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KPV Peptide: Molecular Structure, Mechanisms and Published Research

KPV (Lys-Pro-Val, α-MSH 11-13) is a 342 Da tripeptide cut from α-melanocyte-stimulating hormone. Published research consists of cell-culture experiments, mostly measuring NF-κB activity, and rodent or rabbit models, mostly of colitis; uptake through the PepT1 transporter and partial independence from melanocortin receptors are reported. A PubMed and ClinicalTrials.gov search on November 7, 2026 located no controlled human trial of unmodified KPV. This guide separates KPV from its analogues and formulations and shows what our certificates measure.

Precise Pep Labs Research Editorial Team · November 7, 2026 · 15 min read

Key facts

  • KPV is H-Lys-Pro-Val-OH, residues 11–13 of α-MSH, formula C16H30N4O4, average mass 342.43 Da; it lacks the His-Phe-Arg-Trp core that binds melanocortin receptors.
  • The reproducible in vitro observation is reduced NF-κB activation in stimulated intestinal and airway epithelial cell lines at nanomolar concentrations; uptake into those cells is PepT1-dependent.
  • In mouse colitis models KPV reduced histological inflammation and myeloperoxidase activity, and the effect persisted in mice lacking functional MC1R; a brain-injury study found smaller lesions without reduced TNF-α or IL-1β.
  • Antimicrobial activity is reported for KPV-containing sequences by several groups and was not reproduced by another using acetylated, amidated KPV; the strongest effects involve lipidated or longer fragments.
  • No controlled human trial of unmodified KPV was located in PubMed or ClinicalTrials.gov on November 7, 2026; results from the dimer (CKPV)2, D-valine, lipidated or nanoparticle forms do not transfer to the free tripeptide.
Research use only. This article is reference material for laboratory research. It does not describe or recommend any human or veterinary use, dosing or administration, and nothing here is medical advice. Precise Pep Labs materials are sold for in vitro research only.

What KPV is

KPV is the tripeptide lysine–proline–valine (Lys-Pro-Val). It is the last three residues, positions 11 to 13, of α-melanocyte-stimulating hormone (α-MSH), a 13-residue peptide cut from the precursor pro-opiomelanocortin, which is why the research literature usually calls it α-MSH(11-13) [1]. The tripeptide was first studied because the anti-inflammatory activity of α-MSH in early animal experiments appeared to reside in that C-terminal fragment [2].

Three facts frame everything that follows. First, KPV does not contain the His-Phe-Arg-Trp core (residues 6 to 9) that gives α-MSH its affinity for melanocortin receptors, so whether KPV acts through those receptors at all is a live question in the literature [1][5]. Second, the published evidence consists of cell-culture experiments and rodent or rabbit models, most of them in intestinal inflammation; a search of PubMed and ClinicalTrials.gov on November 7, 2026 located no controlled human trial of unmodified KPV (the search scope is described below). Third, several papers study modified analogues or nanoparticle formulations rather than the free tripeptide, and their results do not transfer to it. This guide separates those categories, explains what each study measured, and shows what the certificates for our own KPV material report.

Precise Pep Labs sells KPV as a lyophilised research material for in vitro use. Nothing here describes or recommends use in people or animals.

Amino acid sequence and molecular identity

PropertyValueSource
SequenceH-Lys-Pro-Val-OH (L-amino acids; free N-terminal amine, free C-terminal acid)PubChem CID 125672 [20]
OriginResidues 11–13 of α-MSH; α-MSH is residues 1–13 of the ACTH sequence within pro-opiomelanocortinBrzoska et al. 2008 [1]
Molecular formulaC16H30N4O4PubChem [20]
Average molecular mass342.43 g/mol (342.44 Da as printed on the Axiom Analytics Klow certificate)PubChem [20]; Axiom AX-2026-2696-CYB5
Monoisotopic mass342.2267 DaPubChem [20]
Charged groupsTwo basic sites (the α-amine and the lysine ε-amine) and one carboxylic acid, so the free peptide carries a net positive charge at neutral pH and is isolated as a saltsequence
Common literature variantsAc-Lys-Pro-Val-NH2 (acetylated, amidated); Lys-Pro-D-Val (KP-D-V); the cyclised dimer (CKPV)2; palmitoyl-α-MSH(11-13)[7][12][15][16]

