KPV

KPV (Lys-Pro-Val) is a naturally occurring tripeptide corresponding to the C-terminal fragment (residues 11-13) of alpha-melanocyte stimulating hormone (α-MSH). Research has demonstrated that this minimal C-terminal sequence retains the anti-inflammatory signaling properties of the full-length α-MSH without melanocortin receptor binding, suggesting a distinct mechanism of action.

KPV has a molecular weight of 358.43 g/mol, making it one of the smallest bioactive peptide fragments studied. Despite lacking the pharmacophore required for melanocortin receptor (MC1R-MC5R) binding, KPV retains anti-inflammatory signaling activity, suggesting a receptor-independent mechanism possibly involving direct NF-κB pathway interaction.

• Inflammatory bowel research: Studies examining KPV effects in colitis models, including oral and nanoparticle-mediated delivery (Dalmasso et al., 2008).
• NF-κB pathway: Research on KPV's interaction with inflammatory transcription factor signaling.
• Dermatological research: Studies examining anti-inflammatory effects in skin cell models.
• Gut epithelial biology: Research on KPV's effects on intestinal epithelial barrier function and permeability.

• NF-κB pathway inhibition (IκBα stabilization)
• IL-10 upregulation in monocyte/macrophage models
• TNF-α and IL-8 suppression in inflammatory models
• Melanocortin-independent anti-inflammatory signaling
• PepT1 transporter-mediated intestinal absorption

Key preclinical findings:

Dalmasso et al. (2008, Gastroenterology): KPV at 12.5 mg/kg/day (oral, nanoparticle-encapsulated) significantly reduced colonic inflammation in murine DSS colitis model. Reduced TNF-α by 65% and IL-6 by 58%. Identified PepT1-mediated intestinal uptake.

Brzoska et al. (2008): KPV at 1-100 µM inhibited NF-κBactivation in human keratinocytes, fibroblasts, and monocytes. IC50 for NF-κB inhibition: ~10 µM. Importantly, KPV did NOT bind melanocortin receptors (MC1R-MC5R), confirming receptor-independent mechanism.

Getting et al. (2006): KPV reduced IL-8 secretion by 50% in TNF-α-stimulated human intestinal epithelial cells at 10 µM concentration.

Typical in vitro concentrations: 1-100 µM. In vivo: 5-15 mg/kg (oral or IP).

All findings from animal or in vitro studies.

Form: Lyophilized powder, 5mg per vial
Appearance: White powder
Molecular Weight: 358.43 g/mol

Reconstitution Guide:
- For 1 mg/mL: Add 5.0 mL bacteriostatic water
- For 5 mg/mL: Add 1.0 mL bacteriostatic water
- Dissolves rapidly due to small size

Solubility: Freely soluble in water (>100 mg/mL). Very high aqueous solubility. Also soluble in DMSO, ethanol.

Stability: Lyophilized stable 24 months at -20°C. Reconstituted: 30 days at 2-8°C. Excellent stability.

Unique Feature: KPV is absorbed via PepT1 transporter in intestinal epithelium, making it one of the few peptides with documented oral absorption pathway in preclinical models.

Analytical Testing: HPLC, ESI-MS, LAL endotoxin, USP sterility.

This content was prepared for informational purposes based on published preclinical research. It does not constitute medical advice or product efficacy claims.

1. 1
   Dalmasso G, et al. "PepT1-mediated tripeptide KPV uptake reduces intestinal inflammation." Gastroenterology. 2008;134(1):166-78. PubMed: 18061177 PubMed
2. 2
   Brzoska T, et al. "Alpha-melanocyte-stimulating hormone and related tripeptides: biochemistry, antiinflammatory and protective effects." Endocr Rev. 2008;29(5):581-602. PubMed: 18612139 PubMed
3. 3
   Getting SJ, et al. "Molecular determinants of the anti-inflammatory function of the neuropeptide alpha-MSH." J Leukoc Biol. 2006;80(1):1-8. PubMed: 16698943 PubMed