KPV

KPV in brief

KPV is the linear tripeptide Lys-Pro-Val (C16H30N4O4, average mass 342.43), residues 11 to 13 of alpha-melanocyte-stimulating hormone, with no modification and none of the His-Phe-Arg-Trp sequence that melanocortin receptors recognise. Its best-supported molecular property is transport: it is a substrate of the oligopeptide transporter PepT1, and in a mouse genetic test the measured effect disappeared when PepT1 was deleted. The evidence base is mostly cell lines, chemically induced rodent models and delivery chemistry in which KPV is the cargo. Whether it engages any melanocortin receptor is contested, and no binding constant has been measured. No experimental 3D structure exists, no medicines regulator has approved it, and the FDA states it has identified no human exposure data for the substance by any route.^{[1,2,3,4,5,6,7]}

KPV regulatory status

No marketing authorisation for KPV was found in Drugs@FDA (queried through openFDA), the EMA medicines database or the Health Canada Drug Product Database, and ClinicalTrials.gov returned no registered study with KPV as an intervention (all searched November 2026). KPV is not named on the 2026 WADA Prohibited List, whose class S0 prohibits at all times any pharmacological substance not addressed elsewhere on the List and with no current approval for human therapeutic use. The FDA's compounding safety-risk page lists KPV among bulk substances previously in category 2 whose nominations were withdrawn by the nominators, stating that the agency has not identified any human exposure data for KPV by any route and lacks important information on whether it would cause harm in humans (page current as of 22 April 2026).^{[8,9,10,11,12,7]}

KPV at a glance

• A three-residue peptide, Lys-Pro-Val, formula C16H30N4O4 and average mass 342.43. All three residues are L and the chain is linear, with no disulfide, no lipid, no sugar and no metal.^[1]
• It is the C-terminal three residues of alpha-melanocyte-stimulating hormone, which pro-opiomelanocortin encodes at residues 138 to 150. The same stretch is positions 11 to 13 of corticotropin, which is why one molecule carries both names.^[2,1]
• It carries none of the His-Phe-Arg-Trp message sequence that melanocortin receptors recognise, and the receptor-pharmacology work read here reports effects that survive a melanocortin MC3/MC4 antagonist and a non-functional MC1 receptor.^[5,13,6]
• The best-supported molecular claim about it is a transport claim rather than a receptor claim: it is a substrate of the oligopeptide transporter PepT1, and in a mouse genetic test the measured effect disappeared when PepT1 was deleted.^[3,4]
• It is not stable in plain aqueous solution: in the one study that tested the point directly, KPV in solution lost measurable activity within two hours at 37 degrees Celsius while the same material held in a hydrogel did not. That is why much of the recent corpus is delivery chemistry rather than work on the free peptide.^[14]

What is KPV?

KPV is what remains of a hormone when all but its last three residues are removed. Alpha-melanocyte-stimulating hormone is a thirteen-residue peptide, Ser-Tyr-Ser-Met-Glu-His-Phe-Arg-Trp-Gly-Lys-Pro-Val, cut out of pro-opiomelanocortin at residues 138 to 150 and released with its first serine acetylated and its last valine amidated. Positions 11, 12 and 13 of that sequence are Lys-Pro-Val. Corticotropin begins with the same thirteen residues, so Lys-Pro-Val is positions 11 to 13 of that hormone as well, and the literature calls the tripeptide alpha-MSH (11-13) and ACTH (11-13) interchangeably, and both mean this molecule.^[2,1]

It entered the literature in 1989, when Hiltz and Lipton reported that graded amounts of alpha-MSH (11-13) changed picryl-chloride-induced ear swelling in mice in a dose-related way, following earlier work that had located the antipyretic message of the hormone in the same three residues. The interest in the fragment from that point on was chemical: the full hormone darkens pigment, a three-residue piece that has lost the receptor-binding tetrapeptide cannot, and the reviews that followed describe KPV as a fragment studied for what remains once the pharmacophore is removed.^[15,6,16]

