
BPC-157
Stable gastric pentadecapeptide, a staple of tissue-repair research.

Alpha-MSH derived tripeptide studied in inflammation research.
KPV 10 mg
Your order ships with the certificate for its own lot.
Alpha-MSH derived tripeptide studied in inflammation research.
10 mg per vial, as a lyophilized powder in a sealed glass vial with a crimped cap. The lot number on the label matches the certificate of analysis in the COA library.
Store lyophilized powder frozen (−20 °C) or refrigerated, sealed and away from light. Once reconstituted, keep refrigerated (2–8 °C).
Handle in a laboratory setting using appropriate protective equipment. Consult the certificate of analysis and safety data for lot-specific information.
KPV is the tripeptide Lys-Pro-Val, the three C-terminal amino acids (positions 11 to 13) of alpha-melanocyte-stimulating hormone (alpha-MSH). Researchers study it because it keeps much of alpha-MSH's anti-inflammatory activity in experimental models without alpha-MSH's pigmentary effect. Most of the published work is in cell culture and mouse models of intestinal inflammation (colitis).
Alpha-MSH is a 13-amino-acid peptide cleaved from proopiomelanocortin. Best known for its role in pigmentation, it has also been studied for anti-inflammatory and protective effects mediated through melanocortin receptors1. Its C-terminal tripeptide, alpha-MSH(11-13) or KPV, was singled out as an anti-inflammatory candidate because it keeps that activity in experimental models while lacking the pigmentary action that limits alpha-MSH itself1,2.
At three residues and a molecular weight of about 342 Da, KPV is one of the smallest peptides in research use. The KPV supplied here is the unmodified tripeptide as a lyophilized powder, and every lot ships with a lot-matched certificate of analysis (HPLC purity and mass-spec identity) from an independent lab, published in the certificate library.
Two findings set KPV apart from its parent hormone. First, it appears to act largely without melanocortin receptors. In a mouse peritonitis model, its effect on leukocyte migration was not blocked by an MC3/MC4 receptor antagonist, it did not raise cAMP in macrophages, and it stayed active in mice with a nonfunctional MC1 receptor; the authors proposed inhibition of IL-1beta signaling instead3. Colitis studies reported similar MC1R-independent activity4.
Second, its size lets it enter cells through PepT1, a di- and tripeptide transporter normally expressed in the small intestine and induced in the colon during inflammation. In human intestinal epithelial cells and T cells, nanomolar KPV inhibited NF-κB and MAP kinase signaling and reduced pro-inflammatory cytokine secretion, an effect that depended on PepT15. In human bronchial epithelial cells, KPV entered the nucleus and interfered with nuclear import of the NF-κB subunit p656.
Most KPV studies use mouse colitis models, with a smaller number in other tissues:
We found no human clinical trial of KPV indexed in PubMed; the evidence is cell culture and animal models, chiefly mice. Much of the colitis work, including the PepT1 and nanoparticle studies, comes from one research group5,7,8,9, so independent replication is limited. Several of the strongest results used engineered delivery systems, which may not reflect the behavior of the free peptide7,8. A 2023 review of the melanocortin system in inflammatory bowel disease notes that the evidence for these peptides comes largely from mouse colitis models11.
For how KPV compares with the most-studied gastric repair peptide, see KPV vs BPC-157. KPV is also one of the four components of the KLOW Blend.
No. KPV is only the last three amino acids (Lys-Pro-Val, positions 11 to 13) of the 13-residue hormone alpha-MSH1. It keeps anti-inflammatory activity in experimental models but lacks alpha-MSH's pigmentary effect, and it appears to act largely without melanocortin receptors1,3.
In intestinal epithelial and immune cells, KPV is carried in by PepT1, the transporter that normally absorbs di- and tripeptides from food. Cell studies indicated that its anti-inflammatory effect depends on PepT15, and KPV had no effect on tumor development in PepT1-knockout mice9.
No. KPV is not an approved drug, and we found no published human trials. It is not named on the World Anti-Doping Agency's 2026 Prohibited List, although WADA's class S0 covers any pharmacological substance without government approval for human therapeutic use.
KPV is a three-residue fragment of alpha-MSH studied mainly as an inhibitor of inflammatory signaling in mouse colitis5. BPC-157 is a 15-residue gastric peptide studied more broadly in tissue-repair models. Their research overlaps in gut inflammation, which is covered in KPV vs BPC-157.
Like most lyophilized research peptides, it is generally kept sealed, cold, dry and protected from light. Our peptide storage guide covers the general principles.
Research summary reviewed 2026-10-26 against the cited literature.

Stable gastric pentadecapeptide, a staple of tissue-repair research.

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