KPV

What Is KPV?

KPV is a synthetic tripeptide consisting of L-lysine, L-proline, and L-valine (Lys-Pro-Val) corresponding to amino acid residues 11 through 13, the C-terminal tripeptide, of α-melanocyte-stimulating hormone (α-MSH).

The 13-residue parent peptide α-MSH is widely studied in the published melanocortin and inflammation research literature; KPV is examined as the minimal C-terminal fragment that retains a substantial portion of the parent peptide’s anti-inflammatory profile in published research models.

A defining feature in the published literature is that, unlike full-length α-MSH, KPV does not appreciably activate melanocortin receptors (MC1R-MC5R) and therefore is not associated with melanogenesis in research models. Its activity in published research is examined through alternative pathways, principally the inhibition of pro-inflammatory transcription factor signaling.

KPV in Plain Language

A non-technical overview of what KPV is, what researchers have studied it for, what early evidence suggests, and what cannot be claimed about it. For research and educational purposes only.

At a glance

KPV is a very small peptide, only three amino acids long, derived from a natural skin and immune hormone (called alpha-MSH), with the pigmentation-causing part removed. In published research, scientists study it for its ability to calm inflammation by quieting the cell-signaling pathways behind it, without suppressing the immune system the way traditional anti-inflammatory drugs do.

Active research areas include gut inflammation (such as ulcerative colitis), skin conditions like eczema, asthma, mouth sores, and overactive immune responses. The compound sold here is a research chemical, not a pharmaceutical, and is not for human or animal use.

What it is

KPV is a synthetic tripeptide made of three amino acids: lysine, proline, and valine (Lys-Pro-Val). Its sequence is identical to the last three amino acids (the C-terminal end) of a much longer natural peptide called α-melanocyte-stimulating hormone (α-MSH), which has been studied in published immunology and skin-biology literature for decades.

One thing that makes KPV interesting to researchers is that, unlike full-length α-MSH, KPV does not meaningfully activate the melanocortin receptors that drive skin pigmentation. Yet in cell and animal experiments, this small fragment still appears to retain a notable portion of the parent peptide’s effects on inflammatory signaling.

Researchers commonly study KPV in laboratory contexts related to inflammation and gut-lining biology.

Research areas being investigated

• Inflammation-pathway research: Studied in cell experiments for effects on NF-κB and p38 MAP-kinase signaling, two of the master switches that turn inflammatory genes on and off.
• Cytokine research: Examined for effects on pro-inflammatory signals such as TNF-α, IL-6, and IL-8 in cell culture.
• Gut-lining research: Investigated in animal models of inflammatory bowel disease, including DSS- and TNBS-induced colitis in rodents.
• Peptide-transporter (PepT1) research: KPV is studied as a substrate of the PepT1 transporter (SLC15A1), which is upregulated in inflamed gut tissue, a mechanism researchers use to investigate tissue-selective peptide uptake.
• α-MSH structure-activity research: Used to dissect which parts of α-MSH are responsible for which biological effects.
• Mast-cell research: A smaller body of preclinical work has examined KPV in histamine-release model systems.

What the research suggests so far

Animal / preclinical findings. Most published KPV evidence comes from rodent inflammatory-bowel-disease (colitis) models, primarily DSS- and TNBS-induced colitis in mice and rats. In these studies, researchers have reported observations consistent with reduced disease-activity scores, lower colonic pro-inflammatory cytokine expression, and improved tissue-level inflammation scores.

Additional preclinical work has examined KPV in colitis-associated cancer models that involve the PepT1 transporter. These findings do not, on their own, demonstrate the same effects in humans.

Cell / lab findings. In cell-culture experiments, KPV has been described as suppressing NF-κB nuclear translocation, inhibiting p38 / MAPK phosphorylation, and reducing the expression of pro-inflammatory cytokines (TNF-α, IL-6, IL-8) at nanomolar concentrations. Mechanistic work has also characterized KPV as a PepT1 substrate, providing a route for selective uptake in inflamed intestinal tissue.

These findings inform hypotheses about how KPV might act in tissue, but they remain mechanistic and several steps removed from clinical outcomes.

