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KPV (Lysine-Proline-Valine) 250mcg/60caps
During our packaging transition, you may receive products with either our previous or updated label. Rest assured, the formulation, purity and quality remain exactly same as standards.
KPV (Lysine-Proline-Valine) is the C-terminal tripeptide fragment of alpha-melanocyte-stimulating hormone (alpha-MSH), corresponding to residues 11-13 and also present within the corresponding region of adrenocorticotropic hormone (ACTH). Research interest centers on KPV's reported melanocortin receptor-independent activity in cell-based inflammatory signalling models, distinguishing it from full-length melanocortin receptor agonists. Research applications include melanocortin fragment structure-activity studies, NF-κB pathway investigation, and tripeptide stability/delivery research.
- High Purity – 99% Purity Guaranteed
- Independently Lab Tested
- Research Grade Quality
- For Laboratory Research Use Only
3D Molecular Structure
Drag to rotate · scroll to zoom| Chemical Formula | C16H30N4O4 |
|---|---|
| Synonyms | Lys-pro-val, L-Valine, N-(1-L-lysyl-L-prolyl)-, Msh (11-13), L-Lysyl-L-prolyl-L-valine, Lysyl-prolyl-valine, ACTH-(11-13) |
| Molar Mass | 342.43 g/mol |
| CAS Number | 67727-97-3 |
| PubChem CID | 125672 |
| Total Compound Content | 15mg (250mcg/capsule) |
| Shelf Life | 36 months |
Every batch is independently lab tested for identity, purity and potency. View our lab testing program →
How does KPV's proposed mechanism differ from full-length alpha-MSH's melanocortin receptor activity?
Full-length alpha-MSH activates the canonical melanocortin receptors (primarily MC1R), a G protein-coupled receptor pathway producing cAMP-dependent downstream signalling. KPV, as a minimal C-terminal tripeptide fragment, is investigated for effects in cell-based models (including NF-κB transcriptional readouts) that appear to occur with reduced dependence on classical MC1R-mediated signalling, making it a research tool for distinguishing melanocortin receptor-dependent from receptor-independent peptide activity. Researchers studying this distinction typically use MC1R antagonists or receptor-knockout/knockdown models alongside KPV exposure to determine the receptor-dependence of observed effects.
What cell-based assays are used to study KPV's effects on NF-κB signaling?
Standard approaches include NF-κB-responsive luciferase reporter assays in cell lines stimulated with a pro-inflammatory trigger (such as LPS or TNF-α) with and without KPV co-treatment, alongside direct measurement of NF-κB nuclear translocation by immunofluorescence or Western blot of nuclear/cytoplasmic fractions. Downstream readouts often include quantification of NF-κB target gene products (pro-inflammatory cytokines, chemokines) by ELISA or qPCR to characterise the functional consequence of any observed transcriptional modulation.
Why is KPV used as a tool for studying the shared C-terminal sequence of alpha-MSH and ACTH?
Because the Lys-Pro-Val sequence is conserved in both alpha-MSH and ACTH at the same relative position, KPV serves as a minimal structural probe for research questions about which biological activities of these larger peptide hormones map to this specific C-terminal motif versus other regions of the parent sequence. Comparative studies using KPV alongside other fragments of alpha-MSH/ACTH (such as the N-terminal or central regions) allow researchers to build structure-activity maps of the full hormone sequence.
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