KPV: The Alpha-MSH Tripeptide, Its PepT1 Uptake Route and What the Research Covers

Evidence at a glance

Preclinical only

KPV has been studied in rodent colitis models and cell culture, with consistent anti-inflammatory findings. Newer work is mostly delivery systems and cell lines. No human trial has been published.

Why researchers are interested

It is the C-terminal fragment of alpha-MSH, keeping the anti-inflammatory activity studied in the full hormone without the receptor-binding core behind pigmentation. A transporter in the gut wall, PepT1, takes it up directly, which made it a natural candidate for colitis models.

What the research found

• Less intestinal inflammationReduced inflammation in colitis models through PepT1 mediated uptake (Dalmasso, Gastroenterology 2008)
• Lower inflammatory markersReduced inflammatory infiltrates in two mouse colitis models (Kannengiesser, 2008)
• Targeted deliveryNanoparticle-delivered KPV reduced mucosal damage and TNF-alpha in a mouse colitis model (Xiao, Mol Ther 2017)
• Antimicrobial activityActivity against bacterial and fungal organisms in vitro (Cutuli, 2000)

Reported in the literature

• No controlled human safety data has been published.
• Not approved by any medicines regulator.

Findings are summarised from the sources listed under References on this page, and from approved product labelling where a compound has one. These are outcomes observed in published studies, not effects claimed for any person, and nothing here is a recommendation for human use.

← All research guides

KPV is the C-terminal tripeptide of α-melanocyte-stimulating hormone (α-MSH), studied primarily in inflammatory-signalling and epithelial-barrier research. This guide covers its identity, why researchers work with the three-residue fragment rather than the whole hormone, what the published literature actually examined, and how the material is handled in a laboratory. It is written for researchers and is not medical guidance.

What KPV is

KPV is a synthetic tripeptide corresponding to residues 11–13 of α-MSH: lysine-proline-valine. It is supplied as a lyophilized powder for laboratory research.

• CAS 67727-97-3 (PubChem CID 125672)
• Molecular formula C₁₆H₃₀N₄O₄
• Molar mass 342.43 g/mol
• Sequence Lys-Pro-Val

These values were checked against PubChem on 2 October 2026. If a listing gives KPV as CAS 69630-60-0, that number belongs to methionine methyl ester hydrochloride and describes a different compound entirely.

Research-use note: KPV is a research chemical supplied strictly for laboratory research. It is not an approved drug, cosmetic, or supplement and is not for human or animal consumption. Every finding below comes from cell-culture or animal-model work.

Why the fragment rather than the whole hormone

This is the point that makes KPV interesting as a research tool, and it is usually skipped.

α-MSH is a 13-residue hormone with two broadly separable activities in the literature: pigmentary signalling, which depends on the receptor-binding core, and anti-inflammatory signalling. KPV retains the Lys-Pro-Val C-terminus while lacking that core.

That separation is the reason the tripeptide is studied at all. Working with KPV rather than α-MSH lets an experiment probe the anti-inflammatory arm of melanocortin signalling without the pigmentary activity confounding the readout. A three-residue peptide is also far cheaper to synthesise and far more tractable to handle than the full hormone.

How it is reported to enter cells

Most peptides do not cross epithelial membranes efficiently. The KPV literature is unusual in naming a specific route.

Dalmasso and colleagues (Gastroenterology, 2008) reported that KPV is taken up through PepT1, a di- and tripeptide transporter expressed in intestinal epithelium, and that at nanomolar concentrations in those models it reduced NF-κB and MAP kinase inflammatory signalling and lowered pro-inflammatory cytokine secretion.

The transporter detail matters for experimental design: an effect that depends on PepT1 expression will behave differently in a cell line that does not express it. That is a question to control for, not an assumption to carry over.

What the published literature covers

The KPV record centres on epithelial inflammation and colitis models. Three older papers carry most of the citations.

• Dalmasso et al. (Gastroenterology, 2008) — PepT1-mediated uptake and reduced inflammatory signalling in intestinal epithelial models.
• Kannengiesser et al. (Inflammatory Bowel Diseases, 2008) — two mouse colitis models, with reduced inflammatory infiltrates and myeloperoxidase activity; the effects appeared at least partly independent of the melanocortin-1 receptor.
• Cutuli et al. (Journal of Leukocyte Biology, 2000) — antimicrobial activity for α-MSH-derived peptides, including the C-terminal tripeptide sequence.

