Bottom line
KPV (Lys-Pro-Val) is a 3-amino-acid peptide corresponding to the C-terminal tripeptide of alpha-melanocyte-stimulating hormone (alpha-MSH). Preclinical models, particularly mouse colitis, show anti-inflammatory effects mediated through PepT1 transporter uptake and NF-κB pathway inhibition. No completed human randomized controlled trial of KPV as a single-ingredient drug exists. The FDA has stated it lacks human exposure data and important safety information for KPV.
Identity and composition
| Field | Verified information |
|---|---|
| Preferred name | KPV |
| Key aliases | Lys-Pro-Val, alpha-MSH(11-13), C-terminal alpha-MSH tripeptide, lysine-proline-valine |
| Molecular/sequence identity | Tripeptide: Lys-Pro-Val (KPV); amidated C-terminus in context of parent alpha-MSH |
| Modifications/form | Linear tripeptide; MW ~342 Da |
| Stable identifiers | No PubChem CID specific to KPV as a discrete entity; part of alpha-MSH sequence |
| Identity caveats | "KVP" (Lys-Val-Pro) is a distinct sequence — not a misspelling of KPV. The free base (Lys-Pro-Val) and acetate salt are chemically distinct forms. K(D)PT is a related analog, not the same molecule. Not interchangeable with full alpha-MSH. |
Development and approval status
| Jurisdiction | Status and indication | Product/source | As of |
|---|---|---|---|
| United States (FDA) | Not approved for any indication. On July 23, 2026, PCAC separately voted 8 yes, 6 no, and 1 abstention to recommend KPV free base and KPV acetate for 503A Bulks List inclusion. The advisory recommendations were nonbinding and did not add either form to the list. | FDA PCAC | 2026-08-06 |
| European Union (EMA) | No marketing authorization | N/A | 2026-08-06 |
| Other jurisdictions | Status not established here; requires current national-register review | — | 2026-08-06 |
Mechanism and pharmacology
KPV is transported into cells via the proton-coupled oligopeptide transporter PepT1 (SLC15A1), which is upregulated on inflamed colonic epithelium. Once internalized, it inhibits NF-κB signaling by preventing IκB degradation and reducing p65 nuclear translocation, thereby suppressing pro-inflammatory cytokines (TNF-α, IL-1β, IL-6, IL-8). Unlike its parent alpha-MSH, KPV does not bind to melanocortin receptors (MC1R-MC5R) and does not cause pigmentation. This receptor-independent mechanism provides tissue selectivity through PepT1 upregulation at inflammation sites.
Evidence by claim
| Claim/indication | Stage | Grade | Best human evidence | Main result | Important limitations |
|---|---|---|---|---|---|
| Inflammatory bowel disease/colitis | Preclinical | D | None (human) | Mouse DSS and TNBS colitis models: reduced inflammation, weight loss, tissue damage | No human trial; animal models only |
| Wound healing | Preclinical | D | None (human) | Rabbit corneal wound model: faster epithelial closure | Animal model only |
| Antimicrobial | Preclinical | D | None | In vitro activity against S. aureus and C. albicans | In vitro only; no in vivo confirmation |
| Anti-inflammatory (general) | Preclinical | D | None | Human cell models: NF-κB inhibition | Cell-based assays; no clinical translation |
Key studies
| Study | Design/population | Exposure studied | Endpoints and result | Limitations |
|---|---|---|---|---|
| Dalmasso et al. 2008 (Gastroenterology) | In vitro and mouse colitis models | Oral KPV via drinking water | Reduced inflammation in DSS and TNBS colitis; PepT1-dependent mechanism identified | Preclinical only |
| Kannengiesser et al. 2008 | Mouse colitis models | KPV in DSS, TNBS, and transfer colitis | Anti-inflammatory effect independent of MC1R signaling | Preclinical; animal models |
| Xiao et al. 2017 | Mouse colitis + nanoparticle delivery | Oral KPV nanoparticles | Reduced colitis severity at doses below standard oral KPV | Preclinical; novel delivery system |
| Bonfiglio et al. 2006 | Rabbit corneal wound | Topical KPV | Improved epithelial wound closure vs controls | Animal model |
Dose and administration evidence
Approved labeled regimen
None.
