KPV is the C-terminal tripeptide (Lys-Pro-Val) of alpha-melanocyte-stimulating hormone (α-MSH), and in laboratory and animal models it has been studied for its ability to dampen pro-inflammatory signaling — notably the NF-κB and MAP-kinase pathways — at nanomolar concentrations without the pigmentary activity of the parent hormone. This article summarizes the research background, proposed mechanism, published literature, and handling guidance for KPV as a research compound. All information is provided strictly for in-vitro and laboratory research use only.
What Is KPV?
KPV corresponds to residues 11–13 of α-MSH, whose full sequence is SYSMEHFRWGKPV. The single-letter code K-P-V denotes lysine, proline, and valine. As a small tripeptide (CAS 67727-97-3; molecular weight ≈342.43 g/mol) it retains much of the anti-inflammatory character associated with α-MSH while lacking the melanocortin-receptor–driven pigmentation signaling of the intact hormone. Because of this, researchers have used KPV as a minimal, well-defined tool for probing how melanocortin-derived sequences influence inflammatory pathways in cultured cells and animal models.
The peptide has been of scientific interest since work in the late 1990s and 2000s established that C-terminal fragments of α-MSH carry anti-inflammatory activity. Investigators have since examined KPV in intestinal epithelial cells, immune cells, and rodent models of colitis. As a freshness marker for readers tracking the field: a 2024 study in Frontiers in Pharmacology described a PepT1-targeted "nanodrug" that co-assembles KPV with an immunosuppressant for combined action in dextran sodium sulfate (DSS)-induced colitis models, indicating the tripeptide remains an active subject of preclinical delivery research. That work concerns laboratory disease models and is noted here only as scientific context; it does not describe or endorse any use of the research compound sold on this page.
Mechanism of Action
A central question in the KPV literature is how such a small peptide produces measurable anti-inflammatory effects. Two mechanistic threads recur across published studies.
NF-κB and MAP-kinase signaling
In human intestinal epithelial cell lines (Caco2-BBE and HT29-Cl.19A) and Jurkat T cells stimulated with pro-inflammatory cytokines such as IL-1β and TNF-α, nanomolar KPV (on the order of 10 nM) has been reported to inhibit activation of the NF-κB pathway — measured by NF-κB–luciferase reporters, preservation of IκB-α from degradation, and reduced phosphorylation of ERK1/2, JNK, and p38 kinases — with a corresponding decrease in interleukin-8 (IL-8) mRNA and protein output (Dalmasso et al., Gastroenterology, 2008). Importantly, in that work the effect did not depend on melanocortin receptors or intracellular cAMP changes in the tested cells, distinguishing KPV's action from classical receptor-mediated α-MSH signaling.
PepT1-mediated uptake
The same research identified the di/tripeptide transporter PepT1 (SLC15A1) as a route by which KPV enters cells. PepT1 is normally expressed in the small intestine and is induced in the colon during inflammatory bowel disease (IBD), providing a plausible mechanism for how an orally delivered tripeptide could reach inflamed intestinal tissue. Uptake experiments using radiolabeled [³H]KPV, with competition by other PepT1 substrates such as Gly-Sar and Gly-Leu, characterized the transport kinetics and supported PepT1 as the carrier. This transporter-based delivery concept has since motivated nanoparticle and prodrug strategies in the laboratory.
Antimicrobial context
Separately, early work reported that α-MSH and its C-terminal KPV fragment exhibited direct antimicrobial activity in vitro against Staphylococcus aureus and Candida albicans, including at low (picomolar) concentrations, an effect linked in part to modulation of cellular cAMP in the microorganisms (Cutuli et al., Journal of Leukocyte Biology, 2000). This places KPV within a broader "host-defense peptide" framing in the literature.
Published Research Overview
A focused peer-reviewed literature has examined KPV in preclinical systems:
- Dalmasso and colleagues (Gastroenterology, 2008) reported that nanomolar KPV inhibits NF-κB and MAP-kinase signaling in human intestinal epithelial and immune cells, that uptake is mediated by PepT1, and that oral KPV reduced the severity of DSS- and TNBS-induced colitis in mice, with lower pro-inflammatory cytokine expression.
- Kannengiesser and colleagues (Inflammatory Bowel Diseases, 2008) found that the melanocortin-derived tripeptide KPV reduced inflammation in two murine colitis models (DSS and CD45RB-high transfer colitis), with earlier weight recovery, reduced histological damage, and lower myeloperoxidase (MPO) activity; effects appeared at least partially independent of melanocortin-1 receptor signaling.
- Cutuli and colleagues (Journal of Leukocyte Biology, 2000) described antimicrobial effects of α-MSH peptides, including the KPV fragment, against representative bacterial and fungal pathogens in vitro.
- Xiao and colleagues (Molecular Therapy, 2017) loaded KPV into hyaluronic-acid–functionalized nanoparticles (~272 nm) designed for oral, colon-targeted delivery, reporting combined anti-inflammatory and mucosal-healing effects in cell and mouse colitis models.
- A 2024 report in Frontiers in Pharmacology described a carrier-free, PepT1-targeted nanodrug co-assembling KPV with the immunosuppressant FK506, accumulating at inflamed sites and outperforming either agent alone in acute and chronic DSS colitis models.
Storage & Handling
Dynamite Research Peptides supplies KPV in lyophilized (freeze-dried) form at 99%+ purity. Store the powder at -20°C, protected from light and moisture; the product carries a stated shelf life of approximately two years when stored properly. Reconstitute immediately before use with a sterile solvent as indicated on the Certificate of Analysis (COA), keep reconstituted material refrigerated, and avoid repeated freeze-thaw cycles that can degrade peptide integrity. Handle with appropriate personal protective equipment in a well-ventilated laboratory setting.
Conclusion
KPV is a compact, well-characterized tool compound for studying melanocortin-derived anti-inflammatory signaling, NF-κB pathway modulation, and PepT1-mediated peptide transport in laboratory models. Our KPV is high-purity, third-party tested, and ships with a COA so experimental results stay reliable and reproducible.
Frequently Asked Questions
What is KPV?
KPV is a tripeptide composed of lysine, proline, and valine that corresponds to the C-terminal fragment (residues 11–13) of α-MSH. It has been studied in cell and animal models for its effects on inflammatory signaling pathways.
How does KPV differ from α-MSH?
KPV is only the last three amino acids of α-MSH. In published cell studies it retains anti-inflammatory activity — such as NF-κB inhibition — but in the systems tested this activity did not require melanocortin receptors, unlike the pigmentation signaling of the full-length hormone.
What is the PepT1 transporter's role in KPV research?
PepT1 (SLC15A1) is a di/tripeptide transporter that research indicates carries KPV into intestinal and immune cells. Because PepT1 expression increases in the colon during inflammation, it has been studied as a delivery route for the peptide in animal models.
What is the purity level of Dynamite Research Peptides' KPV?
Our KPV is typically 99%+ pure, verified by HPLC analysis. Detailed purity data is provided on the Certificate of Analysis (COA) included with each product.
What research applications is KPV suitable for?
It is used in studies of anti-inflammatory peptide mechanisms, NF-κB and MAP-kinase pathway modulation, in-vitro gut inflammation models, and peptide-transport (PepT1) biology.
All products are for research use only — not for human or animal consumption, and not for diagnostic or therapeutic use. Last updated: July 15, 2026.