KPV is a three-amino-acid peptide made of lysine, proline and valine (Lys-Pro-Val). It is the last three amino acids of alpha-melanocyte-stimulating hormone (α-MSH), a hormone cut from the precursor protein proopiomelanocortin that has both pigment-inducing and anti-inflammatory effects. Researchers studied KPV because it seemed to keep much of α-MSH’s anti-inflammatory activity without the pigment effect. Today it is sold online and by some clinics for gut inflammation, skin conditions and “recovery.”

The single most important fact: no study of KPV in humans has ever been published. In its 2026 review, FDA found no clinical trials, no human pharmacokinetic data, no case reports and no adverse event reports. It also found no animal toxicity studies of any kind. Everything known about KPV’s effects comes from cell culture and from mouse, rat and rabbit experiments (FDA briefing document, 2026).

This page summarizes what FDA’s review and the laboratory and animal studies report. It is for education only and is not medical advice.

Property	Detail
Class	Synthetic tripeptide; the C-terminal fragment (positions 11–13) of α-MSH; investigational
Other names	Lys-Pro-Val; α-MSH(11–13); sold as KPV free base or KPV acetate
Formula	C₁₆H₃₀N₄O₄, 342.43 g/mol (free base); acetate salt 402.5 g/mol
Approval	Not part of any FDA-approved drug; no product authorized by the European Medicines Agency
Human studies	None; FDA’s 2026 search, including ClinicalTrials.gov, found no human data
Half-life	Unknown; FDA found no pharmacokinetic studies in humans or animals
Mechanism	Not fully known; does not appear to act through melanocortin receptors; in cells it blocks NF-κB inflammatory signaling and enters gut cells through the PepT1 transporter
US compounding status	Not on the 503A bulks list. FDA staff recommended against adding it; an advisory committee voted 8–6 (1 abstention) in favor in July 2026; FDA is not bound by the vote
WADA	Not named on the 2026 list; the S0 class bans any pharmacological substance without government approval for human use

What it is

KPV’s chemical name is (2S)-2-[[(2S)-1-[(2S)-2,6-diaminohexanoyl]pyrrolidine-2-carbonyl]amino]-3-methylbutanoic acid, CAS number 67727-97-3 (PubChem). It is a short linear peptide made by solid-phase peptide synthesis, the standard method for making peptides by adding one amino acid at a time (FDA briefing document, 2026).

α-MSH is a 13-amino-acid hormone, and KPV is its last three amino acids. By the late 1980s, the fever-lowering activity of α-MSH was thought to reside mainly in this fragment. In 1989 a Dallas group showed that it reduced chemically induced ear swelling in mice in a dose-related way (Hiltz and Lipton, FASEB J 1989). A 2008 review by German dermatology researchers described KPV as an anti-inflammatory alternative to α-MSH that lacks α-MSH’s pigment-inducing effect (Brzoska et al., Endocr Rev 2008). No drug program has taken it into human trials.

Two forms are sold, and FDA treats them as different substances:

Form	Formula / weight	Note
KPV (free base)	C₁₆H₃₀N₄O₄ / 342.43 g/mol	The peptide itself
KPV acetate	C₁₆H₃₀N₄O₄·CH₃COOH / 402.5 g/mol	Acetate salt; same active peptide. Public sources usually give it the same CAS number as the free base

Other α-MSH-related peptides in this library include Melanotan I (afamelanotide), Melanotan II and PT-141 (bremelanotide). Unlike KPV, these are longer peptides with their own pages.

How it is thought to work

KPV’s molecular target is unknown (FDA briefing document, 2026). Several lines of laboratory evidence suggest that it does not act like α-MSH:

No melanocortin receptor activity in most tests. In cell and tissue studies, KPV did not displace α-MSH from its binding sites and did not raise cyclic AMP, the signal that melanocortin receptors normally trigger (as summarized by FDA).
Effects persist without the receptors. In mice, KPV reduced white blood cell influx in two peritonitis models (inflammation of the abdominal lining). A drug that blocks MC3 and MC4 receptors did not stop the effect, and it also occurred in mice with a non-working MC1 receptor. Unlike α-MSH, KPV did not reduce cytokine release from activated macrophages in the dish. The authors concluded that KPV more likely works by interfering with interleukin-1β (IL-1β), an inflammatory signal (Getting et al., J Pharmacol Exp Ther 2003).
NF-κB blockade inside cells. NF-κB is a protein switch that turns on many inflammatory genes. In human airway cells grown in the lab, KPV entered the cell nucleus and blocked NF-κB from moving into the nucleus, which lowered release of the inflammatory signals IL-8 and eotaxin (Land, Int J Physiol Pathophysiol Pharmacol 2012).
Uptake by PepT1. PepT1 is a transporter that carries small peptides from food into intestinal cells. It is normally found in the small intestine, and inflamed colon tissue makes more of it. In human intestinal and T-cell lines, nanomolar KPV concentrations blocked NF-κB and MAP kinase signaling, and this effect depended on PepT1 uptake (Dalmasso et al., Gastroenterology 2008).