The mass figures matter for reading a certificate. A laboratory that confirms identity by mass spectrometry compares the observed mass with the theoretical value for the form being tested. For the free tripeptide that value is 342.43 Da; an acetylated and amidated analogue (Ac-KPV-NH2) is about 383 Da; a palmitoylated analogue is heavier still. A certificate that reports a mass near 342 Da is therefore describing unmodified KPV, not one of the analogues. Because the free peptide has two basic sites, the lyophilised powder also contains counter-ions, which add to the vial's mass but not to the peptide; Article 2 explains why that separates purity from net content.

Historical discovery and early experiments

The first dedicated study of the tripeptide is Hiltz and Lipton's 1989 report in the FASEB Journal [2]. α-MSH was already known to be antipyretic and to inhibit histamine-induced increases in vascular permeability; the authors tested graded amounts of α-MSH(11-13) against ear swelling induced by picryl chloride in mice, with saline and a corticosteroid as comparators, and reported dose-related inhibition of swelling. That single mouse model is the origin of the claim that KPV carries α-MSH's anti-inflammatory "message sequence".

Through the 1990s Lipton, Catania and colleagues extended the α-MSH and α-MSH(11-13) work to other models of inflammation and summarised three proposed mechanisms: direct effects on peripheral host cells, actions on melanocortin receptors in the brain that dampen peripheral inflammation, and local effects within the central nervous system [3]. These are proposals derived from animal pharmacology, not demonstrated human mechanisms.

Cell-culture findings

The in vitro literature on unmodified KPV is small and concentrated on epithelial and immune cell lines. The table lists the principal experiments.

StudyCellsStimulusWhat was measuredReported resultWhat it does not show
Dalmasso et al. 2008 [4]Two intestinal epithelial lines (Caco2-BBE, HT29-Cl.19A); Jurkat T cellsPro-inflammatory cytokinesNF-κB reporter activity, MAP-kinase signalling, cytokine secretion; radiolabelled-KPV uptake with competition for the PepT1 transporterNanomolar KPV reduced NF-κB and MAP-kinase activation and cytokine secretion; uptake was PepT1-dependentNothing about intact tissue or about cells that do not express PepT1
Land 2012 [8]16HBE14o- human bronchial epithelial cellsTNF-α; respiratory syncytial virusNF-κB reporter, MMP-9 activity, IL-8 and eotaxin secretion, p65 nuclear importDose-dependent suppression of NF-κB signalling and chemokine release; KPV was associated with blocked nuclear import of p65 and appeared to interact with the importin-α binding siteA single immortalised line; the importin interaction was inferred from competition assays
Elliott et al. 2004 [7]HaCaT and normal human keratinocytes; MC1R-transfected CHO cellsα-MSH, KPV, KP-D-V, ACTH peptidesCyclic AMP; intracellular calciumNo cAMP rise to α-MSH or KPV in keratinocytes; rapid calcium signals under specific conditions; in MC1R-transfected cells α-MSH and the KPV peptides raised calciumDoes not establish which receptor, if any, mediates the calcium response in keratinocytes
Gatti et al. 2006 [16]Human peripheral blood mononuclear cellsLipopolysaccharideTNF-α productionThe dimer (CKPV)2 inhibited TNF-α; KPV and an α-MSH analogue were run as comparatorsThe headline finding concerns the dimer, not KPV

Two patterns recur. The readout is almost always NF-κB activity or a cytokine downstream of it, so "anti-inflammatory" in this literature means "reduced NF-κB-driven signalling in a stimulated cell line". And the concentrations reported as active are in the nanomolar range in the intestinal and airway lines, which is one reason the uptake mechanism attracted attention.