Studied regimens (not recommendations)
Mouse studies: oral KPV via drinking water at ~mg/kg range. No human dose-finding trial has been conducted.
What is not established
No established or recommended human dose.
Safety
Established label risks
None — no approved label.
Human-study signals
No human exposure data exist for KPV drug products administered by any route. FDA states it "lacks important information regarding any safety issues raised by KPV, including whether it would cause harm if administered to humans."
Unknowns and product-quality risks
Zero human safety data.
Regulatory status remains unresolved: the July 2026 PCAC recommendations were advisory, and neither reviewed form was thereby added to the 503A Bulks List.
Products marketed as research chemicals have no quality assurance.
Theoretical risk of immune modulation in autoimmune conditions is uncharacterized.
Interactions and special populations
No data available. No human studies for any population.
Regulatory, compounding, and sport notes
FDA: Not approved. On July 23, 2026, PCAC separately voted 8-6 with one abstention to recommend KPV free base and KPV acetate for the 503A Bulks List. PCAC recommendations are nonbinding; they are not marketing approval and do not themselves place a substance on the list.
WADA: KPV is not explicitly named in the 2026 List. S0 would prohibit it at all times only if both conditions in S0 are met: KPV is not addressed by a later section of the List and it has no current approval by any governmental regulatory health authority for human therapeutic use.
No FDA-approved product or EMA-authorized medicine was identified as of 2026-08-06; status elsewhere requires a current national-register check.
K(D)PT (a related analog) has one human UC trial; this does not constitute KPV safety or efficacy data.
Evidence gaps
No completed human clinical trial of KPV as a single-ingredient drug.
No pharmacokinetic, dose-finding, or safety study in humans.
Translational relevance of mouse colitis models to human IBD is unconfirmed.
A final FDA regulatory determination following the July 2026 advisory votes was not identified as of 2026-08-06.
All anti-inflammatory claims rely on preclinical data.
Search notes
Databases and registries: PubMed, ClinicalTrials.gov, FDA Federal Register, FDA PCAC materials
Search terms: KPV, Lys-Pro-Val, alpha-MSH 11-13, KPV colitis
Last searched: 2026-08-06
Inclusion emphasis: Human evidence prioritized; clear distinction from K(D)PT analog
Sources
https://pubmed.ncbi.nlm.nih.gov/18061177/ (Dalmasso et al. 2008 — PepT1-mediated KPV uptake, mouse colitis)
https://pubmed.ncbi.nlm.nih.gov/18092346/ (Kannengiesser et al. 2008 — anti-inflammatory in murine IBD models)
https://pmc.ncbi.nlm.nih.gov/articles/PMC2095288/ (Brzoska et al. 2008 — α-MSH related tripeptides review)
https://pubmed.ncbi.nlm.nih.gov/12750433/ (Getting et al. 2003 — KPV anti-inflammatory effect core vs C-terminal)
https://pubmed.ncbi.nlm.nih.gov/28143741/ (Xiao et al. 2017 — oral KPV nanoparticles for UC)
https://pubmed.ncbi.nlm.nih.gov/18612139/ (Brzoska et al. 2008 — α-MSH tripeptides biochemistry review)
https://pmc.ncbi.nlm.nih.gov/articles/PMC3403564/ (Mechanism of KPV action — NF-κB nuclear import inhibition)
FDA. July 23-24, 2026 Pharmacy Compounding Advisory Committee meeting page, agenda, materials, and official webcast links. https://www.fda.gov/advisory-committees/advisory-committee-calendar/july-23-24-2026-meeting-pharmacy-compounding-advisory-committee-07232026 Official July 23 webcast: https://www.youtube.com/watch?v=DhDC0DAYdBI
WADA. 2026 Prohibited List, section S0. https://www.wada-ama.org/sites/default/files/2025-09/2026list_en_final_clean_september_2025.pdf