One study in human skin cells reported that KPV raised calcium inside cells, including cells engineered to express the MC1 receptor (Elliott et al., J Invest Dermatol 2004). How these findings fit together has not been worked out.

Pharmacokinetics

No pharmacokinetic data exist. FDA found no study measuring KPV’s absorption, distribution, breakdown or half-life in people, and none in animals (FDA briefing document, 2026). Any half-life quoted for KPV online is not backed by a published measurement.

The few relevant laboratory findings:

Finding	Detail	Source
Skin penetration (donated human skin, in the lab)	Passive permeation was below the limit of detection (0.01 µg/mL)	Pawar et al., J Pharm Sci 2017
With microneedles	Permeation rose to 4.4 µg/cm²/h	Pawar et al. 2017
Iontophoresis (a small electric current) plus microneedles	35-fold higher permeation than microneedles alone	Pawar et al. 2017
Intestinal uptake (cell lines)	Taken up by the PepT1 transporter	Dalmasso et al., Gastroenterology 2008
Chemical breakdown	Under acid, alkaline and oxidizing stress, KPV acetate breaks down mainly to a lysine–proline ring compound (a diketopiperazine); with hydrogen peroxide it also releases proline and valine	FDA briefing document, 2026

FDA noted two sides to the skin finding. Poor penetration through intact skin may limit whole-body exposure from a cream. It may also mean that a cream delivers little KPV to the deeper skin layers where it would need to act.

Regulatory status

KPV is not an approved drug. FDA found that it is not a component of any FDA-approved product. It has no monograph in the US, European or Japanese pharmacopeias, and the European Medicines Agency lists no authorized product containing it (FDA briefing document, 2026).

FDA compounding review (2026)

US pharmacies can compound a drug from a bulk substance that has no monograph and is not in an approved drug only if the substance is on the “503A bulks list.” The key steps for KPV were:

Withdrawn nomination. A compounding pharmacy nominated KPV as a 0.1% topical cream or gel for wound healing and inflammatory skin conditions such as psoriasis and eczema. The nomination was later withdrawn. FDA’s page of substances that may present significant safety risks lists KPV among the withdrawn nominations. It states that FDA “has not identified any human exposure data” on KPV by any route (FDA, updated April 22, 2026).
FDA’s own evaluation. FDA then evaluated KPV free base and KPV acetate on its own initiative. Its staff concluded that neither form is well characterized, that there is no evidence of effectiveness in humans, and that safety in humans is unknown. Staff recommended not adding either form to the list (FDA briefing document, 2026).
Advisory committee vote. The Pharmacy Compounding Advisory Committee discussed KPV on July 23, 2026, together with BPC-157, TB-500 and MOTS-c (Federal Register notice, 2026). Trade press reported that the committee voted 8–6, with one abstention, in favor of allowing KPV to be compounded. The vote is advisory: FDA is not bound by it, and any change requires formal rulemaking (Pharmaceutical Executive, July 2026).

FDA also found that the nomination was inconsistent about which form it meant. Its certificate of analysis named one form in its title and gave the other form’s molecular formula. FDA said that such naming confusion is a patient safety risk, because a patient may receive a different substance than the one prescribed (FDA briefing document, 2026).

Related pages: BPC-157, TB-500 and MOTS-c went through the same 2026 review.

What the research shows

All of the evidence below comes from cell culture or animals. None of it shows that KPV works in people. FDA’s search found no human data for either proposed use, wound healing or inflammatory conditions (FDA briefing document, 2026).

Colitis (mouse models of inflammatory bowel disease)

Colitis models are the most studied area. Researchers trigger colon inflammation in mice with chemicals (DSS or TNBS) or by transferring certain immune cells.

Study	Model	How KPV was given	Main finding
Dalmasso et al., Gastroenterology 2008	DSS and TNBS colitis in mice	In drinking water	Less colitis and lower inflammatory cytokine levels
Kannengiesser et al., Inflamm Bowel Dis 2008	DSS colitis and T-cell transfer colitis in mice	Not stated in abstract	Faster weight regain and less inflammation under the microscope. In mice without a working MC1 receptor, all KPV-treated animals survived DSS colitis
Viennois et al., Cell Mol Gastroenterol Hepatol 2016	Colitis-associated colon cancer in mice	Not stated in abstract	Prevented tumor formation in normal mice but not in mice lacking PepT1
Xiao et al., Mol Ther 2017	Ulcerative colitis model in mice	Oral, packed in colon-targeted nanoparticles	Hyaluronic-acid-coated nanoparticles protected the colon lining and lowered TNF-α more than uncoated KPV nanoparticles

Several later studies have used KPV as a building block in experimental drug-delivery systems for colitis, such as hydrogels and nanoparticles. These test delivery technology in animals. They do not provide human evidence for KPV itself.