Animal-model findings

StudyModelRoute in the studyEndpointsReported resultLimits
Hiltz & Lipton 1989 [2]Picryl-chloride ear swelling, mouseSystemicEar thicknessDose-related reduction in swellingOne acute model; the paper predates modern cytokine assays
Dalmasso et al. 2008 [4]DSS and TNBS colitis, mouseAdded to drinking waterHistology; pro-inflammatory cytokine mRNAReduced incidence and cytokine expression in both modelsChemical colitis models; no survival or long-term data
Kannengiesser et al. 2008 [5]DSS colitis and CD45RB-high T-cell transfer colitis, mouse; DSS colitis in MC1R-deficient (e/e) miceSystemicWeight, histology, myeloperoxidase activity, survivalEarlier recovery and weight regain, fewer infiltrates, lower MPO; in MC1R e/e mice KPV prevented death during DSS colitisEffects described as "at least partially" MC1R-independent; group sizes typical of exploratory work
Bonfiglio et al. 2006 [9]Mechanical corneal abrasion, rabbitTopical dropsEpithelial defect area over timeFaster re-epithelialisation than vehicle; the effect was blocked by a nitric-oxide-synthase inhibitorWound closure, not inflammation; eight corneas per group
Schaible et al. 2013 [10]Controlled cortical impact, mouseSingle intraperitoneal injection after injuryLesion volume, TNF-α and IL-1β expression, microglial morphology, cleaved caspase-3Smaller lesion and less microglial activation and apoptosis; TNF-α and IL-1β were not reducedSingle time point; one injury model
Viennois et al. 2016 [19]Colitis-associated cancer (AOM/DSS), wild-type and PepT1-knockout miceOralTumour number and size, inflammationFewer tumours in wild-type mice; no effect in PepT1-knockout miceA model of chemically induced tumours; the paper's primary subject is PepT1

Across these studies the consistent observation is reduced tissue inflammation or injury in rodent models. The inconsistent observation is mechanism: cytokine readouts fell in the colitis papers but not in the brain-injury paper, and receptor dependence differs between reports. None of this translates to a human outcome; animal models of colitis in particular have a poor record of predicting effects in people, and the trials that would answer that question do not exist.

NF-κB and other signalling observations

Across cell types the most reproducible molecular observation is reduced NF-κB activation after KPV exposure [4][8]. NF-κB is the transcription factor that switches on many pro-inflammatory genes; reporter assays measure its transcriptional activity, and Western blots of IκBα and p65 measure the steps before it. Dalmasso and colleagues also reported reduced MAP-kinase signalling [4]. Land's airway study went one step further and proposed a physical explanation: KPV was associated with stabilised IκBα and blocked nuclear import of p65, with competition data pointing to the importin-α binding site [8]. That proposal has not, to our knowledge, been reproduced by another group, and it sits awkwardly with the receptor-mediated explanations in the review literature [1][6]. The signalling picture is best summarised as "NF-κB activity goes down in several stimulated cell lines; the upstream mechanism is unresolved".

PepT1-mediated transport

PepT1 is the intestinal di- and tripeptide transporter. It is expressed in the small intestine, is low in healthy colon and is induced in colonic epithelium during inflammatory bowel disease [4][19]. Dalmasso and colleagues showed that KPV is a PepT1 substrate: radiolabelled KPV uptake into epithelial and immune cells was saturable and was competed by other PepT1 substrates, and the anti-inflammatory effect in cells depended on the transporter [4]. Viennois and colleagues then showed, in the colitis-associated cancer model, that oral KPV had no effect in mice lacking PepT1 [19]. The practical consequence for interpreting the colitis studies is that they describe a peptide delivered to inflamed colon through a transporter that is up-regulated there; they say nothing about tissues or conditions where PepT1 is absent.

Melanocortin-receptor and receptor-independent mechanisms

α-MSH signals through five melanocortin receptors, and its anti-inflammatory effects on immune cells are generally attributed to MC1R and the resulting cAMP rise [1]. KPV lacks the receptor-binding core, which is why its mechanism is contested:

  • Luger and colleagues reported that KPV "was able to bind to MC-1R" and modulate antigen-presenting cells, and reviewed in vivo contact-hypersensitivity data for both α-MSH and KPV [6].
  • Elliott and colleagues found no cAMP response to KPV in keratinocytes, though calcium responses appeared in MC1R-transfected cells [7].
  • Kannengiesser and colleagues found that KPV still protected mice carrying a non-functional MC1R, and concluded the effect was at least partly receptor-independent [5].
  • Dalmasso and colleagues and Land proposed intracellular routes (PepT1 uptake; direct interference with p65 nuclear import) that do not require a surface receptor at all [4][8].