Newer work has mostly been about delivery and cell lines rather than new animal efficacy studies. Xiao and colleagues (Molecular Therapy, 2017) loaded KPV into hyaluronic-acid-functionalised nanoparticles aimed at colonic epithelial cells and macrophages, and reported less mucosal damage and lower TNF-α in a mouse colitis model. Two 2026 cell-culture studies took it beyond the gut: in HepG2 liver cells KPV reduced oleic-acid-induced lipid accumulation (Lee et al., Cytotechnology), and in 3T3-L1 preadipocytes it suppressed adipocyte differentiation (An et al., Tissue and Cell), in both cases alongside reduced reactive-oxygen-species signalling.

That is still a small evidence base. No controlled human study is cited here, the animal work is in colitis models, and the newest findings come from cell lines. Results in those models describe what happened in those models.

KPV as a blend component

KPV is the component that distinguishes the four-peptide KLOW blend from the three-peptide formulation, where it contributes 10 mg of the 80 mg total. Of the four components, it is the only one with a substantial inflammatory-signalling literature, so its presence is what makes a blend relevant to that class of question. The composition breakdown is in our KLOW research guide.

In a blend the components are reconstituted together and cannot be varied independently. A study that needs to isolate KPV’s contribution needs the single compound.

Form, reconstitution and storage

KPV is supplied as a lyophilized powder. Standard laboratory practice is to reconstitute with bacteriostatic water, swirl rather than shake until dissolved, and store the reconstituted solution refrigerated at 2–8 °C. The lyophilized powder is kept frozen and protected from light, and repeated freeze-thaw cycles are avoided. Our walkthrough covers the general procedure: how to reconstitute peptides.

(General lab-handling notes, not usage instructions, and no substitute for the protocol in force in the receiving laboratory.)

For research use only

All products and information referenced here are intended strictly for laboratory and scientific research use only. They are not for human or animal consumption and are not drugs, foods, supplements, cosmetics, or medical devices. Nothing here should be interpreted as medical advice, and no outcome in a person is described, implied or promised. Products are supplied against a stated purity specification.

Explore KPV and related research peptides

• KPV 10 mg — specifications and stated purity
• KLOW 80 mg — the four-peptide blend that includes KPV
• GHK-Cu — copper tripeptide, also a KLOW component
• Full research catalog

Common questions about KPV

What does KPV stand for?

The single-letter codes of its three amino acids: lysine (K), proline (P) and valine (V). It is the C-terminal end of α-melanocyte-stimulating hormone.

How is KPV different from α-MSH?

KPV keeps the C-terminal Lys-Pro-Val of α-MSH but lacks the core sequence associated with pigmentation, which is why researchers use it to study the anti-inflammatory side of melanocortin signaling separately.

Which blend contains KPV?

KLOW, alongside GHK-Cu, BPC-157 and TB-500. KPV is also sold on its own.

References

1. Dalmasso G, et al. PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation. Gastroenterology. 2008. PubMed
2. Kannengiesser K, et al. Melanocortin-derived tripeptide KPV has anti-inflammatory potential in murine models of inflammatory bowel disease. Inflamm Bowel Dis. 2008. PubMed
3. Cutuli M, et al. Antimicrobial effects of alpha-MSH peptides. J Leukoc Biol. 2000. PubMed
4. Xiao B, et al. Orally Targeted Delivery of Tripeptide KPV via Hyaluronic Acid-Functionalized Nanoparticles Efficiently Alleviates Ulcerative Colitis. Mol Ther. 2017. PubMed
5. Lee JY, et al. Lysine-proline-valine peptide attenuates hepatic lipid accumulation through ROS-dependent regulation of the PPARγ pathway in HepG2 cells. Cytotechnology. 2026. PubMed
6. An SH, et al. KPV attenuates adipogenesis and lipid metabolism through modulation of ROS-mediated AKT/mTORC1/PPARγ signaling. Tissue Cell. 2026. PubMed
7. Compound identity verified against the PubChem database, retrieved 2 October 2026. PubChem