KPV Peptide: What the Research Shows

Research summary. KPV is the C-terminal tripeptide of alpha-melanocyte-stimulating hormone (lysine-proline-valine). The published literature describes it as an inhibitor of NF-kB signaling in cell and animal models of inflammation, taken up by the PepT1 transporter. The evidence base is small and entirely preclinical: there are no controlled human studies. It is a reference material characterized by identity and purity, not a consumer product.

Author: Nox Amino Research Team Reviewed by: the Nox Amino Research Team Published: July 16, 2026 · Updated: July 16, 2026 Editorial methodology: /learn/editorial-standards

Research Use Only (RUO). All materials referenced on this page are intended exclusively for laboratory research and analytical use. They are not drugs, dietary supplements, or articles for human or veterinary consumption, and nothing here constitutes medical advice or a recommendation for use in or on the body. Statements below describe published third-party studies in their own terms; they are not claims about outcomes for any reader. See our Certificates of Analysis for identity and purity data on stocked reference materials.

What KPV is, in the published literature

KPV is a three-residue peptide: lysine-proline-valine. PubChem records it under CID 125672 with the synonyms alpha-MSH (11-13) and MSH (11-13), which is the authoritative basis for the description of KPV as the C-terminal fragment of alpha-melanocyte-stimulating hormone. Its molecular formula is C16H30N4O4, molecular weight 342.43, CAS 67727-97-3.

The interest in this fragment dates to a 1989 report in FASEB Journal, where Hiltz and Lipton found that the COOH-terminal fragment of alpha-MSH retained activity on its own, reporting that "alpha-MSH [11-13] inhibited swelling in a dose-related fashion" in a mouse ear-swelling model (Hiltz & Lipton, FASEB J 1989; PMID 2550304). That observation, that the smallest fragment carried the activity, is why a tripeptide became a subject of study at all.

For laboratory work, the relevant point is that KPV is a reference material: a defined tripeptide characterized by analytical identity and purity, not by any outcome in a person.

What the research reports: NF-kB signaling and PepT1 uptake

The most-cited KPV paper is a 2008 study in Gastroenterology. Dalmasso and colleagues reported that "nanomolar concentrations of KPV inhibit the activation of NF-κB and MAP kinase" in human intestinal epithelial cells and T cells, and that the peptide entered cells through the PepT1 di- and tripeptide transporter rather than through a melanocortin receptor (Dalmasso et al., Gastroenterology 2008; PMID 18061177). The same work reported reduced inflammation in mouse DSS and TNBS colitis models.

A 2012 paper in International Journal of Physiology, Pathophysiology and Pharmacology examined the mechanism more closely in human bronchial epithelial cells in vitro, reporting that "KPV and γMSH evoked a dose-dependent inhibition of NFκB, matrix metalloproteinase-9 activity" (Land, Int J Physiol Pathophysiol Pharmacol 2012; PMID 22837805).

The receptor question was addressed directly in 2003, when Getting and colleagues dissected the core and C-terminal alpha-MSH peptides and concluded that "KPV is unlikely to mediate its effects through melanocortin receptors" (Getting et al., J Pharmacol Exp Ther 2003; PMID 12750433). A 2004 study in Journal of Investigative Dermatology was consistent with this, reporting that "no elevation in cyclic AMP was detected in either HaCaT or normal human keratinocytes" after exposure (Elliott et al., J Invest Dermatol 2004; PMID 15102092). This receptor-independence is the distinguishing feature of KPV in the melanocortin literature.

Further murine colitis work was published the same year as the Dalmasso paper, reporting that "the melanocortin-derived tripeptide KPV showed significant anti-inflammatory effects in 2 murine models of colitis" (Kannengiesser et al., Inflamm Bowel Dis 2008; PMID 18092346), and a 2016 study in Cellular and Molecular Gastroenterology and Hepatology extended the PepT1 line of investigation into a colitis-associated cancer model (Viennois et al., Cell Mol Gastroenterol Hepatol 2016; PMID 27458604).

Research-findings table: what studies describe

The table below summarizes how the cited publications describe KPV. It reflects published research observations and study context, not outcomes for any reader, and contains no dosing or therapeutic guidance.

Attribute (per literature)	What the research describes	Representative citation
Molecule	Lysine-proline-valine tripeptide; C16H30N4O4; MW 342.43; CAS 67727-97-3	PubChem CID 125672
Origin	C-terminal fragment (residues 11 to 13) of alpha-MSH	PMID 2550304
Cellular uptake	Reported as PepT1-mediated transporter uptake	PMID 18061177
Signaling (in vitro)	Reported inhibition of NF-kB and MAP kinase at nanomolar concentrations	PMID 18061177 · PMID 22837805
Receptor pharmacology	Described as unlikely to act through melanocortin receptors; no cAMP elevation reported	PMID 12750433 · PMID 15102092
Animal models	Murine colitis models (DSS, TNBS)	PMID 18092346
Controlled human data	None identified. No clinical trials indexed in PubMed or registered on ClinicalTrials.gov	PubMed / ClinicalTrials.gov searches, July 2026

Table reflects how third-party publications describe this compound in research contexts. It is not a statement of effectiveness, safety, or suitability for any use in humans.

