KPV

OA treatment enhanced hepatic lipid deposition via upregulation of fatty acid synthase (FAS) expression.; KPV (100 g/mL) significantly attenuated OA-induced lipid accumulation and suppressed FAS expression without inducing cytotoxicity.; KPV reduced reactive oxygen species generation, preventing activation of extracellular signal-regulated kinase.; KPV downregulated AKT phosphorylation, inhibiting mTORC1 phosphorylation and regulating PPARγ phosphorylation to normalize FAS expression.

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.

HDPs are promising IBD candidates due to their antimicrobial and immunomodulatory properties.; HDPs cited include cathelicidins (e.g., LL-37-T 1, LTP, C-L, KR-12), defensins (e.g., HD-5, hBD2), cecropins (e.g., CC34), microcins (e.g., MccJ25), brevinins (e.g., chensinin-1), PrAMPs (e.g., abaecin), type V peptides (e.g., VP-NP), and α-MSH (e.g., KPV).; HDPs downregulate the NF-κB pathway, modulate cytokine release, and restore homeostasis.; HDPs may offer a way to reduce side effects compared with current IBD treatments.

Tripeptides regulate cell migration, proliferation, differentiation, inflammation, angiogenesis, and ECM remodeling to accelerate tissue repair.; GHK-based formulations (e.g., nanoparticle conjugates, hydrogels, TriHex, TriHex 2.0) enhance fibroblast migration, ECM remodeling, collagen and elastin synthesis, wound closure, and provide antimicrobial activity.; KdPT mitigates hyperglycemia-induced oxidative stress and restores keratinocyte function; KPV-loaded hydrogels reduce inflammation, promote regeneration, and combat MRSA infections.; Lipotripeptides (DICAMs) inhibit and disrupt bacterial biofilms, while GPE supports neuroprotection and regeneration via ERK and PI3K/Akt signaling activation.

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.

KPV and RAPA self-assembled into carrier-free spherical nanoparticles with good stability and biosafety.; KPV-RAPA nanoparticles significantly inhibited vascular calcification in mice compared to other treatment groups.; The mechanism involved inhibition of inflammatory responses and activation of autophagy.; The nanoparticles show potential as therapeutic agents for vascular calcification combination therapy.

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 91 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).