These results are not necessarily contradictory, because they come from different cells and endpoints, but together they mean that no single mechanism is established for KPV. Claims that KPV "works by activating melanocortin receptors" or "stabilises mast cells" are not supported by the primary literature; neither phrase describes an experiment in the papers above.

Antimicrobial findings and conflicting evidence

A separate line of work examines α-MSH and its C-terminal fragments as antimicrobial peptides. Singh and Mukhopadhyay reported that α-MSH(6-13) and α-MSH(11-13) killed more than 90 % of methicillin-sensitive and methicillin-resistant Staphylococcus aureus at micromolar concentrations in vitro, with membrane depolarisation and permeabilisation similar to the full-length peptide, while the N-terminal fragment was inactive [11]. Charnley and colleagues found Ac-Lys-Pro-Val-NH2 and Ac-Lys-Pro-D-Val-NH2 active against S. aureus and Escherichia coli, with no potency difference between the L- and D-valine forms and no requirement for the lysine's positive charge [12]. Carotenuto and colleagues reported candidacidal activity for α-MSH and its C-terminal sequence and then optimised longer analogues for that purpose [13].

The conflicting datum is Songok and colleagues' 2018 study, which tested Ac-KPV-NH2 and glycoalkylated analogues under a variety of assay conditions and found no antimicrobial activity for any of them [14]. Assay medium, peptide form (acetylated and amidated versus free) and bacterial growth phase all differ between these papers, so the honest summary is that antimicrobial activity has been reported for KPV-containing sequences by some groups and not reproduced by others, and that the strongest results involve longer fragments or lipidated analogues rather than unmodified KPV.

Experimental delivery formulations

Because a free tripeptide is rapidly degraded and, when given orally, is absorbed in the small intestine before it reaches the colon, several groups have built delivery systems around KPV. These studies test the system, not the free peptide:

  • Laroui and colleagues loaded KPV into 400 nm polymer nanoparticles embedded in an alginate–chitosan hydrogel that collapses in the colon, and reported reduced inflammatory responses in Caco2-BBE cells and in DSS colitis at a far lower KPV load than free peptide required [17].
  • Xiao and colleagues functionalised KPV nanoparticles with hyaluronic acid to target colonic epithelial cells and macrophages, again in a hydrogel, and reported faster mucosal healing and lower TNF-α in a mouse colitis model than non-targeted particles [18].
  • Zhang and colleagues co-assembled KPV with the immunosuppressant tacrolimus into PepT1-targeted nanoparticles and compared the combination with each agent alone in DSS colitis [21].

What these papers show is that colon-targeted carriers can deliver the tripeptide to inflamed tissue in mice. What they do not show is anything about the pharmacology of KPV in solution, which is the form a research vial provides.

Unmodified KPV and its analogues

FormWhat it isWhere it appearsTransferable to unmodified KPV?
H-Lys-Pro-Val-OHThe free tripeptide; the form our certificates describeHiltz 1989, Dalmasso 2008, Kannengiesser 2008, Bonfiglio 2006, Schaible 2013 [2][4][5][9][10]—
Ac-Lys-Pro-Val-NH2N-acetylated, C-amidated; mass about 383 DaCharnley 2008, Songok 2018 [12][14]Partly; the terminal modifications change charge and protease stability
Lys-Pro-D-Val (KP-D-V)D-valine at position 3Elliott 2004, Charnley 2008 [7][12]No; a stereoisomer
(CKPV)2Two Cys-KPV units joined by a disulfideGatti 2006 [16]No; a dimer with its own pharmacology
Palmitoyl-α-MSH(11-13)Lipid-tailed KPVMumtaz 2020 [15]No; the lipid tail drives the membrane activity reported
Nanoparticle- or hydrogel-formulated KPVFree KPV inside a carrierLaroui 2010, Xiao 2017, Zhang 2024 [17][18][21]No; the carrier determines where and how much peptide is released
KdPT (Lys-D-Pro-Thr)A different tripeptide, from IL-1β residues 193–195Reviewed in Brzoska 2008 [1]No; a different sequence