What the primary studies measure is inflammatory readouts, and saying so plainly places the compound better than its chemistry does. Across the works read here the endpoints are leukocyte accumulation in the mouse peritoneal cavity, NF-kappaB reporter activity and cytokine release in human intestinal, bronchial and T-cell lines, and tissue damage, cytokine and tumour counts in chemically induced rodent colitis and colitis-associated cancer models. A smaller set of papers measured microbial growth, and a larger recent set measured a gel or a particle carrying KPV rather than the peptide itself. Every one of those is a measurement in a named cell line or animal model, and none of them is a finding about a person.^{[5,3,13,4,17,14]}

As a class it is a short linear peptide of three proteinogenic residues with both termini free, which is a different kind of object from the hormone it comes from. It is small enough to be a substrate for the intestinal di- and tripeptide transporter PepT1, which is the property most of the recent work turns on. It is also unstable enough in plain solution that several groups have built gels and films to hold it and have measured the difference, so the material and its behaviour in a vial are not the same question as its sequence.^{[3,14,18,19,1]}

The names it is confused with matter more than usual here, because the three letters are a sequence rather than a code. PubChem resolves the bare string KPV to 2-oxo-5-phenylpentanoic acid, an unrelated molecule with no amino acids in it, so a lookup that trusts the abbreviation returns the wrong formula. KdPT, KP-D-V, GKPV and the disulfide-linked dimer [Ac-CKPV]2 are separate molecules appearing in the same papers, and the structured list above keeps them apart.^{[20,1,21,22,23,16]}

KPV structure and sequence

There is very little chain to describe. Lysine contributes a four-carbon side chain ending in a primary amine; proline contributes a pyrrolidine ring whose nitrogen is part of the backbone; valine contributes an isopropyl side chain and the free C-terminal carboxylate. Three chiral centres, one per residue, all (S) in the record's isomeric SMILES. The interesting feature is the middle residue: because proline's nitrogen is tied into a ring, the peptide bond preceding it has no amide hydrogen to donate and the backbone torsions around it are restricted, so a Lys-Pro-Val chain is conformationally poorer than three free residues would be. Near neutral pH there are charged groups at both ends and on the lysine side chain, a net charge near +1, and a single hydrophobic patch at the valine.^[1]

The view on this page is a calculated conformer from the PubChem record for CID 125672, and the status line says so. No experiment placed those atoms. A three-residue peptide with two free termini and a proline hinge is a flexible object in water, so it should be read as a connectivity diagram drawn in three dimensions rather than as a determined shape: it shows the connectivity, the stereochemistry and the relative bulk of the three side chains, and nothing about which conformation the molecule adopts in solution, at a transporter, or at any protein surface.^[1]

Nothing better is available. A Protein Data Bank motif search for KPV restricted to short polymer entities returns one hit, Ac-YKPVD-CHO in entry 7RNE, a synthetic pentapeptide aldehyde that contains the three letters and is not this compound. The nearest real structural work in the family is a proton NMR study of the designed dimer [Ac-CKPV]2, reporting an extended backbone with a beta-turn-like feature; that molecule has an acetyl cap, a cysteine at each N-terminus and a disulfide joining two chains, so its geometry is not transferable here.^[24,22]

Three chiral centres, one per residue, all L in the canonical molecule: the record's isomeric SMILES fixes lysine, proline and valine each as (S). The chain is linear and uncyclised. There is no cysteine and therefore no disulfide, no lipidation, no PEG, no glycosylation, no linker, no metal coordination and no non-proteinogenic residue. Charge is simple enough to count by hand: the lysine side-chain amine and the free N-terminal amine are protonated near neutral pH and the valine carboxylate is deprotonated, giving a net charge near +1. Proline in the middle position removes the only backbone amide hydrogen the three-residue chain would otherwise have there and restricts the backbone angles around it, which is the usual reason a proline-containing tripeptide has fewer accessible conformations than its residue count suggests.^[1]

What studies on KPV show

Each card names the experimental system and what was measured. A result in one system is not evidence about another.

