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KPV

Also called Lys-Pro-Val, Lysyl-prolyl-valine, alpha-MSH(11-13), alpha-MSH 11-13, H-Lys-Pro-Val-OH, KPV acetate.

KPV is a tiny protein piece made of three building blocks. It is the last three letters of a natural hormone called alpha-MSH. In lab dishes and mice it calmed inflammation. No human studies have been found and no regulator has approved it as a medicine.

KPV is not an approved medicine for these uses in most countries. This page explains the science and the law; it does not give dosing, sourcing or usage advice.

How strong is the evidence?

AnecdoteAnimalsHuman trialsApproved
Animals. Tested in animals, not properly in people.The evidence is cell and animal work only. Human intestinal and T-cell lines and mouse colitis models (DSS, TNBS and T-cell transfer colitis) support an anti-inflammatory effect. A mouse peritonitis model and rodent wound models add to this. FDA's 2026 review states that neither the nomination nor its own searches of PubMed, Embase and ClinicalTrials.gov found any study of KPV given to humans by any route. Animal and cell results often do not carry over to people. The oral delivery work in mice is early-stage and used nanoparticle or hydrogel carriers.

Last verified 2026-09-29 · how we verify

3. V · ValineV2. P · ProlineP1. K · LysineKNC

Schematic

  • Positive charge
  • Glycine or proline
  • Water-avoiding

Schematic from the amino-acid sequence — not an experimental structure

3 amino acids, one bead each, coloured by type, N-terminus to C-terminus. The chain shape is illustrative; it is not the real 3D shape of KPV.

Acts on
PepT1 (SLC15A1, di/tripeptide transporter): proposed route into cells, shown in human cell lines and mice, NF-kB and MAP kinase inflammatory signalling: proposed downstream effect, shown in cell studies, Interleukin-1 beta signalling: proposed in a mouse study, Melanocortin receptors: studies indicate they are probably not the main target
Taken as
Not given by any approved route, because it is not approved anywhere. In research it has been studied by adding it to drinking water in mice (colitis models), by systemic injection in mouse inflammation models, in nanoparticle or hydrogel carriers designed for oral delivery to the colon in mice, and, in the laboratory only, across excised human skin. No human route has been studied in a published trial.
Structure
Lys-Pro-Val tripeptide, C16H30N4O4, molecular weight 342.43 g/mol (free acid); the acetate salt is about 402.5 g/mol.[src]
Origin
The C-terminal three residues (11-13) of alpha-melanocyte-stimulating hormone.[src]
US regulatory status
Not a component of any FDA-approved drug and has no USP monograph. In its briefing document dated 12 May 2026 FDA proposed that KPV (free base) and KPV acetate not be added to the 503A bulk drug substances list.[src]
FDA advisory committee vote
On 23 July 2026 the Pharmacy Compounding Advisory Committee voted 8 in favour, 6 against and 1 abstention to recommend adding KPV to the 503A bulks list. The vote is advisory; FDA would still need notice-and-comment rulemaking.[src]

Inside the body

What KPV does, step by step

Watch the 3D journey →
  1. 01Brain

    A piece of a natural hormone

    Your body makes a hormone called alpha-MSH, including in the pituitary, a small gland at the base of the brain. KPV is just its last three building blocks, cut off from the rest.

    For experts

    KPV corresponds to residues 11-13 of alpha-MSH, the 13-residue melanocortin derived from pro-opiomelanocortin, which is produced in the pituitary and other tissues. The C-terminal tripeptide was reported to keep anti-inflammatory activity in mice (Hiltz and Lipton, 1989) while lacking the pigmentary activity of the full hormone (Brzoska 2008). Whether endogenous KPV-length fragments have a physiological role in people is not established.[src][src][src]

  2. 02Gut

    Getting into gut cells through a peptide doorway

    Cells lining the gut have a doorway (a transporter called PepT1) that pulls in tiny protein pieces. In lab tests with human cells, KPV seemed to use this doorway, and the doorway becomes more common when the gut is inflamed.