The D-valine and palmitoylated analogues deserve a sentence each because they are frequently conflated with KPV. KP-D-V was designed to resist proteolysis; in the antibacterial comparison it was no more potent than the L-form [12]. Palmitoyl-α-MSH(11-13) was more active than the unlipidated fragment against stationary-phase S. aureus in vitro, an effect the authors attribute to improved membrane interaction from the lipid tail [15], so it is evidence about lipidation, not about KPV.

Major limitations of the existing research

  • No controlled human trial located. On November 7, 2026 we searched PubMed for KPV, Lys-Pro-Val and α-MSH(11-13) restricted to clinical-trial and randomised-controlled-trial publication types (0 records), reviewed the 38 records returned for the same terms under the "humans" subject heading (all were in vitro work on human cells or tissue, reviews, or studies of other peptides), and searched ClinicalTrials.gov by intervention for KPV, Lys-Pro-Val, α-MSH(11-13) and CKPV (no registered study of the tripeptide; the dimer (CKPV)2 was described as under clinical investigation for antimicrobial use in 2006 [16], but no trial record was located). The statement is limited to those two databases on that date and to unmodified KPV.
  • Few groups, mostly one disease model. The in vivo evidence comes largely from murine chemical colitis studied by a small number of laboratories; independent replication across groups is thin.
  • Endpoints are surrogates. Reporter assays, cytokine mRNA, histology scores and MPO activity are informative but are not clinical outcomes.
  • Mechanism unresolved. Receptor-dependent, receptor-independent and transporter-mediated explanations coexist; the airway importin finding has not been independently confirmed.
  • Routes and vehicles vary. Drinking water, intraperitoneal injection, topical drops and engineered carriers appear across the studies; results obtained with one cannot be assumed for another.
  • Stability. A free tripeptide is a substrate for peptidases; Sun and colleagues note that KPV solution is unstable under the conditions of their rectal-delivery experiments, which is one reason hydrogels and nanoparticles were developed [22][17][18]. Stability of KPV in solution at bench conditions is poorly characterised in the open literature.
  • Analogue contamination of the narrative. Much secondary writing attributes dimer, D-amino-acid and lipidated-analogue results to KPV itself.

Precise Pep Labs certificates for KPV

Two kinds of certificate in our COA Library describe KPV, and they should be read differently.

Single-compound KPV. The KPV 5 mg certificate is from Freedom Diagnostics Testing (accession 2607200745, search code Prec2607200745, received July 20 and reported July 22, 2026, lot recorded by cap colour as "White Cap"). It reports identity confirmed by LC-MS as KPV, purity 99.05 % by HPLC-UV, and net content of 5.23 mg in vial 1 and 5.11 mg in vial 2, giving the 5.17 mg shown in the library, against a 5 mg label. The certificate prints no specification column and identifies the lot only by cap colour, so it cannot be matched to a numbered batch; it describes the two vials tested.

KPV as a blend component. Klow 80 mg is a four-component blend labelled as 10 mg KPV, 50 mg GHK-Cu, 10 mg BPC-157 and 10 mg TB-500. Its certificates measure KPV inside that mixture, which is a different sample from a single-compound vial, and the values below describe the blend lot, not standalone KPV material.

