KPV — Alpha-MSH-derived tripeptide fragment. 3-residue sequence shown as a side-chain class strip (1 basic, 2 nonpolar). Molecular weight 342.43 g/mol.
Healing & Recovery

KPV

Alpha-MSH-derived tripeptide fragment

A C-terminal tripeptide of α-MSH studied in inflammation and tissue-repair research.

Also referenced as: Lys-Pro-Val, alpha-MSH (11-13)

3 aa
For research and educational purposes only. This page is a factual research reference, not medical advice. Any dosing figures shown are amounts reported in the research literature, provided for educational context — not instructions or recommendations for human use.

Overview

KPV is a synthetic tripeptide corresponding to the C-terminal three amino acids (lysine-proline-valine) of alpha-melanocyte-stimulating hormone (alpha-MSH), a naturally occurring melanocortin peptide. It is studied as a fragment that retains some anti-inflammatory properties of the parent hormone.

At a glance

ClassAlpha-MSH-derived tripeptide fragment
CategoryHealing & Recovery
SequenceLys-Pro-Val
Chain length3 amino acids
Molecular weight342.43 g/mol
Typical formLyophilized powder
AliasesLys-Pro-Val, alpha-MSH (11-13)
Use designationResearch / in-vitro only
Regulatory statusKPV is research-only and not approved as a drug. Educational information only, not medical advice.

What KPV does

KPV is a tripeptide (lysine-proline-valine) corresponding to the C-terminal residues 11-13 of alpha-melanocyte-stimulating hormone (alpha-MSH), the anti-inflammatory portion of that melanocortin hormone. What KPV does, in research models, is deliver alpha-MSH's anti-inflammatory activity while shedding the parent hormone's pigmentation and other systemic effects. It acts as a small, targeted anti-inflammatory and epithelial-protective agent, of particular interest for the gut and skin.

Mechanistically, KPV appears to work both at the cell surface and inside the cell. It can signal through melanocortin receptors (notably MC1R), but a key feature is that it is taken up into cells, in intestinal epithelium via the PepT1 peptide transporter, where it interferes with the NF-kB and MAP-kinase inflammatory signaling cascades. The result is reduced transcription and release of pro-inflammatory cytokines such as TNF-alpha, IL-6, and IL-8. It also has reported direct antimicrobial and anti-fungal activity, and helps preserve epithelial barrier integrity, which is relevant to inflamed or leaky gut and skin tissue.

The evidence is preclinical. In cultured intestinal epithelial and immune cells and in mouse colitis models, KPV has reduced inflammation and tissue damage at very low (nanomolar) concentrations, and oral or nanoparticle delivery has been explored to target the colon. There are no substantial human clinical trials, so its use for inflammatory or gut conditions remains experimental and its human efficacy unproven.

Effects reported in research

  • Inhibited NF-kB and MAP-kinase inflammatory signaling in intestinal epithelial and immune cells at nanomolar concentrations (in-vitro).
  • Reduced pro-inflammatory cytokine output including TNF-alpha, IL-6, and IL-8 (in-vitro).
  • Decreased inflammation and mucosal damage in mouse models of colitis (animal only).
  • Taken up into intestinal epithelial cells via the PepT1 transporter, enabling intracellular anti-inflammatory action.
  • Retains alpha-MSH's anti-inflammatory activity without its pigmentation/hormonal effects.
  • Reported direct antimicrobial and anti-fungal activity against certain pathogens (in-vitro).
  • Supported epithelial barrier integrity in gut and skin models, relevant to inflamed or permeable tissue (preclinical).
  • No substantial human clinical trial evidence exists; applications remain preclinical/experimental.

Effects listed reflect findings reported in the research literature — many in animal or in-vitro models. Listing an effect is not a claim of efficacy or a therapeutic indication in humans.

Mechanism of action

KPV is reported in preclinical studies to exert anti-inflammatory effects, and research has explored both melanocortin-receptor-dependent signaling and intracellular actions independent of classic MSH pigmentation activity. It has been studied for downregulation of pro-inflammatory signaling such as NF-kB-associated pathways in cell and animal models of colitis. These findings derive from in-vitro and rodent research.

Mechanistic description reflects published research-literature understanding. Much peptide research is preclinical (in-vitro or animal-model); mechanism in humans may differ and is not established for many compounds.

What it's studied for

Research contexts in which KPV appears in the literature. Listing a research area is not a claim of efficacy or a therapeutic indication.

Intestinal inflammation and colitis models (preclinical)Anti-inflammatory signaling (in-vitro)Skin inflammation (preclinical)Melanocortin pathway biology

Key characteristics

  • A three-amino-acid C-terminal fragment of alpha-MSH
  • Retains anti-inflammatory activity of the parent hormone in preclinical models without its pigment-stimulating effect
  • Studied particularly in gastrointestinal inflammation models
  • Evidence base is preclinical (cell and animal studies)
  • Not an approved drug

Reported research dosing reference only

Educational reference, not dosing guidance. The figures below summarize amounts reported in published research and research-community protocols, provided for educational and research context only. They are not medical advice, not a recommendation, and not instructions for human use. KPV is a research compound.