Why KPV is studied as a transported peptide rather than as a receptor ligand

The sequence argument comes first and it is arithmetic on the hormone. Melanocortin receptors read the His-Phe-Arg-Trp tetrapeptide at positions 6 to 9 of alpha-MSH. KPV is positions 11 to 13 and contains no part of it, so on sequence alone there is no reason to expect it to act as a melanocortin agonist. The pharmacology is consistent with that: in a mouse peritonitis comparison the KPV effect survived an MC3/MC4 antagonist and persisted in animals with a non-functional MC1 receptor, and KPV did not raise cyclic AMP in macrophages where the core peptides did. A colitis study reported the same persistence in MC1R-deficient mice.^[6,5,13,2]

What takes the receptor's place is a transporter. PepT1 carries di- and tripeptides across intestinal epithelium, and KPV is the right size to be a substrate. Uptake of tritiated KPV in human intestinal epithelial and T-cell lines was competed by a PepT1 substrate, a fluorescent conjugate built on KPV has been used to report PepT1 expression, and most of the delivery chemistry since has been designed around that transporter rather than around a receptor. The decisive test is genetic: in PepT1 knockout mice the changes seen in wild-type animals did not occur. That establishes that entry through this transporter is required for the readout in that model. It does not identify what the peptide engages once inside.^[3,4,26,27]

One study proposes a named intracellular partner. NF-kappaB sits in the cytoplasm held by an inhibitory protein, IkappaB alpha; when that inhibitor is degraded, the transcription-activating subunit p65RelA is carried through the nuclear pore by a carrier protein, importin-alpha3, and switches genes on. In human bronchial epithelial cells KPV was found in the nucleus, was associated with stabilised IkappaB alpha and reduced nuclear translocation of tagged p65RelA, and competition experiments pointed at the importin-alpha3 binding site on p65RelA, with the authors suggesting interference with specific armadillo repeats, the repeated helical units making up that carrier's cargo-binding groove. That is the most structurally specific hypothesis available for this molecule, and it remains a hypothesis: there is no structure of KPV bound to importin-alpha or to p65RelA, and no dissociation constant. Reduced NF-kappaB activity is the one readout that recurs across cell types, reported since 2000 and attributed in the earlier work to preservation of IkappaB alpha, but the molecular event behind it has one candidate and no structural confirmation.^{[25,3,28,29,30]}

What is still unknown about KPV

Whether KPV engages a melanocortin receptor at all is genuinely contested in the works read, and the disagreement is not a matter of emphasis. A 2003 review from the Muenster group states that the C-terminal tripeptide was able to bind MC1R, and a 2004 study found calcium responses to KPV in MC1 receptor-transfected CHO cells. Against that, a 2003 pharmacology paper reported the KPV effect insensitive to an MC3/MC4 antagonist and intact in mice with a non-functional MC1 receptor, a 2008 colitis study reported the same insensitivity in MC1R-deficient animals, and a 2010 review from the same Muenster group states flatly that KPV lacks the entire sequence motif required to bind any known melanocortin receptor. No measured binding constant at any melanocortin receptor was located in any of them, which is why the question is open: it is being argued from sequence and from models rather than settled by a measurement.^{[31,21,5,13,6]}

The structural gap is total. There is no deposited experimental structure of the free tripeptide, no structure of it bound to PepT1, and no structure of it bound to importin-alpha or to p65RelA. The only three-dimensional structural work in the family is NMR on the designed dimer [Ac-CKPV]2, whose acetyl caps and disulfide make it a different molecule. Everything shown on this page in three dimensions is calculated.^[24,22,1]