  • Axiom Analytics Laboratories, certificate AX-2026-2696-CYB5, lot PPL-2610-KLOW, issued October 15, 2026, two vials: KPV identity by LC-MS accurate mass, observed 342.426 Da against a theoretical 342.44 Da (−0.014 Da, within the ± 1 Da criterion); KPV purity 99.62 % mean of the two vials (99.88 % and 99.36 %) against a criterion of not less than 99.25 area %; KPV content 10.47 mg mean (10.49 and 10.45 mg) against a 9–11 mg criterion; container-to-container consistency for KPV 0.27 % CV. The blend as a whole reported 99.67 % purity and 83.45 mg net peptide content.
  • Kovera Labs, report KVR-2026-84DDA5, certified July 20, 2026, an earlier lot with no batch number on the certificate: KPV measured at 10.27 mg against 10 mg labelled, by RP-HPLC on a C18 column with diode-array detection at 214 nm, with blend identity by LC-MS and a blend-average purity of 99.881 %. This certificate reports one purity figure for the whole blend, not a KPV-specific purity.

The difference between the two certificate types is the point. A blend certificate that resolves KPV by mass and quantifies it separately, as the Axiom report does, gives real information about that component; a blend-average purity does not tell a reader how pure the KPV in the mixture was. Article 1 covers how to read those fields, and Article 2 covers why a purity percentage and a milligram figure answer different questions. Where a lot on a vial does not match a library entry, contact us with the lot number.

Frequently asked scientific questions

Is KPV the same thing as α-MSH? No. α-MSH is a 13-residue hormone; KPV is its last three residues. KPV lacks the receptor-binding core of α-MSH, has no pigmentary activity in the studies that looked for it, and its mechanism is debated [1][5].

What has KPV actually been tested in? Human intestinal, airway and keratinocyte cell lines and T cells in culture; mouse models of chemically induced and T-cell-transfer colitis, ear swelling, brain injury and colitis-associated cancer; a rabbit corneal wound model [2][4][5][7][8][9][10][19].

Does KPV act through melanocortin receptors? The evidence is mixed: one group reported MC1R binding [6], another found protection persisted in mice without functional MC1R [5], and two others proposed receptor-independent intracellular routes [4][8].

Is KPV antimicrobial? Activity against S. aureus, E. coli and Candida has been reported for KPV-containing sequences by several groups [11][12][13] and not reproduced by another using acetylated, amidated KPV [14]. The strongest effects involve longer or lipidated fragments.

Are there human studies of KPV? None located: no clinical-trial publication in PubMed and no registered study in ClinicalTrials.gov for the unmodified tripeptide as of November 7, 2026, within the search scope described above.

What is on a KPV certificate of analysis? Identity by LC-MS (a mass near 342 Da for the free peptide), chromatographic purity, and net content per vial; for a blend, whether KPV was identified and quantified as a component or only averaged into the mixture.

Evidence from our lab reports

Each row is one certificate on file, identified by product and report date. Values are the figures the testing laboratory reported for that lot; they are not re-measured or adjusted here. "Latest COA in Library" and "Earlier COA" describe the certificate's place in the COA Library for that product. The lot currently shipping is identified by each product's inventory batch number, not by which certificate is newest.

ProductReport dateTestPurityNet contentCertificate
KPV 5mgLatest COA in LibraryAug 5, 2026HPLC purity99.05%5.17 mg View
Klow 80mgLatest COA in LibraryOct 15, 2026HPLC purity99.67%83.45 mg View
Klow 80mgEarlier COAAug 5, 2026HPLC purity99.88%88.61 mg View

