KPV

What is KPV?

KPV (Lysine-Proline-Valine) represents molecular dissection of anti-inflammatory signaling. As the C-terminal tripeptide of alpha-melanocyte stimulating hormone, KPV retains the parent molecule's remarkable anti-inflammatory properties while eliminating melanocortin receptor-mediated effects like pigmentation. This separation of functions makes KPV uniquely valuable: it modulates inflammatory gene transcription through NF-κB pathway inhibition and reduces pro-inflammatory cytokine production without the broader melanocortin system effects.

Research has demonstrated KPV's effectiveness in inflammatory bowel disease models, dermal inflammation studies, and wound healing research where inflammation must be controlled without suppressing the entire immune response. Its ability to penetrate epithelial barriers and concentrate in inflamed tissues makes it particularly relevant for mucosal inflammation research.

Mechanism of Action

KPV operates primarily through inhibition of the NF-κB signaling pathway, a master regulator of inflammatory gene transcription. The tripeptide penetrates cells and translocates to the nucleus where it interferes with NF-κB DNA binding activity, preventing transcription of pro-inflammatory cytokines including TNF-α, IL-1β, IL-6, and IL-8. This mechanism occurs independently of melanocortin receptor activation—unlike the parent molecule α-MSH which also signals through MC1R, MC3R, and MC4R receptors.

The peptide demonstrates selective accumulation in inflamed tissues, with studies showing 3-5 fold higher concentrations in areas of active inflammation compared to healthy tissue. KPV also modulates immune cell function by reducing neutrophil infiltration and decreasing production of reactive oxygen species (ROS) from activated macrophages. In intestinal epithelial cells, the peptide enhances barrier function through upregulation of tight junction proteins zonula occludens-1 (ZO-1) and occludin. These combined mechanisms make KPV particularly effective in inflammatory conditions affecting mucosal barriers.

Key Research Findings

• Reduces DSS-induced colitis severity scores by 65% through NF-κB inhibition and decreased TNF-α expression in murine models [Dalmasso et al., 2008]
• Demonstrates 72% reduction in IL-6 secretion from LPS-stimulated human peripheral blood mononuclear cells at 100 μM concentration [Cutolo et al., 2015]
• Enhances intestinal barrier integrity with 45% improvement in transepithelial electrical resistance (TEER) in Caco-2 cell monolayers [Kannengiesser et al., 2008]
• Shows superior anti-inflammatory potency compared to α-MSH in dermal inflammation models despite lacking melanocortin receptor binding [Brzoska et al., 2008]
• Reduces neutrophil infiltration by 58% in carrageenan-induced paw edema model through suppression of adhesion molecule expression [Hiltz et al., 2003]

Research Applications

• NF-κB signaling inhibition
• Inflammatory cytokine modulation
• Inflammatory bowel disease models
• Mucosal immunity research
• Wound healing inflammation control
• Melanocortin peptide fragment studies

Reconstitution & Use

Reconstitute with bacteriostatic water for injection. For detailed reconstitution instructions and dosing protocols for your specific research application, see our reconstitution guide.

Storage & Handling

Store lyophilized at -20°C. Upon reconstitution with bacteriostatic water, maintain at 2-8°C and use within 30 days. This small peptide demonstrates excellent stability in solution.