colonic cells and mice
Colonic cell systems and mice with experimental ulcerative colitis
The formulation was reported to improve mucosal-healing and inflammatory outcomes in preclinical colitis models.
Study administration: Orally administered HA-KPV nanoparticles and experimental comparators
Limitations: HA-KPV nanoparticles are a distinct engineered formulation. This is not evidence that unformulated KPV works orally in humans.
Diffusion testing across excised human cadaver skin with passive delivery, microporation, and iontophoresis
Excised human cadaver skin
Passive KPV permeation was poor; microporation and iontophoresis increased delivery into or across the excised skin.
Study administration: KPV applied with passive delivery, microneedle microporation, iontophoresis, or both
Limitations: Cadaver-skin permeation is not a topical clinical trial and does not establish wound healing, systemic absorption, tolerability, or a consumer-use protocol.
Controlled experiments in wild-type and PepT1-knockout mice exposed to a colitis-associated carcinogenesis protocol
Wild-type and PepT1-knockout mice
KPV reduced tumor development in wild-type mice, while the reported effect was absent in PepT1-knockout mice.
Study administration: KPV during experimental colitis-associated carcinogenesis
Limitations: This is an animal mechanism study. It does not show that KPV prevents or treats cancer in humans and should never be presented as a human anticancer result.
KPV-loaded nanoparticles embedded in a colon-targeted polysaccharide hydrogel and tested in cells and mice
Intestinal cell models and mice with experimental colitis
The specialized nanoparticle/hydrogel system delivered KPV to the colon and reduced experimental colitis measures in mice.
Study administration: Colon-targeted KPV nanoparticle/hydrogel formulation versus experimental controls
Limitations: The delivery system is part of the intervention. Results cannot be assigned to ordinary oral free KPV, capsules, injections, or human use.
Controlled experiments in two murine colitis models
Mice with chemically induced or T-cell-transfer colitis
KPV reduced several measures of inflammation in both mouse colitis models.
Study administration: KPV compared with model controls
Limitations: Animal models do not demonstrate effectiveness for ulcerative colitis, Crohn disease, or nonspecific gut healing in people.
Transport experiments in intestinal epithelial and immune-cell lines plus chemically induced mouse colitis models
Caco2-BBE and HT29-Cl.19A intestinal cells, Jurkat T cells, and mice with experimental colitis
The study reported PepT1-mediated cellular uptake, reduced inflammatory signaling in cell models, and reduced inflammation in mouse colitis models.
Study administration: KPV exposure in cell systems and oral KPV in mouse colitis models
Limitations: This was not a human intervention study. Cell-line transport and mouse-colitis outcomes do not establish human oral bioavailability, efficacy, dose, or safety.
Safety snapshot
No human exposure, pharmacokinetic, safety, or effectiveness study of KPV was identified by FDA via any route.
No direct evidenceNo reported human exposure is not proof of safety. It means benefits, adverse effects, bioavailability, dose-response, and repeated-use risks remain unknown.
Open sourceThe current record does not support a reliable common-versus-uncommon frequency split.
Evidence boundaryUnder-detected or under-reported events must not be described as rare.
No source-qualified compound-specific warning or contraindication is encoded in the current record.
Evidence boundaryNo FDA-approved KPV drug product was located. FDA proposed against adding KPV free base and acetate to the 503A Bulks List; on July 23, 2026, PCAC voted 8-6 with one abstention to recommend both forms for inclusion. That nonbinding recommendation is not FDA approval or a final determination. Whether KPV produces any clinically meaningful human effect; human bioavailability, pharmacokinetics, acute and repeated-use safety, immunogenicity, dose-response, route differences, and combination effects.
The current record does not identify a reliable compound-specific pattern of events that caused study discontinuation.
Evidence boundaryThis is an evidence gap, not proof that discontinuations did not occur.
No compound-specific patient-facing urgent-action threshold is established in the current Relay record.
Evidence boundaryRelay does not infer emergency guidance from study discontinuations, mechanism, or incomplete adverse-event reporting.
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