Frequently asked questions

What is KPV peptide?
KPV is the tripeptide lysine–proline–valine, the last three residues (11–13) of α-melanocyte-stimulating hormone. It has the formula C16H30N4O4 and an average mass of 342.43 Da. It is studied as a research material because early animal work suggested the anti-inflammatory activity of α-MSH resides in this fragment.
What is the difference between KPV and α-MSH?
α-MSH is a 13-residue hormone that binds melanocortin receptors through its His-Phe-Arg-Trp core; KPV is only the C-terminal three residues and lacks that core. KPV shows no pigmentary activity in the studies that looked, and whether it acts through melanocortin receptors is contested in the literature.
What research models has KPV been studied in?
Cell culture: human intestinal epithelial lines (Caco2-BBE, HT29-Cl.19A), Jurkat T cells, 16HBE14o- bronchial epithelial cells and keratinocytes, mostly with NF-κB and cytokine readouts. Animals: mouse ear swelling, DSS and TNBS colitis, T-cell transfer colitis, controlled cortical impact and colitis-associated cancer; rabbit corneal abrasion.
How does KPV enter cells?
Dalmasso and colleagues showed in 2008 that KPV is a substrate of PepT1, the intestinal di- and tripeptide transporter that is induced in inflamed colon, and that its anti-inflammatory effect in cells depended on that transporter. A 2016 study found oral KPV had no effect in mice lacking PepT1.
Are there human clinical trials of KPV?
None were located. A PubMed search restricted to clinical-trial publication types returned no record for KPV, Lys-Pro-Val or α-MSH(11-13), and ClinicalTrials.gov had no registered study of the tripeptide by intervention, as of November 7, 2026. The dimer (CKPV)2 was described as under clinical investigation in 2006, but that is a different molecule.
What does a certificate of analysis show for KPV?
Identity by LC-MS (a mass close to 342 Da for the free tripeptide), chromatographic purity by HPLC, and net content in milligrams per vial. Our KPV 5 mg certificate from Freedom Diagnostics reports 99.05 % purity and 5.17 mg mean content; the Axiom certificate for the Klow 80 mg blend identifies and quantifies KPV as a component (10.47 mg mean, 99.62 % purity).

