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
Peptides like growth hormone secretagogues and analogues are marketed for muscle growth and recovery but lack clinical evidence for supraphysiological use.; Potential risks include cardiovascular strain, insulin resistance, dyslipidemia, and psychiatric instability.; Unregulated supply chains lead to mislabeled or contaminated products, exacerbating health dangers.; Prevalence data on recreational use, especially among younger individuals, is critically lacking.
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.
SIPPC platform integrates PEG, ROS-responsive self-immolative module, and hydrolyzable scaffold to form nanoparticles with GI stability and mucus penetration.; proKPV achieved 3.8-fold higher colonic accumulation than free KPV in colitis mice, with efficacy at a 20-fold lower dose.; Oral proKPV accumulated in inflamed lungs and showed potent anti-inflammatory efficacy in acute lung injury mice.; Ac-QAW and IRW-based conjugates showed comparable benefits, supporting SIPPC as a general platform for oral peptide delivery.
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.
The oil layer protects encapsulated materials from the acidic stomach environment during digestion.; Hydrogel cores provide high stability under high osmolarity conditions in the stomach.; Fine-tuning the shell composition enables selective release in response to gut pH conditions.; The system preserves anti-inflammatory activities of 5-ASA and KPV and their effects on colonic epithelial cell migration and proliferation.
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 89 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).
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