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KPV: Compound Profile

KPV is the smallest peptide in the tissue-repair class and the anti-inflammatory specialist among its compounds. This profile covers its identity, the mechanism the literature attributes to it, and how it fits the class. It is also a component of the KLOW research blend. For the wider class, see the tissue-repair peptides overview.

What is KPV?#

KPV is a tripeptide made of lysine, proline, and valine, corresponding to the C-terminal segment (residues 11-13) of α-melanocyte-stimulating hormone (α-MSH). Although it derives from a melanocortin sequence, its studied activity is anti-inflammatory and is generally reported to act independently of the melanocortin receptors, which distinguishes it from the melanocortin agonists. Its small size is central to how it is studied, since short peptides reach intracellular compartments more readily than larger ones.

AttributeValue
Common nameKPV (lysine-proline-valine)
ClassAnti-inflammatory tripeptide; C-terminal α-MSH fragment
SequenceLys-Pro-Val (KPV)
Molecular weight≈ 342.4 g/mol
CAS number67727-97-3
Primary study areaInflammatory-signaling and intestinal-barrier research
KPV molecular identity, as commonly reported in the literature and chemical databases.
Two-dimensional structure of KPV, a tripeptide Lys-Pro-Val (α-MSH C-terminal fragment). Surgical-green heteroatoms (N, O) over a white skeleton on a dark background.
KPV · tripeptide Lys-Pro-Val (α-MSH C-terminal fragment) · structure rendered from PubChem CID 13294447 via RDKit.

What does the research literature study?#

The KPV literature centers on anti-inflammatory activity, with reported effects on inflammatory-signaling pathways such as NF-κB and on pro-inflammatory cytokine levels. A recurring research theme is intestinal-barrier and gut-inflammation models, where the tripeptide's small size and reported uptake are studied. As with the rest of the class, this is preclinical research and does not establish outcomes in people.

Where KPV sits in the tissue-repair class#

KPV is the anti-inflammatory member of the class, complementing the angiogenic (BPC-157), cytoskeletal (TB-500), and matrix (GHK-Cu) mechanisms of the other compounds. That mechanistic breadth is why it is one of the four components of the KLOW research blend. The class is mapped in the tissue-repair cornerstone.

Handling and storage#

KPV ships as a lyophilized powder for reconstitution. As a very small tripeptide it is comparatively stable, though handling still follows standard practice: the reconstitution primer covers solvent selection, and the cold-chain article covers storage of reconstituted material.

Nexara catalogs KPV (10mg) at ≥99% purity for laboratory research. Independent third-party COA delivery is paused during the laboratory-partner transition; see research compliance.

Frequently asked

What is KPV?
KPV is a tripeptide (Lys-Pro-Val) corresponding to the C-terminal three residues of α-melanocyte-stimulating hormone. Research studies it for anti-inflammatory activity, reportedly via inflammatory-signaling pathways such as NF-κB, and in intestinal-barrier models. It is a laboratory research compound and is not for human use.
Is KPV a melanocortin peptide?
KPV derives from the C-terminal sequence of α-MSH, a melanocortin, but its studied anti-inflammatory activity is generally reported to act independently of the melanocortin receptors. That makes it distinct from the melanocortin agonists like PT-141 and Melanotan-2, despite the shared parent sequence.
Why is KPV in the KLOW blend?
KLOW combines four peptides with complementary mechanisms: GHK-Cu (matrix), BPC-157 (angiogenic signaling), TB-500 (cytoskeletal), and KPV (anti-inflammatory). KPV contributes the anti-inflammatory arm. In research the blend is studied for the combined activity of its separate components, not for an additive-benefit claim.

Sources and further reading#

For research use only. Not for human consumption, diagnosis, treatment, or prevention of any disease. All products are intended solely for laboratory research purposes.

Last updated: 2026-05-27