References

  1. Brzoska T, Luger TA, Maaser C, Abels C, Böhm M. α-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. 2008;29(5):581–602. doi:10.1210/er.2007-0027
  2. Hiltz ME, Lipton JM. Antiinflammatory activity of a COOH-terminal fragment of the neuropeptide α-MSH. FASEB Journal. 1989;3(11):2282–2284. PMID 2550304. https://pubmed.ncbi.nlm.nih.gov/2550304/
  3. Lipton JM, Catania A. Mechanisms of antiinflammatory action of the neuroimmunomodulatory peptide α-MSH. Annals of the New York Academy of Sciences. 1998;840:373–380. doi:10.1111/j.1749-6632.1998.tb09576.x
  4. Dalmasso G, Charrier-Hisamuddin L, Nguyen HTT, Yan Y, Sitaraman S, Merlin D. PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation. Gastroenterology. 2008;134(1):166–178. doi:10.1053/j.gastro.2007.10.026
  5. Kannengiesser K, Maaser C, Heidemann J, Luegering A, Ross M, Brzoska T, et al. Melanocortin-derived tripeptide KPV has anti-inflammatory potential in murine models of inflammatory bowel disease. Inflammatory Bowel Diseases. 2008;14(3):324–331. doi:10.1002/ibd.20334
  6. Luger TA, Scholzen TE, Brzoska T, Böhm M. New insights into the functions of α-MSH and related peptides in the immune system. Annals of the New York Academy of Sciences. 2003;994:133–140. doi:10.1111/j.1749-6632.2003.tb03172.x
  7. Elliott RJ, Szabo M, Wagner MJ, Kemp EH, MacNeil S, Haycock JW. α-Melanocyte-stimulating hormone, MSH 11-13 KPV and adrenocorticotropic hormone signalling in human keratinocyte cells. Journal of Investigative Dermatology. 2004;122(4):1010–1019. doi:10.1111/j.0022-202X.2004.22404.x
  8. 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. International Journal of Physiology, Pathophysiology and Pharmacology. 2012;4(2):59–73. PMID 22837805. https://pubmed.ncbi.nlm.nih.gov/22837805/
  9. Bonfiglio V, Camillieri G, Avitabile T, Leggio GM, Drago F. Effects of the COOH-terminal tripeptide α-MSH(11-13) on corneal epithelial wound healing: role of nitric oxide. Experimental Eye Research. 2006;83(6):1366–1372. doi:10.1016/j.exer.2006.07.014
  10. Schaible EV, Steinsträßer A, Jahn-Eimermacher A, Luh C, Sebastiani A, Kosel F, et al. Single administration of tripeptide α-MSH(11-13) attenuates brain damage by reduced inflammation and apoptosis after experimental traumatic brain injury in mice. PLoS One. 2013;8(8):e71056. doi:10.1371/journal.pone.0071056
  11. Singh M, Mukhopadhyay K. C-terminal amino acids of α-melanocyte-stimulating hormone are requisite for its antibacterial activity against Staphylococcus aureus. Antimicrobial Agents and Chemotherapy. 2011;55(5):1920–1929. doi:10.1128/AAC.00957-10
  12. Charnley M, Moir AJG, Douglas CWI, Haycock JW. Anti-microbial action of melanocortin peptides and identification of a novel X-Pro-D/L-Val sequence in Gram-positive and Gram-negative bacteria. Peptides. 2008;29:1004–1009. doi:10.1016/j.peptides.2008.02.004
  13. Carotenuto A, Saviello MR, Auriemma L, Campiglia P, Catania A, Novellino E, Grieco P. Structure-function relationships and conformational properties of α-MSH(6-13) analogues with candidacidal activity. Chemical Biology & Drug Design. 2007;69:68–74. doi:10.1111/j.1747-0285.2007.00473.x
  14. Songok AC, Panta P, Doerrler WT, Macnaughtan MA, Taylor CM. Structural modification of the tripeptide KPV by reductive "glycoalkylation" of the lysine residue. PLoS One. 2018;13:e0199686. doi:10.1371/journal.pone.0199686
  15. Mumtaz S, Behera S, Mukhopadhyay K. Lipidated short analogue of α-melanocyte stimulating hormone exerts bactericidal activity against the stationary phase of methicillin-resistant Staphylococcus aureus and inhibits biofilm formation. ACS Omega. 2020;5:28425–28440. doi:10.1021/acsomega.0c01462
  16. Gatti S, Carlin A, Sordi A, Leonardi P, Colombo G, Fassati LR, Lipton JM, Catania A. Inhibitory effects of the peptide (CKPV)2 on endotoxin-induced host reactions. Journal of Surgical Research. 2006;131(2):209–214. doi:10.1016/j.jss.2005.08.009
  17. Laroui H, Dalmasso G, Nguyen HTT, Yan Y, Sitaraman SV, Merlin D. Drug-loaded nanoparticles targeted to the colon with polysaccharide hydrogel reduce colitis in a mouse model. Gastroenterology. 2010;138(3):843–853. doi:10.1053/j.gastro.2009.11.003
  18. Xiao B, Xu Z, Viennois E, Zhang Y, Zhang Z, Zhang M, et al. Orally targeted delivery of tripeptide KPV via hyaluronic acid-functionalized nanoparticles efficiently alleviates ulcerative colitis. Molecular Therapy. 2017;25(7):1628–1640. doi:10.1016/j.ymthe.2016.11.020
  19. Viennois E, Ingersoll SA, Ayyadurai S, Zhao Y, Wang L, Charania M, 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. Cellular and Molecular Gastroenterology and Hepatology. 2016;2(3):340–357. doi:10.1016/j.jcmgh.2016.01.006
  20. PubChem. Lys-Pro-Val (CID 125672): molecular formula C16H30N4O4, molecular weight 342.43, monoisotopic mass 342.2267. National Library of Medicine. https://pubchem.ncbi.nlm.nih.gov/compound/125672
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  22. Sun J, Xue P, Liu J, Huang L, Lin G, Ran K, et al. Self-cross-linked hydrogel of cysteamine-grafted γ-polyglutamic acid stabilized tripeptide KPV for alleviating TNBS-induced ulcerative colitis in rats. ACS Biomaterials Science & Engineering. 2021;7:4859–4869. doi:10.1021/acsbiomaterials.1c00792

How this article was checked

  • Written by: Precise Pep Labs Research Editorial Team
  • Last reviewed: November 7, 2026
  • Published: November 7, 2026
  • Last updated: November 7, 2026
  • Lab reports cited: 3
  • Sources: the numbered references above and the certificates of analysis in the COA Library. Editorial content is reviewed for research-use-only compliance before publication.

Related research materials

Reference materials discussed in this article, each with its certificate of analysis

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KPV

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