Human findings. Human evidence for KPV itself is very limited. There are no large, published Phase III randomized controlled trials demonstrating efficacy for any condition. The broader α-MSH-related peptide literature includes some early-phase work, but this does not transfer directly to KPV. KPV is not approved by the FDA, EMA, or other major regulators for any use.

Limitations of the evidence. The KPV literature is dominated by cell-culture and rodent colitis-model work. Long-term human safety data, large-scale efficacy trials, and standardized human dosing studies are lacking. Independent multi-laboratory replication is uneven. Reviewers in the peer-reviewed literature have specifically called out the need for more rigorous human studies before any therapeutic conclusions can be drawn.

Research relevance

KPV is most often discussed in research involving inflammation pathways (NF-κB, p38 MAPK), pro-inflammatory cytokine biology, gut inflammation models, PepT1-transporter biology and tissue-selective peptide uptake, and the structure-activity of α-MSH-derived peptides. Most published findings are preclinical, so it should not be presented as a proven treatment for any condition.

Its scientific interest lies in its potential use as a research tool for studying inflammation and gut-lining biology in the laboratory.

What cannot be claimed about KPV

• It cannot be claimed to treat, cure, heal, or repair any human or animal condition.
• It cannot be claimed to treat inflammatory bowel disease, ulcerative colitis, Crohn’s disease, or leaky gut in humans.
• It cannot be claimed to treat skin conditions such as eczema, psoriasis, acne, or rosacea.
• It cannot be claimed to treat allergies, asthma, or autoimmune disease.
• It cannot be claimed to be safe or effective for human or veterinary use.
• It cannot be claimed to be approved by the FDA or any other regulatory authority.

Summary

KPV is a synthetic tripeptide (lysine-proline-valine) corresponding to the last three amino acids of α-melanocyte-stimulating hormone (α-MSH). It is studied in laboratory and animal research related to inflammation pathways, pro-inflammatory cytokine biology, gut inflammation models, and PepT1-transporter biology. Published evidence comes mainly from cell-culture work and rodent colitis models; human evidence is very limited.

KPV is not approved by the FDA or any other regulatory authority and is sold here strictly as a research-use-only chemical for laboratory investigation. It is not intended for human consumption, medical use, or veterinary use.

Short version

KPV is a synthetic tripeptide derived from the C-terminus of α-MSH, most often studied in cell and animal research on inflammation pathways and gut-lining biology. Human evidence is very limited and it is not approved for any medical use. Sold for research and laboratory use only.

Source notes

• Brzoska T, et al. Alpha-melanocyte-stimulating hormone and related tripeptides, biochemistry, anti-inflammatory and protective effects in vitro and in vivo, and future perspectives for the treatment of immune-mediated inflammatory diseases. Endocr Rev, 2008, review article. (PMC2095288.)
• Dalmasso G, et al. PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation. Gastroenterology, 2008, animal/cell study. (PMC2431115.)
• Charrier L, Merlin D. The oligopeptide transporter PepT1 in inflammation and inflammatory bowel disease. Lab Invest, 2006, review article. (PMC3311434.)
• Viennois E, et al. The critical role of PepT1 in colitis-associated cancer and therapeutic benefits of KPV. Cell Mol Gastroenterol Hepatol, 2016, animal/cell study.
• KPV tripeptide, encyclopedic reference (Wikipedia, secondary source).

Source types: entries 1, 3 are review articles; entries 2, 4 are animal / cell-culture studies; entry 5 is a secondary reference work.

SEO meta description

KPV is a synthetic tripeptide (Lys-Pro-Val) studied in preclinical research on inflammation pathways, gut-lining biology, and the PepT1 transporter. Research-use only.

Reminder. BioChain USA sells KPV strictly as a research-use-only chemical for qualified laboratory and educational use. It is not intended for human consumption, medical treatment, veterinary treatment, diagnosis, prevention, or cure of disease.

Certificate of Analysis (COA)

• COA provided where available for the specific batch shipped.
• The batch COA is the authoritative reference for analytical methods, purity data, and lot-specific testing for that shipment.
• COA information is batch-specific and is not interchangeable between lots.

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