    For experts

    Dalmasso et al. reported that KPV is taken up by PepT1 in human Caco2-BBE and HT29-Cl.19A epithelial cells and Jurkat T cells, in uptake and competition assays; the reported Km in Caco2-BBE cells was about 160 uM, which the authors describe as high affinity for this transporter. PepT1 is expressed in the small intestine and induced in the colon in inflammatory bowel disease. These are cell-culture and mouse findings; PepT1 uptake of KPV has not been demonstrated in people.[src]

  3. 03Immune system

    Turning down inflammation signals inside the cell

    Once inside, KPV lowered the switches cells use to sound the inflammation alarm. In these dish experiments the cells then released fewer alarm chemicals.

    For experts

    In human cell lines stimulated with pro-inflammatory cytokines, nanomolar KPV inhibited activation of NF-kB and MAP-kinase pathways and reduced pro-inflammatory cytokine secretion (Dalmasso 2008). Earlier mouse work suggested KPV acts by inhibiting IL-1 beta functions (Getting 2003). The direct molecular target is unknown, as FDA's 2026 review also notes.[src][src][src]

  4. 04Immune system

    Probably not through the usual hormone receptors

    The full alpha-MSH hormone works by docking onto special receptors. KPV did not seem to need them. It still calmed inflammation in mice whose receptor did not work, so scientists think it acts a different way.

    For experts

    KPV did not raise cAMP or inhibit cytokine release in macrophages, and its anti-migratory effect in mouse peritonitis was not blocked by an MC3/4 receptor antagonist. It remained active in MC1R-deficient (recessive yellow, e/e) mice, in peritonitis and in DSS colitis (Getting 2003; Kannengiesser 2008). This is why KPV is generally not classed with melanocortin receptor agonists such as bremelanotide, although the authors of the colitis study describe the independence from MC1R as at least partial.[src][src][src]

  5. 05Gut

    Less gut inflammation in mice, not yet tested in people

    In mice with chemically triggered bowel inflammation, KPV given by mouth or in special carriers reduced the damage. Nobody has published a test of KPV in people with bowel disease.

    For experts

    KPV added to drinking water reduced the incidence of DSS- and TNBS-induced colitis in mice, with lower pro-inflammatory cytokine mRNA (Dalmasso 2008). KPV also aided recovery in DSS and CD45RBhi transfer colitis (Kannengiesser 2008). It prevented tumour formation in a wild-type mouse model of colitis-associated cancer, but not in PepT1-knockout mice (Viennois 2016). Carrier-based oral delivery has been tested in mice (Xiao 2017). All findings are animal-only.[src][src][src][src]

  6. 06Skin

    Skin and wound healing: rodent and lab-only evidence

    KPV has also been studied for skin healing, but only in animals and in lab tests on donated human skin. In those tests, plain KPV barely got through the skin's outer layer.

    For experts

    Rodent wound-healing models have been reported, and Bohm and Luger (2019) proposed that KPV and KdPT are candidates for clinical study in cutaneous wounds and ulcers. FDA found no human data for the nominated topical uses (wound healing and inflammatory conditions such as psoriasis and eczema). In excised human skin, passive permeation was below the assay limit (0.01 ug/mL), and measurable delivery required microneedle pretreatment, iontophoresis (a small electric current) or both (Pawar 2017).[src][src][src]