Why the KPV evidence base is small, and why that matters

A PubMed title-level search for KPV returns roughly fourteen records in total, and several of those are drug-delivery-vehicle papers in which KPV is the cargo rather than the subject. The 2017 Molecular Therapy nanoparticle study, for example, is primarily about hyaluronic-acid-functionalized carriers (Xiao et al., Mol Ther 2017; PMID 28143741). That is the entire title-level literature on this tripeptide.

Two distinctions are worth stating plainly, because they are frequently blurred:

Human cells are not human data. The keratinocyte and bronchial-epithelial studies above used human cell lines in culture. That is in vitro work, not evidence about people.
Ex vivo tissue is not a human study. A 2017 iontophoresis paper carries "human skin" in its title but was conducted on excised skin in a diffusion cell (Pawar et al., J Pharm Sci 2017; PMID 28343991). It involved no living subjects.

Filtering PubMed to clinical trials and randomized controlled trials returns no results for KPV, and ClinicalTrials.gov lists zero registered studies. The accurate research-voice summary is that KPV's mechanistic and animal literature is coherent and consistent, while controlled human evidence does not exist. Broader reviews of alpha-MSH-related peptides describe the class in similar mechanistic terms (Luger & Brzoska, Ann Rheum Dis 2007; PMID 17934097; Brzoska et al., Adv Exp Med Biol 2010; PMID 21222263).

For laboratory use, KPV is selected and handled as a reference material defined by analytical attributes: identity (for example by mass spectrometry) and purity (for example by HPLC). Those attributes, documented on a batch-specific Certificate of Analysis, are the appropriate basis for choosing a research compound. Our approach to reading those reports is covered in how to read a peptide COA.

Sourcing COA-verified KPV

Nox Amino stocks research-grade reference materials with batch-specific Certificates of Analysis. To view COA-verified KPV, see the product detail page at /shop/kpv, or review the current batch report at /coas/NoxR2605270158. KPV is also a constituent of the KLOW blend. Browse the full catalog at /shop.

Create a free account to view COA-verified KPV, access batch-specific analytical data, and see member pricing. → Create your account

This article cites third-party research and registry records for informational and laboratory-research purposes only. Nox Amino sells research compounds intended for laboratory and analytical use only, not for human or animal consumption. Nothing on this page is medical advice. Editorial methodology and review process: /learn/editorial-standards.

Frequently Asked Questions

What is KPV?

KPV is a tripeptide composed of lysine, proline, and valine. PubChem (CID 125672) lists it under the synonyms alpha-MSH (11-13) and MSH (11-13), which identifies it as the C-terminal three-residue fragment of alpha-melanocyte-stimulating hormone. Its molecular formula is C16H30N4O4 with a molecular weight of 342.43 and CAS 67727-97-3. As stocked by Nox Amino, KPV is a reference material for laboratory research use only, characterized by identity and purity rather than by any effect in a person.

What does the published research report about KPV?

The published literature is centered on inflammatory signaling in laboratory models. Dalmasso et al. (Gastroenterology 2008, PMID 18061177) reported that nanomolar concentrations of KPV inhibited activation of NF-kB and MAP kinase in intestinal epithelial cells, and that uptake was mediated by the PepT1 transporter. Land (Int J Physiol Pathophysiol Pharmacol 2012, PMID 22837805) reported dose-dependent inhibition of NF-kB in human bronchial epithelial cells in vitro. These describe findings in research models, not outcomes for any individual.

Are there human studies on KPV?

No. A PubMed search filtered to clinical trials and randomized controlled trials returns no results for KPV, and a ClinicalTrials.gov query returns zero registered studies. Every biological finding in the KPV literature comes from in vitro work or animal models. Some studies use human cell lines, such as HaCaT keratinocytes or 16HBE14o- bronchial cells, but human cells in culture are not human subject data. The accurate summary is that KPV has no controlled human evidence of any kind.

How does KPV relate to alpha-MSH?

KPV corresponds to residues 11 to 13 of alpha-melanocyte-stimulating hormone. Hiltz and Lipton (FASEB J 1989, PMID 2550304) first reported that this C-terminal fragment carried anti-inflammatory activity in a mouse model independently of the full peptide. Getting et al. (J Pharmacol Exp Ther 2003, PMID 12750433) later reported that KPV is unlikely to mediate its effects through melanocortin receptors, which is why the literature discusses it as receptor-independent rather than as a melanocortin agonist.

How do I verify the identity and purity of a research peptide like KPV?

Identity and purity are documented on a batch-specific Certificate of Analysis (COA), typically using mass spectrometry for identity and HPLC for purity. These analytical attributes, not biological outcomes, are the appropriate basis for selecting a research compound. You can review the KPV COA and other batch reports on the /coas page, and create a free account to access batch-specific analytical data and member pricing.