Skin, eye and wound healing

Skin inflammation (mice). KPV reduced ear swelling caused by a skin irritant in a dose-related way (Hiltz and Lipton, FASEB J 1989).
Corneal wounds (rabbits). After the surface layer of the cornea was scraped off, KPV eye drops (1–10 mg/mL, four times a day for 4 days) sped healing. At 60 hours, 8 of 8 KPV-treated corneas had fully healed compared with none of the controls. A drug that blocks nitric oxide production reduced the effect (Bonfiglio et al., Exp Eye Res 2006).
Proposed for human wounds, untested. Researchers who study melanocortin peptides have proposed KPV-type peptides as future candidates for skin wounds and ulcers. They outline the studies still needed and do not report human results (Böhm and Luger, Exp Dermatol 2019).

Antimicrobial activity (lab only)

In the dish, α-MSH and KPV reduced growth of Staphylococcus aureus and the yeast Candida albicans. They did not reduce the ability of human white blood cells to kill these microbes (Cutuli et al., J Leukoc Biol 2000). No animal infection or human data support an antimicrobial use.

Muscle, performance and “recovery”

No study has tested KPV for muscle growth, strength, body composition, injury recovery or athletic performance in people or animals. A 2026 review of peptide use in sport lists KPV among peptides promoted for anti-inflammatory effects. It notes that clinical evidence for such peptides in sport is limited (Coutinho et al., J Sports Med Phys Fitness 2026).

Side effects and risks

Unknown safety in humans

Because KPV has never been formally given to people, its side effects in humans are unknown. FDA searched its adverse event database (FAERS) and the medical literature through December 3, 2025 and found no reports. It also searched its food and supplement complaint system from 2004 to December 2025 and found no cases. The absence of reports does not show that KPV is safe. It reflects the absence of any studied or tracked human use. FDA also notes that compounders generally do not report adverse events (FDA briefing document, 2026).

No toxicity testing

FDA found no studies of KPV free base or acetate for any of the standard safety tests:

acute (single-dose) toxicity;
repeat-dose toxicity;
genotoxicity (damage to DNA);
effects on fertility, pregnancy or development;
cancer risk.

FDA also found no animal pharmacokinetic or toxicokinetic data (FDA briefing document, 2026).

Immunogenicity and aggregation

Immunogenicity means the chance that the body makes antibodies against a drug. FDA notes that peptides, like protein drugs, can trigger immune responses. These range from harmless antibodies to severe reactions, and can include antibodies that neutralize the drug. Peptides as short as two amino acids can aggregate, meaning that molecules clump together, and aggregation raises immunogenicity risk. FDA found no data on whether KPV aggregates or triggers antibodies, and said there is insufficient information to conclude that it does not (FDA briefing document, 2026).

Quality and identity of products

FDA’s review raised several product-quality problems:

Name confusion. “KPV” is a common name, not an official drug name. Different salts and derivatives, including different active molecules, are sold under the same name.
Missing quality tests. Certificates of analysis FDA found for the free base usually reported only a purity figure. They gave no impurity limits, no aggregate testing and no microbial testing.
Gaps even in the best example. The acetate certificate from the nomination reported total impurities of 0.9% (limit ≤2.0%), but did not identify them. It included no aggregate or microbial testing, which FDA noted is required for topical products.

FDA also noted that KPV is promoted online in injectable, oral, nasal spray and topical forms. It is promoted alone and in combination with other unapproved peptides such as BPC-157, TB-500 and AOD-9604 (FDA briefing document, 2026). None of these routes or combinations has been studied in humans.

Use in sport

KPV is not named on the WADA list. The S0 class prohibits at all times any pharmacological substance with no current approval by any government health authority for human therapeutic use (WADA 2026 Prohibited List). KPV has no approval from FDA or the European Medicines Agency, so it appears to fall under this catch-all class.

Key takeaways

A three-amino-acid fragment of α-MSH. KPV (Lys-Pro-Val) is the end of the α-MSH hormone. In laboratory studies it seems to keep anti-inflammatory activity without causing pigmentation, and it does not appear to work through melanocortin receptors.
Animal and cell data only. Mouse colitis models, a rabbit corneal wound study and mouse skin-inflammation models showed benefits. No human study has been published.
Nothing is known about its kinetics or toxicity. FDA found no pharmacokinetic studies and no standard toxicity studies in any species. Its half-life in the body has never been measured.
FDA staff recommended against compounding it. In 2026 FDA staff cited poor characterization, no evidence of effectiveness and unknown safety. An advisory committee nevertheless voted 8–6 in favor. The vote is not binding, and KPV remains off the 503A bulks list unless FDA completes rulemaking.
Product identity is uncertain. “KPV” is not an official name, free base and acetate are sold interchangeably, and typical certificates of analysis lack impurity, aggregate and microbial testing.
Likely banned in sport. As an unapproved substance, it appears to fall under WADA’s S0 class, which is prohibited at all times.