The shape of the corpus is a limit, and so is the access. Most of what has been published since the transporter work is delivery chemistry (nanoparticles, hydrogels, films, a fluorescent conjugate) in which KPV is a cargo or a targeting group and the thing measured is the vehicle; the papers studying the free peptide tend to report one organism-level endpoint in one named system without replication, a rabbit cornea in 2006 and mouse preadipocytes in 2026 among them, and a 2025 tripeptide review confirms the pattern rather than resolving it. Nothing read here has followed the 2012 importin proposal with a target identification. Separately, the two papers carrying the key mechanistic numbers, the PepT1 uptake kinetics and the importin competition, sit outside the PubMed Central open-access subset, so those constants and curves were not opened: one full text was read in full and the rest is abstract-level reading.^{[32,33,26,34,35,36,37,3,25,4]}

There is no human safety data, and that is a documented absence rather than an inference from silence. ClinicalTrials.gov returns no registered study with KPV as an intervention, and the FDA's compounding safety-risk page records that the agency identified no human exposure data for KPV by any route and lacks important information on whether the substance would cause harm in humans. No toxicology study in any species appears among the works read here, so the organism-level findings on this page are the inflammatory and tumour endpoints the papers set out to measure and carry no statement about tolerability.^[11,7]

The chemistry of the material is also a live question separate from the chemistry of the molecule. KPV in plain aqueous solution lost measurable activity within two hours at 37 degrees Celsius in the one study that tested it directly, which is why several later papers hold it in a gel or a particle, and no work read here identifies the degradation products. The salt form is not resolvable from a label reading only KPV: the synonym list carries both free-acid and acetate-salt spellings, and a counterion changes the mass of a weighed powder without changing the peptide.^[14,1]

Key papers on KPV

1. Critical role of PepT1 in promoting colitis-associated cancer and therapeutic benefits of the anti-inflammatory PepT1-mediated tripeptide KPV in a murine model

   Viennois E, Ingersoll SA, Ayyadurai S, Zhao Y, Wang L, Zhang M, Han MK, Garg P, Xiao B, Merlin D (2016), Cellular and Molecular Gastroenterology and Hepatology · Mouse genetic test with a chemically induced tumour model

   The one genetic test in this literature, and the only full text read here: deleting PepT1 abolished the measured effect, which is the strongest available statement about how the peptide has to reach a cell.

2. Dissection of the anti-inflammatory effect of the core and C-terminal (KPV) alpha-melanocyte-stimulating hormone peptides

   Getting SJ, Schioth HB, Perretti M (2003), Journal of Pharmacology and Experimental Therapeutics · Receptor pharmacology

   The careful dissection of what KPV does not need, run against the core melanocortin peptides, a receptor antagonist and an MC1R-deficient strain in one study.

3. PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation

   Dalmasso G, Charrier-Hisamuddin L, Nguyen HT, Yan Y, Sitaraman S, Merlin D (2008), Gastroenterology · Radiolabelled uptake and reporter assays

   The paper that identified KPV as a PepT1 substrate and set the direction of everything written about it since.

4. 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

   Land SC (2012), International Journal of Physiology, Pathophysiology and Pharmacology · Reporter-gene, imaging and competition assays

   The only work read that names a candidate intracellular binding partner, the importin-alpha3 site on p65RelA, and is worth reading for how far short of a structure that evidence falls.

5. Antiinflammatory activity of a COOH-terminal fragment of the neuropeptide alpha-MSH

   Hiltz ME, Lipton JM (1989), FASEB Journal · Primary study, mouse

   The 1989 report that made the fragment a subject in its own right, and the origin of the claim that the hormone's message sits in its last three residues.

6. Terminal signal: anti-inflammatory effects of alpha-melanocyte-stimulating hormone related peptides beyond the pharmacophore

   Brzoska T, Bohm M, Lugering A, Loser K, Luger TA (2010), Advances in Experimental Medicine and Biology · Review

   The review that states the sequence argument most plainly: the tripeptide lacks the entire motif required to bind any known melanocortin receptor. Read it beside R07, which says the opposite.

