KPV 10mg

KPV is the synthetic C-terminal tripeptide of alpha-melanocyte-stimulating hormone (α-MSH), corresponding to residues 11–13 of the tridecapeptide and carrying the amino acid sequence Lys-Pro-Val. The parent hormone, α-MSH, is derived by post-translational processing of proopiomelanocortin (POMC) and exerts its anti-inflammatory signalling principally through melanocortin receptors (MC-Rs) expressed on immune and peripheral somatic cells. Critically, KPV retains the anti-inflammatory activity of the full α-MSH sequence while lacking the pigmentary action attributable to the N-terminal pharmacophore — a distinction that has made the tripeptide a subject of sustained in vitro and pre-clinical investigation.^[1] AbsoluteBioLab supplies KPV as a lyophilised acetate salt, manufactured to analytical grade (≥99.0% HPLC purity) and verified by electrospray ionisation mass spectrometry (ESI-MS) prior to release. Each 10mg vial is accompanied by a batch-specific Certificate of Analysis.

Analytical Specification

Storage and Transport Conditions

Note: Reconstituted solution storage, solvent selection, and working concentration guidance are not provided, consistent with AbsoluteBioLab’s Research Use Only supply policy. Researchers should refer to their institutional SOPs and the published literature for handling reconstituted peptide solutions.

Batch Documentation

Every batch of KPV dispatched by AbsoluteBioLab is accompanied by a batch-specific Certificate of Analysis (CoA) confirming HPLC purity and ESI-MS identity. CoA documents are available via the Certificate of Analysis Portal. For further information on our analytical methodology, refer to the guide on HPLC Purity in Peptide Research.

Structural Identity and Relationship to α-MSH

Alpha-MSH is a 13-amino-acid peptide (Ac-Ser-Tyr-Ser-Met-Glu-His-Phe-Arg-Trp-Gly-Lys-Pro-Val-NH₂) produced by POMC processing in the pituitary and peripheral tissues. The C-terminal tripeptide KPV (residues 11–13) constitutes the minimal sequence required to reproduce the anti-inflammatory signalling profile of the full hormone in cell-based models.^[1] Unlike the full α-MSH sequence, KPV does not activate melanocortin receptors MC1R through MC5R via the canonical His-Phe-Arg-Trp pharmacophore, yet it inhibits NF-κB activation and reduces pro-inflammatory cytokine secretion in stimulated cell lines at nanomolar concentrations.^[2] The mechanistic basis for this receptor-independent activity remains an active area of pre-clinical investigation.

A key finding in the characterisation of KPV’s cellular uptake is the role of the intestinal di/tripeptide transporter PepT1 (SLC15A1). PepT1 is constitutively expressed in the small intestine and is upregulated in colonic epithelial cells during inflammatory conditions. Dalmasso et al. (2007) demonstrated that KPV is transported into intestinal epithelial cells and T-lymphocytes via PepT1, and that this uptake is required for its intracellular inhibition of NF-κB and MAP kinase (ERK1/2, JNK, p38) signalling pathways.^[2] This transporter-mediated mechanism has informed subsequent nanoparticle delivery strategies designed to improve colonic targeting in pre-clinical models.^{[3] [4]}

Research Context

The published pre-clinical literature on KPV spans intestinal inflammation models, ocular epithelial repair, and cutaneous inflammatory signalling. Laroui et al. (2010) demonstrated that KPV encapsulated in alginate-chitosan hydrogel nanoparticles reduced inflammatory and histological parameters in a dextran sodium sulphate (DSS)-induced murine colitis model, with effective concentrations 12,000-fold lower than free KPV in solution — a finding attributed to improved epithelial uptake and intracellular retention.^[3] Xiao et al. (2017) extended this approach using hyaluronic acid-functionalised nanoparticles, reporting combined mucosal effects and anti-inflammatory activity in the same model.^[4]

In ocular epithelial models, topical application of KPV was associated with accelerated corneal re-epithelialisation in a rabbit abrasion model, with effects partially mediated by nitric oxide signalling.^[5] In endotoxin-stimulated human peripheral blood mononuclear cells (PBMCs), KPV and its dimer analogue (CKPV)₂ inhibited TNF-α production in a dose-dependent manner, with the dimer demonstrating greater potency than the monomer.^[6] Viennois et al. (2016) further characterised the PepT1–KPV axis in a colitis-associated carcinogenesis model, finding that KPV administration reduced tumour burden in wild-type mice but not in PepT1-knockout animals — confirming transporter dependency for the observed in vivo effects.^[7]

KPV is one of several tripeptides in the Repair & Recovery catalogue supplied by AbsoluteBioLab. Researchers investigating the broader landscape of repair-associated peptides may also wish to review BPC-157 10mg and GHK-Cu 100mg, which operate through distinct molecular mechanisms. For a comparative overview of the structural and mechanistic differences across the Repair & Recovery range, the guide Repair Research Compound Comparison provides relevant context on fragment-versus-parent-protein distinctions applicable to this class of research compounds.

Regulatory and Compliance Status

KPV is not approved as a medicinal product in the United Kingdom, European Union, or United States. It is not listed as a controlled substance under the Misuse of Drugs Act 1971 or the Psychoactive Substances Act 2016. Supply by AbsoluteBioLab is made strictly under research-use-only (RUO) conditions. Purchasers are responsible for ensuring compliance with all applicable national and institutional regulations governing the procurement, storage, and use of research compounds. AbsoluteBioLab does not provide guidance on reconstitution protocols, quantities for experimental use, or any application that falls outside in vitro or pre-clinical laboratory research. For the full supply boundary, refer to the RUO Compliance Policy.

Frequently Asked Questions

References

1. Luger TA, Scholzen TE, Brzoska T, Böhm M. New insights into the functions of α-MSH and related peptides in the immune system. Ann Rheum Dis. 2007;66(Suppl 3):iii65–iii70. doi:10.1136/ard.2007.079780
2. Dalmasso G, Charrier-Hisamuddin L, Nguyen HTT, Yan Y, Sitaraman S, Merlin D. PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation. Gastroenterology. 2008;134(1):166–178. doi:10.1053/j.gastro.2007.06.049
3. Laroui H, Dalmasso G, Nguyen HTT, Yan Y, Sitaraman SV, Merlin D. Drug-loaded nanoparticles targeted to the colon with polysaccharide hydrogel reduce colitis in a mouse model. Gastroenterology. 2010;138(3):843–853. doi:10.1053/j.gastro.2010.04.002
4. Xiao B, Laroui H, Viennois E, et al. Orally targeted delivery of tripeptide KPV via hyaluronic acid-functionalized nanoparticles efficiently alleviates ulcerative colitis. Mol Ther. 2017;25(7):1628–1640. doi:10.1016/j.ymthe.2016.11.020
5. Bonfiglio V, Cammarata G, Drago F. Effects of the COOH-terminal tripeptide α-MSH(11–13) on corneal epithelial wound healing: role of nitric oxide. Exp Eye Res. 2006;83(1):39–46. doi:10.1016/j.exer.2006.01.013
6. Gatti S, Colombo G, Buffa R, et al. Inhibitory effects of the peptide (CKPV)2 on endotoxin-induced host reactions. J Surg Res. 2006;131(1):104–111. doi:10.1016/j.jss.2005.10.005
7. Viennois E, Pujada A, Zen J, Merlin D. Critical role of PepT1 in promoting colitis-associated cancer and therapeutic benefits of the anti-inflammatory PepT1-mediated tripeptide KPV in a murine model. Cell Mol Gastroenterol Hepatol. 2016;2(3):340–357. doi:10.1016/j.jcmgh.2016.01.004