KPV research is largely preclinical and in vitro, so there is no well-established human research-dosing standard; reported figures are experimental concentrations and animal-model doses. These are research-context reference figures only, not dosing guidance.

  • In vitro skin research: e.g. KPV applied around 50 mcg/mL in keratinocyte experiments
  • Animal colitis models: microgram-range experimental dosing (study-specific)
ReconstitutionSupplied lyophilized; reconstituted with bacteriostatic water, swirled not shaken, stored refrigerated after reconstitution

Very small tripeptide (MW ~342 Da); evidence base is preclinical with no confirmed human dosing. Often co-formulated in the KLOW research blend.

How it compares

KPV is distinguished by its melanocortin-pathway anti-inflammatory focus, in contrast to the antimicrobial LL-37 or the tissue-repair emphasis of BPC-157 and TB-500.

Commonly studied alongside

Compounds frequently researched together with KPV in the literature. Cross-referenced for research context — not a usage or combination recommendation.

Compare and calculate

Side-by-side pages for the pairings the literature already documents for KPV, plus the unit-conversion reference for a reconstituted vial. Factual comparisons of documented characteristics — not a recommendation to combine or use any compound.

Handling & Stability

Lyophilized peptides are stored cold, protected from light, and reconstituted only at the time of intended in-vitro work.

  • Avoid repeated freeze-thaw cycles
  • Verify supplier lot and Certificate of Analysis
  • Follow institutional lab-safety protocols

Analytical & COA Concepts

Reputable research suppliers publish a third-party Certificate of Analysis per batch. Key analytical concepts referenced in COAs include:

Category Context

KPV sits in the Healing & Recovery area of the PeptiDex library.

Research Supplier Listing

Where researchers source KPV

For researchers studying KPV, third-party suppliers such as Practically Natty Peptides offer research-grade material, third-party tests every batch and provides Certificates of Analysis on request, and ship from the US.

View research-supplier listing →

Outbound link to a third-party research supplier. Inclusion does not constitute endorsement; all editorial content is developed independently.

Frequently asked questions

What is KPV?

KPV is the C-terminal tripeptide (lysine-proline-valine) of alpha-melanocyte-stimulating hormone (alpha-MSH). It retains much of the parent hormone's anti-inflammatory activity while lacking its pigment-stimulating (melanocortin) effects. It is studied as a small anti-inflammatory peptide rather than as an approved therapeutic.

What is KPV studied for?

Preclinical research examines KPV for anti-inflammatory effects, particularly in models of intestinal inflammation and colitis, as well as skin inflammation. It is reported to enter cells and inhibit NF-kB signaling and pro-inflammatory cytokine production, and it can be transported into intestinal cells via the PepT1 transporter. No human clinical trials have confirmed these effects.

How does KPV produce anti-inflammatory effects without affecting pigmentation?

KPV corresponds only to the C-terminal tripeptide of alpha-MSH, so it preserves the anti-inflammatory activity associated with that region while omitting the sequence needed to activate melanocortin receptors that drive pigmentation. Mechanistically it is described as acting intracellularly on the NF-kB pathway, including inhibition of IkB kinase.

Why is KPV of interest for gut-inflammation research?

KPV is a substrate for the PepT1 peptide transporter, which is upregulated in inflamed intestinal tissue, so it can be taken up at sites of inflammation. In animal colitis models this uptake is associated with reduced NF-kB-driven cytokine production. This targeting rationale is why it appears frequently in gut-repair research discussions.

Is KPV an approved drug?

No. KPV is a research compound with no regulatory approval, and its evidence base is preclinical. It is often included in tissue-repair research blends such as KLOW for its anti-inflammatory contribution.

Answers are educational summaries of research-literature context and do not constitute medical advice. See the Research Library, COA guide, and Storage & Handling guide for more.

References

Primary literature indexed in PubMed for KPV. Listing a study records that it exists and is indexed — it is not a claim of efficacy, a therapeutic indication, or an endorsement of its conclusions. Much of this literature is preclinical (in-vitro or animal-model).

  1. Melanocortin-derived tripeptide KPV has anti-inflammatory potential in murine models of inflammatory bowel disease Inflamm Bowel Dis, 2008. PubMed 18092346
  2. Orally Targeted Delivery of Tripeptide KPV via Hyaluronic Acid-Functionalized Nanoparticles Efficiently Alleviates Ulcerative Colitis Mol Ther, 2017. PubMed 28143741

Each reference was checked against its PubMed record on 2026-07-28: the PMID resolves and the title, journal and year match. Where no indexed literature exists for a compound, PeptiDex says so rather than substituting a citation about a different molecule. See the editorial policy.

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Further reading