7. Three-dimensional structure of the alpha-MSH-derived candidacidal peptide [Ac-CKPV]2

   Catania A, Grieco P, Randazzo A, Novellino E, Gatti S, Rossi C, Colombo G, Lipton JM (2005), Journal of Peptide Research · Proton NMR with restrained mechanics and dynamics

   The only three-dimensional structural study in the family, and a precise illustration of why it is not a structure of KPV.

8. Msh (11-13) (Lys-Pro-Val), Compound Summary for CID 125672

   PubChem, PubChem, National Center for Biotechnology Information · Database record

   The compound record carrying the formula, the masses, the stereochemistry and the calculated conformer shown here. Reach it by the name Lys-Pro-Val, never by the abbreviation.

References

1. 1.PubChem. Msh (11-13) (Lys-Pro-Val), Compound Summary for CID 125672. PubChem, National Center for Biotechnology Information. source · database record
2. 2.UniProt Consortium. P01189, Pro-opiomelanocortin (POMC), Homo sapiens. UniProtKB. source · database record
3. 3.Dalmasso G, Charrier-Hisamuddin L, Nguyen HT, Yan Y, Sitaraman S, Merlin D. (2008). PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation. Gastroenterology. 134:166-178. doi:10.1053/j.gastro.2007.10.026 · abstract only
4. 4.Viennois E, Ingersoll SA, Ayyadurai S, Zhao Y, Wang L, Zhang M, Han MK, Garg P, Xiao B, Merlin D. (2016). Critical role of PepT1 in promoting colitis-associated cancer and therapeutic benefits of the anti-inflammatory PepT1-mediated tripeptide KPV in a murine model. Cellular and Molecular Gastroenterology and Hepatology. 2:340-357. doi:10.1016/j.jcmgh.2016.01.006 · full text read
5. 5.Getting SJ, Schioth HB, Perretti M. (2003). Dissection of the anti-inflammatory effect of the core and C-terminal (KPV) alpha-melanocyte-stimulating hormone peptides. Journal of Pharmacology and Experimental Therapeutics. 306:631-637. doi:10.1124/jpet.103.051623 · abstract only
6. 6.Brzoska T, Bohm M, Lugering A, Loser K, Luger TA. (2010). Terminal signal: anti-inflammatory effects of alpha-melanocyte-stimulating hormone related peptides beyond the pharmacophore. Advances in Experimental Medicine and Biology. 681:107-116. doi:10.1007/978-1-4419-6354-3_8 · abstract only
7. 7.U.S. Food and Drug Administration. (2026). Certain Bulk Drug Substances for Use in Compounding that May Present Significant Safety Risks (content current as of 22 April 2026). U.S. Food and Drug Administration, Human Drug Compounding. source · full text read
8. 8.U.S. Food and Drug Administration. (2026). Drugs@FDA (openFDA drugsfda endpoint): approved-product active ingredient search for KPV or lysyl-prolyl-valine, no matches. Drugs@FDA. source · database record
9. 9.European Medicines Agency. (2026). Medicines output: European public assessment reports for human and veterinary medicines (full list, JSON report). European Medicines Agency medicines database. source · database record
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11. 11.U.S. National Library of Medicine. (2026). ClinicalTrials.gov study search by intervention for KPV, no records. ClinicalTrials.gov. source · database record
12. 12.World Anti-Doping Agency. (2026). The 2026 Prohibited List: International Standard. World Anti-Doping Agency. source · full text read