For experts

The detail

KPV (Lys-Pro-Val, C16H30N4O4, 342.43 g/mol) is the C-terminal tripeptide of alpha-melanocyte-stimulating hormone (residues 11-13). It is a linear, unmodified, unconjugated tripeptide with no engineered stabilising features; native alpha-MSH is C-terminally amidated, whereas the form FDA and PubChem describe is the free acid, and the acetate salt, N-acetylated KPV, the KdPT analogue and the (CKPV)2 dimer are different substances that the literature sometimes conflates. An early report of anti-inflammatory activity for the alpha-MSH(11-13) fragment came from a mouse ear-swelling model (Hiltz and Lipton, 1989). It does not appear to work through the melanocortin receptors that mediate alpha-MSH's pigmentary and many of its anti-inflammatory effects: it did not raise cAMP in macrophages and it acted in mice with a non-functional MC1R (Getting 2003; Kannengiesser 2008). Proposed mechanisms are uptake by the transporter PepT1 followed by inhibition of NF-kB and MAP-kinase signalling (human Caco2-BBE, HT29-Cl.19A and Jurkat cells) and interference with IL-1 beta effects; the molecular target remains unidentified. In mice, KPV reduced DSS- and TNBS-induced colitis and CD45RBhi transfer colitis, and rodent wound-healing models have been reported. FDA identified no pharmacokinetic study in any species, so there is no half-life. In vitro, KPV did not cross human skin by passive diffusion at detectable levels (Pawar 2017). KPV is not a component of any approved drug, and it has no USAN, USP monograph or UNII. FDA found no study of KPV given to humans, and its search of FAERS and the medical literature for adverse events through 3 December 2025 found no reports. FDA's briefing document (12 May 2026), prepared for the 23-24 July 2026 Pharmacy Compounding Advisory Committee, judged KPV not well characterised and proposed against adding it to the 503A bulks list. The committee voted 8-6 with one abstention to recommend adding it; the vote is advisory only and needs notice-and-comment rulemaking.

Evidence: The evidence is cell and animal work only. Human intestinal and T-cell lines and mouse colitis models (DSS, TNBS and T-cell transfer colitis) support an anti-inflammatory effect. A mouse peritonitis model and rodent wound models add to this. FDA's 2026 review states that neither the nomination nor its own searches of PubMed, Embase and ClinicalTrials.gov found any study of KPV given to humans by any route. Animal and cell results often do not carry over to people. The oral delivery work in mice is early-stage and used nanoparticle or hydrogel carriers.[src][src][src][src]

Known safety signals

  • No human safety data exist. FDA states that it did not find clinical studies or human exposure data for KPV, so its safety risks in people are unknown.[src]
  • FDA searched its adverse event database (FAERS) through 3 December 2025 and found no reports for KPV. FDA notes that this cannot show safety: reporting is voluntary and compounded or unregulated products are rarely reported.[src]
  • FDA did not identify acute-toxicity, repeat-dose toxicity, genotoxicity, reproductive or carcinogenicity studies of KPV, and no pharmacokinetic studies.[src]
  • FDA flagged unassessed risks of peptide immunogenicity (anti-drug antibody formation) and aggregation for KPV, and found the substance not well characterised: it is sold under one common name in different salt and derivative forms, and public certificates of analysis lack impurity, aggregate and microbiological testing.[src]
  • Health Canada listed KPV among unauthorized injectable peptides it had seized and warned that such products can carry contamination, infection and allergic-reaction risks, and that 'research use only' labelling does not make them legal.[src]
  • FDA's list of compounding substances that may present significant safety risks now places KPV under 'nominated but withdrawn' (page content current as of 22 April 2026). The entry says FDA has not identified any human exposure data for KPV by any route and lacks important information on whether it would cause harm in people. Moving off Category 2 is not the same as being added to the 503A bulks list.[src]

Around the world

Is KPV legal where you live?

CountryStatusWhat it meansVerified
AustraliaNot approvedNo KPV product is on the ARTG. It counts as an unapproved peptide, and advertising or supplying it is likely unlawful.Details →source2026-09-29
BrazilNot approvedNo Brazilian registration for KPV; the same unregistered-peptide rules applyDetails →source2026-09-29
CanadaProhibitedNot authorised; named in Health Canada's April 2026 advisory of seized unauthorised injectablesDetails →source2026-09-29
ChinaNot approvedNo NMPA approval found for KPV; it cannot lawfully be sold as a medicine in China.Details →source2026-09-29
European UnionNot approvedNo EU marketing authorisation; not listed in EMA or Union Register dataDetails →source2026-09-29
IndiaNot approvedNot approved in India: no CDSCO marketing permission found for KPV; making or selling it as a medicine would be unapprovedDetails →source2026-09-29
JapanNot approvedNot an approved medicine in Japan; KPV is absent from PMDA's approved-drug lists and package-insert databaseDetails →source2026-09-29
MexicoNot approvedNo registration for KPV found in COFEPRIS listsDetails →source2026-09-29
New ZealandNot approvedNo Medsafe-approved medicine contains KPV; unapproved peptide products are unlawful to supplyDetails →source2026-09-29
United Arab EmiratesNot approvedNot approved in the UAE: no marketing authorisation for KPV; unapproved peptide products are under EDE enforcementDetails →source2026-09-29
United KingdomNot approvedKPV is not licensed in the UKDetails →source2026-09-29
United StatesNot approvedNo FDA approval; FDA found no human exposure data for KPV, and an advisory panel recommended considering it in July 2026 (non-binding)Details →source2026-09-29

