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Pathways Recommended: MAPK/ERK Pathway Neuronal Signaling JAK/STAT Signaling
Results for "

p38 MAPK/NLRP3 signaling

" in MedChemExpress (MCE) Product Catalog:

6

Inhibitors & Agonists

1

Peptides

3

Natural
Products

Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-161834
    RG100204
    1 Publications Verification

    		 Pyroptosis Aquaporin NOD-like Receptor (NLR) p38 MAPK Infection Metabolic Disease Inflammation/Immunology
    RG100204 is a selective, orally available inhibitor of the aquaporin AQP9. RG100204 directly inhibits AQP9 channel function, preventing the transmembrane transport of water, glycerol, and H 2O 2. RG100204 reduces the activation of the NLRP3 inflammasome and p38 MAPK signaling pathways, thereby alleviating inflammation and pyroptosis. RG100204 reduces multi-organ dysfunction in a mouse sepsis model and shows glucose-regulating effects in diabetic db/db mice .
    RG100204
  • HY-P10408
    Candidalysin

    		EGFR MMP Calcium Channel NOD-like Receptor (NLR) ERK p38 MAPK Infection Inflammation/Immunology
    Candidalysin is a cytolytic peptide toxin secreted by the fungus Candida albicans. Candidalysin drives epithelial immune responses by activating the EGFR-MAPK signaling pathway, inducing MMP expression and calcium influx, and regulating the c-Fos transcription factor and MKP1 via p38 MAPK and ERK1/2 respectively. Candidalysin is essential for mucosal and systemic infections, activating NLRP3 to promote inflammatory responses, neutrophil recruitment, and Th17 immunity. Candidalysin activates LDH causing membrane damage and exhibiting cytotoxicity
    Candidalysin
  • HY-N1431
    Tabersonine
    3 Publications Verification

    		 NOD-like Receptor (NLR) Apoptosis Cytochrome P450 NF-κB PI3K Akt CDK Caspase Interleukin Related p38 MAPK Inflammation/Immunology Cancer
    Tabersonine is a selective, orally active NLRP3 inhibitor. Tabersonine directly binds to the NACHT domain of NLRP3, inhibiting its ATPase activity and oligomerization, thereby blocking ASC spot formation and caspase-1 activation, and reducing the release of pro-inflammatory cytokines such as IL-1β. Tabersonine also inhibits K63-linked ubiquitination of TRAF6, blocking NF-κB, PI3K/Akt, and p38 MAPK signaling pathways. Tabersonine can inhibit inflammatory responses, induce apoptosis of liver cancer cells through mitochondrial pathways and death receptor pathways, reduce mitochondrial membrane potential, promote cytochrome c release, and activate caspase proteins. Tabersonine is mainly used in the study of NLRP3-driven inflammatory diseases (such as acute lung injury, sepsis, peritonitis) and tumors such as liver cancer .
    Tabersonine
  • HY-W923189
    Neral

    		Interleukin Related COX TNF Receptor NOD-like Receptor (NLR) NO Synthase PERK p38 MAPK Reactive Oxygen Species (ROS) Caspase Autophagy Herbicide Inflammation/Immunology Cancer
    Neral is a plant-derived anti-inflammatory, antioxidant and anticancer agent. Neral inhibits the phosphorylation of ERK1/2, p38 MAPK and IκB in macrophages induced by LPS (HY-D1056), suppresses the secretion of TNF-α and IL-6, as well as the expression of pro-IL-1β, iNOS and COX-2 in cells, and reduces the production of ROS in cells. Neral inhibits the activation of the NLRP3 inflammasome, and decreases the activation of caspase-1 and the secretion of IL-1β in mouse macrophages. Neral induces autophagy, and exhibits antiproliferative activity both in in vitro breast cancer cell models and mouse xenograft models. Neral regulates brassinosteroid, jasmonic acid and ethylene signaling pathways, and induces the expression of AP2/ERF-ERF and bHLH family genes in rice roots. Neral acts as a herbicide safener, alleviates the damage induced by Fenoxaprop-P-ethyl (HY-B2013), and promotes the elongation of rice roots. Neral can be used in research related to breast cancer, inflammatory and immune system diseases, and herbicide safeners .
    Neral
  • HY-126941
    Hecogenin acetate

    		ERK MMP Reactive Oxygen Species (ROS) NF-κB p38 MAPK NOD-like Receptor (NLR) TRP Channel TNF Receptor Interleukin Related Infection Neurological Disease Inflammation/Immunology Endocrinology
    Hecogenin acetate is an orally active steroid saponin aglycone with extensive biological activities. Hecogenin acetate inhibits the phosphorylation of NF-κB and p38 MAPK signaling pathways, antagonizes TRPA1/TRPM8 channels, inhibits the production of pro-inflammatory cytokines, and has anti-inflammatory and analgesic effects. Hecogenin acetate inhibits the production of ROS and the activation of NLRP3 inflammasome; downregulates the expression of MMP-2, and has neuroprotective and anti-tumor activities. Hecogenin acetate enhances gastric mucosal defense and promotes ulcer healing. Hecogenin acetate can be used in combination with certain antibiotics to regulate bacterial efflux pumps and restore antibiotic sensitivity .
    Hecogenin acetate
  • HY-N1431A
    Tabersonine hydrochloride
    3 Publications Verification

    		 NOD-like Receptor (NLR) Apoptosis Cytochrome P450 NF-κB PI3K Akt CDK Caspase Interleukin Related p38 MAPK Neurological Disease Inflammation/Immunology
    Tabersonine hydrochloride is a selective, orally active NLRP3 inhibitor. Tabersonine hydrochloride directly binds to the NACHT domain of NLRP3, inhibiting its ATPase activity and oligomerization, thereby blocking ASC spot formation and caspase-1 activation, and reducing the release of pro-inflammatory cytokines such as IL-1β. Tabersonine hydrochloride also inhibits K63-linked ubiquitination of TRAF6, blocking NF-κB, PI3K/Akt, and p38 MAPK signaling pathways. Tabersonine hydrochloride can inhibit inflammatory responses, induce apoptosis of liver cancer cells through mitochondrial pathways and death receptor pathways, reduce mitochondrial membrane potential, promote cytochrome c release, and activate caspase proteins. Tabersonine hydrochloride is mainly used in the study of NLRP3-driven inflammatory diseases (such as acute lung injury, sepsis, peritonitis) and tumors such as liver cancer .
    Tabersonine hydrochloride

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