13. 13.Kannengiesser K, Maaser C, Heidemann J, Luegering A, Ross M, Brzoska T, Bohm M, Luger TA, Domschke W, Kucharzik T. (2008). Melanocortin-derived tripeptide KPV has anti-inflammatory potential in murine models of inflammatory bowel disease. Inflammatory Bowel Diseases. 14:324-331. doi:10.1002/ibd.20334 · abstract only
14. 14.Sun J, Xue P, Liu J, Huang L, Lin G, Ran K, Yang J, Lu C, Zhao YZ, Xu HL. (2021). Self-Cross-Linked Hydrogel of Cysteamine-Grafted gamma-Polyglutamic Acid Stabilized Tripeptide KPV for Alleviating TNBS-Induced Ulcerative Colitis in Rats. ACS Biomaterials Science and Engineering. 7:4859-4869. doi:10.1021/acsbiomaterials.1c00792 · abstract only
15. 15.Hiltz ME, Lipton JM. (1989). Antiinflammatory activity of a COOH-terminal fragment of the neuropeptide alpha-MSH. FASEB Journal. 3:2282-2284. PMID 2550304 · abstract only
16. 16.Brzoska T, Luger TA, Maaser C, Abels C, Bohm M. (2008). 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. Endocrine Reviews. 29:581-602. doi:10.1210/er.2007-0027 · abstract only
17. 17.Cutuli M, Cristiani S, Lipton JM, Catania A. (2000). Antimicrobial effects of alpha-MSH peptides. Journal of Leukocyte Biology. 67:233-239. doi:10.1002/jlb.67.2.233 · abstract only
18. 18.Shao W, Chen R, Lin G, Ran K, Zhang Y, Yang J, Pan H, Shangguan J, Zhao Y, Xu H. (2021). In situ mucoadhesive hydrogel capturing tripeptide KPV: the anti-inflammatory, antibacterial and repairing effect on chemotherapy-induced oral mucositis. Biomaterials Science. 10:227-242. doi:10.1039/d1bm01466h · abstract only
19. 19.Zhao Y, Huang L, Lin G, Tong M, Xie Y, Pan H, Shangguan J, Yao Q, Xu S, Xu H. (2022). Skin-adaptive film dressing with smart-release of growth factors accelerated diabetic wound healing. International Journal of Biological Macromolecules. 222:2729-2743. doi:10.1016/j.ijbiomac.2022.10.054 · abstract only
20. 20.PubChem. 5-Phenyl-2-keto-valeric acid (2-oxo-5-phenylpentanoic acid), Compound Summary for CID 13294447. PubChem, National Center for Biotechnology Information. source · database record
21. 21.Elliott RJ, Szabo M, Wagner MJ, Kemp EH, MacNeil S, Haycock JW. (2004). alpha-Melanocyte-stimulating hormone, MSH 11-13 KPV and adrenocorticotropic hormone signalling in human keratinocyte cells. Journal of Investigative Dermatology. 122:1010-1019. doi:10.1111/j.0022-202X.2004.22404.x · abstract only
22. 22.Catania A, Grieco P, Randazzo A, Novellino E, Gatti S, Rossi C, Colombo G, Lipton JM. (2005). Three-dimensional structure of the alpha-MSH-derived candidacidal peptide [Ac-CKPV]2. Journal of Peptide Research. 66:19-26. doi:10.1111/j.1399-3011.2005.00265.x · abstract only
23. 23.Kelly JM, Moir AJ, Carlson K, Yang Y, MacNeil S, Haycock JW. (2006). Immobilized alpha-melanocyte stimulating hormone 10-13 (GKPV) inhibits tumor necrosis factor-alpha stimulated NF-kappaB activity. Peptides. 27:431-437. doi:10.1016/j.peptides.2005.03.062 · abstract only
24. 24.RCSB Protein Data Bank. Polymer entity 7RNE_3, Ac-YKPVD-CHO. RCSB PDB. source · database record
25. 25.Land SC. (2012). 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. International Journal of Physiology, Pathophysiology and Pharmacology. 4:59-73. PMID 22837805 · abstract only
