KPV
preclinicalAlso known as: Lysine-Proline-Valine, α-MSH (11-13)
**Mechanism of Action** KPV (Lysine-Proline-Valine), the C-terminal tripeptide of α-melanocyte-stimulating hormone (α-MSH 11-13), exerts anti-inflammatory effects primarily through PepT1-mediated cellular uptake. Once internalized, it inhibits nuclear factor-κB (NF-κB) activation, reducing pro-inflammatory cytokine production (e.g., TNF-α, IL-1β, IL-6). This pathway is particularly relevant in intestinal epithelial cells and immune cells, where KPV modulates oxidative stress and apoptosis. **Key Research Findings** Preclinical studies in inflammatory bowel disease (IBD) models (e.g., DSS-induced colitis in mice) demonstrate that KPV reduces colonic inflammation, mucosal damage, and neutrophil infiltration. It also enhances tight junction protein expression (e.g., occludin, ZO-1), improving intestinal barrier integrity. In vitro, KPV suppresses LPS-induced NF-κB signaling in Caco-2 cells and macrophages. Notably, its effects are dose-dependent and require PepT1 expression, as PepT1 knockout models show diminished efficacy. **Clinical Relevance** KPV remains in preclinical development, with no human trials reported. Its potential lies in targeted therapy for IBD, particularly ulcerative colitis and Crohn’s disease, where PepT1 is upregulated in inflamed tissue. However, challenges include rapid enzymatic degradation and limited oral bioavailability. Future research may focus on formulation strategies (e.g., nanoparticle encapsulation) to enhance stability and delivery. For research purposes only — not medical advice.
Key data
C11H12O3Research & studies
NLRP3 expression is significantly increased in melanocytes of vitiligo patients and melanoma-Treg-induced vitiligo mice.; Knockout of NLRP3 effectively alleviates vitiligo progression in the mouse model.; Downregulation of β-TrCP1 reduces K27-linked ubiquitination of NLRP3, weakening its interaction with autophagy receptor NDP52 and impairing selective autophagic degradation.; Melanocyte-specific knockdown of NLRP3 using KPV-Lipos with Nlrp3 shRNA significantly alleviates vitiligo development.
PM10 exposure suppressed HaCaT cell proliferation and induced IL-1 secretion.; KPV (50 μg/mL) restored cell viability and reduced IL-1 secretion in PM10-treated cells.; KPV inhibited ROS production and suppressed MAPK (ERK, p38) activation and NF-κB signaling.; KPV decreased apoptosis-related proteins (Bax, Bcl-2, cleaved caspase-3) and blocked ROS-mediated caspase-1 activation, reducing IL-1 secretion.
Vimentin knockout (KPV-/-) mice showed attenuated tumor growth and improved survival compared to controls.; Therapeutic disruption of vimentin with withaferin A suppressed tumor growth and reduced lung tumor burden.; Mature vimentin intermediate filaments are required for cell-autonomous metastasis.; Vimentin loss upregulates ferroptosis genes, reduces GPX4, and increases toxic lipid peroxides.
DCM-KPV specifically targets PepT1 overexpressed in chronic ulcerative colitis epithelial cells.; The probe exhibits long emission, low photobleaching, negligible cytotoxicity, and high cytocompatibility.; It enables direct noninvasive observation of colon inflammation and distinguishes chronic, acute, and normal groups.; The method provides real-time tracking of intracellular KPV, replacing time-consuming and invasive H&E staining.
NPs (400 nm) did not affect cell viability or barrier functions.; Alginate-chitosan hydrogel containing NPs collapsed in the colon, enabling targeted delivery.; NP-KPV reduced inflammatory responses in Caco2-BBE cells in a dose-dependent manner.; Mice given DSS and NP-KPV were protected against inflammatory and histologic damage compared to DSS-only controls.
Frequently asked questions
What is KPV?
**Mechanism of Action** KPV (Lysine-Proline-Valine), the C-terminal tripeptide of α-melanocyte-stimulating hormone (α-MSH 11-13), exerts anti-inflammatory effects primarily through PepT1-mediated cellular uptake. Once internalized, it inhibits nuclear factor-κB (NF-κB) activation, reducing pro-inflammatory cytokine pro
How does KPV work?
C-terminal tripeptide of α-MSH with anti-inflammatory action via PepT1 uptake and NF-κB inhibition, studied in IBD models.
What is the research status of KPV?
KPV is currently classified as preclinical, with 88 research references on record. This is for research purposes only and is not medical advice.
What is the molecular weight of KPV?
KPV has a molecular weight of approximately 192.21 g/mol (formula C11H12O3).
Related peptides
28-aa neuropeptide acting on VPAC1/2 receptors; vasodilatory, bronchodilatory, and anti-inflammatory.
38-aa neuropeptide of the VIP/secretin family acting on PAC1 receptors; neuroprotective and vasoregulatory.
43-aa actin-sequestering peptide that drives cell migration, angiogenesis, and repair in cardiac, corneal, and dermal tissue.
Gastric-juice-derived pentadecapeptide that promotes angiogenesis (VEGF) and tissue repair via FAK-paxillin and NO-system modulation.
Copper-binding tripeptide that stimulates collagen synthesis, wound healing, and remodeling gene expression.
Erythropoietin-derived 11-aa peptide targeting the innate repair receptor (EPOR/CD131) for tissue protection without erythropoiesis.
Build on KPV data programmatically
Structured peptide data, semantic search, and AI summaries via one API.
Get a free API key