Sources

Food and Drug Administration. FDA briefing document: Evaluation of KPV-related bulk drug substances (KPV (free base) and KPV acetate) for inclusion on the 503A bulk drug substances list. Pharmacy Compounding Advisory Committee meeting, July 23–24, 2026 (memo dated May 12, 2026). FDA.
Food and Drug Administration. Certain bulk drug substances for use in compounding that may present significant safety risks. Content current as of April 22, 2026. FDA.
Food and Drug Administration. Pharmacy Compounding Advisory Committee; notice of meeting; establishment of a public docket; request for comments—bulk drug substances nominated for inclusion on the section 503A bulk drug substances list. Federal Register. April 16, 2026;91:20465 (FR Doc 2026-07361). Federal Register.
Jacobus N. FDA panel votes to loosen restrictions for four peptides. Pharmaceutical Executive. July 24, 2026. PharmExec.
National Center for Biotechnology Information. PubChem compound summary for CID 125672, Msh (11-13). PubChem.
Hiltz ME, Lipton JM. Antiinflammatory activity of a COOH-terminal fragment of the neuropeptide alpha-MSH. FASEB J. 1989;3(11):2282–2284. PubMed.
Brzoska T, Luger TA, Maaser C, et al. Alpha-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 diseases. Endocr Rev. 2008;29(5):581–602. PubMed.
Getting SJ, Schiöth HB, Perretti M. Dissection of the anti-inflammatory effect of the core and C-terminal (KPV) alpha-melanocyte-stimulating hormone peptides. J Pharmacol Exp Ther. 2003;306(2):631–637. PubMed.
Land SC. Inhibition of cellular and systemic inflammation cues in human bronchial epithelial cells by melanocortin-related peptides: mechanism of KPV action and a role for MC3R agonists. Int J Physiol Pathophysiol Pharmacol. 2012;4(2):59–73. PubMed.
Elliott RJ, Szabo M, Wagner MJ, et al. alpha-Melanocyte-stimulating hormone, MSH 11-13 KPV and adrenocorticotropic hormone signalling in human keratinocyte cells. J Invest Dermatol. 2004;122(4):1010–1019. PubMed.
Dalmasso G, Charrier-Hisamuddin L, Nguyen HT, et al. PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation. Gastroenterology. 2008;134(1):166–178. PubMed.
Kannengiesser K, Maaser C, Heidemann J, et al. Melanocortin-derived tripeptide KPV has anti-inflammatory potential in murine models of inflammatory bowel disease. Inflamm Bowel Dis. 2008;14(3):324–331. PubMed.
Viennois E, Ingersoll SA, Ayyadurai S, et al. Critical role of PepT1 in promoting colitis-associated cancer and therapeutic benefits of the anti-inflammatory PepT1-mediated tripeptide KPV in a murine model. Cell Mol Gastroenterol Hepatol. 2016;2(3):340–357. PubMed.
Xiao B, Xu Z, Viennois E, et al. Orally targeted delivery of tripeptide KPV via hyaluronic acid-functionalized nanoparticles efficiently alleviates ulcerative colitis. Mol Ther. 2017;25(7):1628–1640. PubMed.
Pawar K, Kolli CS, Rangari VK, et al. Transdermal iontophoretic delivery of lysine-proline-valine (KPV) peptide across microporated human skin. J Pharm Sci. 2017;106(7):1814–1820. PubMed.
Bonfiglio V, Camillieri G, Avitabile T, et al. Effects of the COOH-terminal tripeptide alpha-MSH(11-13) on corneal epithelial wound healing: role of nitric oxide. Exp Eye Res. 2006;83(6):1366–1372. PubMed.
Böhm M, Luger T. Are melanocortin peptides future therapeutics for cutaneous wound healing? Exp Dermatol. 2019;28(3):219–224. PubMed.
Cutuli M, Cristiani S, Lipton JM, et al. Antimicrobial effects of alpha-MSH peptides. J Leukoc Biol. 2000;67(2):233–239. PubMed.
Coutinho LFD, de Oliveira Neves LF, Camilo RP. A new era of doping? Use of peptide and peptide-analog drugs in recreational and professional sport and bodybuilding: a critical review. J Sports Med Phys Fitness. 2026;66(7):880–885. PubMed.
World Anti-Doping Agency. The 2026 Prohibited List. In effect January 1, 2026. WADA.

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