26. 26.Zeng M, Shao A, Li H, Tang Y, Li Q, Guo Z, Wu C, Cheng Y, Tian H, Zhu WH. (2017). Peptide Receptor-Targeted Fluorescent Probe: Visualization and Discrimination between Chronic and Acute Ulcerative Colitis. ACS Applied Materials and Interfaces. 9:13029-13036. doi:10.1021/acsami.7b00936 · abstract only
27. 27.Wu Y, Sun M, Wang D, Li G, Huang J, Tan S, Bao L, Li Q, Li G, Si L. (2019). A PepT1 mediated medicinal nano-system for targeted delivery of cyclosporine A to alleviate acute severe ulcerative colitis. Biomaterials Science. 7:4299-4309. doi:10.1039/c9bm00925f · abstract only
28. 28.Barcellini W, Colombo G, La Maestra L, Clerici G, Garofalo L, Brini AT, Lipton JM, Catania A. (2000). Alpha-melanocyte-stimulating hormone peptides inhibit HIV-1 expression in chronically infected promonocytic U1 cells and in acutely infected monocytes. Journal of Leukocyte Biology. 68:693-699. PMID 11073109 · abstract only
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31. 31.Luger TA, Scholzen TE, Brzoska T, Bohm M. (2003). New insights into the functions of alpha-MSH and related peptides in the immune system. Annals of the New York Academy of Sciences. 994:133-140. doi:10.1111/j.1749-6632.2003.tb03172.x · abstract only
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33. 33.Xiao B, Xu Z, Viennois E, Zhang Y, Zhang Z, Zhang M, Han MK, Kang Y, Merlin D. (2017). Orally Targeted Delivery of Tripeptide KPV via Hyaluronic Acid-Functionalized Nanoparticles Efficiently Alleviates Ulcerative Colitis. Molecular Therapy. 25:1628-1640. doi:10.1016/j.ymthe.2016.11.020 · abstract only
34. 34.Bonfiglio V, Camillieri G, Avitabile T, Leggio GM, Drago F. (2006). Effects of the COOH-terminal tripeptide alpha-MSH(11-13) on corneal epithelial wound healing: role of nitric oxide. Experimental Eye Research. 83:1366-1372. doi:10.1016/j.exer.2006.07.014 · abstract only
35. 35.An SH, Park JY, Lee SJ. (2026). KPV attenuates adipogenesis and lipid metabolism through modulation of ROS-mediated AKT/mTORC1/PPARgamma signaling. Tissue & Cell. 104:103837. doi:10.1016/j.tice.2026.103837 · abstract only
36. 36.Can VC, Locke IC, Kaneva MK, Kerrigan MJP, Merlino F, De Pascale C, Grieco P, Getting SJ. (2020). Novel anti-inflammatory and chondroprotective effects of the human melanocortin MC1 receptor agonist BMS-470539 dihydrochloride and human melanocortin MC3 receptor agonist PG-990 on lipopolysaccharide activated chondrocytes. European Journal of Pharmacology. 872:172971. doi:10.1016/j.ejphar.2020.172971 · abstract only
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38. 38.Bohm M, Luger T. (2019). Are melanocortin peptides future therapeutics for cutaneous wound healing?. Experimental Dermatology. 28:219-224. doi:10.1111/exd.13887 · abstract only
39. 39.Luger TA, Brzoska T. (2007). alpha-MSH related peptides: a new class of anti-inflammatory and immunomodulating drugs. Annals of the Rheumatic Diseases. 66 Suppl 3:iii52-iii55. doi:10.1136/ard.2007.079780 · abstract only
40. 40.Gatti S, Carlin A, Sordi A, Leonardi P, Colombo G, Fassati LR, Lipton JM, Catania A. (2006). Inhibitory effects of the peptide (CKPV)2 on endotoxin-induced host reactions. Journal of Surgical Research. 131:209-214. doi:10.1016/j.jss.2005.08.009 · abstract only
41. 41.ChemSpider, Royal Society of Chemistry. L-Lysyl-L-prolyl-L-valine, C16H30N4O4, ChemSpider ID 111779. ChemSpider. source · database record
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