Recent history

  1. 2026-07-23

    FDA advisory committee votes on seven peptides for the 503A compounding list, against FDA staff advice

  2. 2026-04-15

    FDA removes 12 peptides from the 'Category 2' safety-risk list

Full timeline →

Related molecules

Melanotan IIBremelanotide (PT-141)SetmelanotideBPC-157TB-500 (thymosin beta-4 fragment)GHK-Cu (copper peptide)

Sources (54)

  1. 01PepT1-mediated tripeptide KPV uptake reduces intestinal inflammationGastroenterology (Dalmasso G et al.) · 2008-01 · accessed 2026-09-29
  2. 02Melanocortin-derived tripeptide KPV has anti-inflammatory potential in murine models of inflammatory bowel diseaseInflammatory Bowel Diseases (Kannengiesser K et al.) · 2008-03 · accessed 2026-09-29
  3. 03Dissection of the anti-inflammatory effect of the core and C-terminal (KPV) alpha-melanocyte-stimulating hormone peptidesJournal of Pharmacology and Experimental Therapeutics (Getting SJ et al.) · 2003-08 · accessed 2026-09-29
  4. 04FDA Briefing Document: Evaluation of KPV-related Bulk Drug Substances (KPV (free base) and KPV acetate) for Inclusion on the 503A Bulk Drug Substances ListU.S. Food and Drug Administration (Pharmacy Compounding Advisory Committee) · 2026-05-12 · accessed 2026-09-29
  5. 05Antiinflammatory activity of a COOH-terminal fragment of the neuropeptide alpha-MSHFASEB Journal (Hiltz ME, Lipton JM) · 1989-09 · accessed 2026-09-29
  6. 06Alpha-melanocyte-stimulating hormone and related tripeptides: biochemistry, antiinflammatory and protective effects in vitro and in vivo, and future perspectives for the treatment of immune-mediated inflammatory diseasesEndocrine Reviews (Brzoska T et al.) · 2008-08 · accessed 2026-09-29
  7. 07Critical role of PepT1 in promoting colitis-associated cancer and therapeutic benefits of the anti-inflammatory PepT1-mediated tripeptide KPV in a murine modelCellular and Molecular Gastroenterology and Hepatology (Viennois E et al.) · 2016-05 · accessed 2026-09-29
  8. 08Orally Targeted Delivery of Tripeptide KPV via Hyaluronic Acid-Functionalized Nanoparticles Efficiently Alleviates Ulcerative ColitisMolecular Therapy (Xiao B et al.) · 2017-07-05 · accessed 2026-09-29
  9. 09Are melanocortin peptides future therapeutics for cutaneous wound healing?Experimental Dermatology (Böhm M, Luger TA) · 2019-03 · accessed 2026-09-29
  10. 10Transdermal Iontophoretic Delivery of Lysine-Proline-Valine (KPV) Peptide Across Microporated Human SkinJournal of Pharmaceutical Sciences (Pawar K et al.) · 2017-07 · accessed 2026-09-29
  11. 11Msh (11-13) / Lys-Pro-Val (L-lysyl-L-prolyl-L-valine), PubChem CID 125672National Center for Biotechnology Information (PubChem) · 2005-08-08 · accessed 2026-09-29
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