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NLRP3 signaling pathways

" in MedChemExpress (MCE) Product Catalog:

62

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2

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35

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4

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2

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Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-100573
    Necrosulfonamide
    Maximum Cited Publications
    139 Publications Verification

    Mixed Lineage Kinase Necroptosis Pyroptosis Caspase NOD-like Receptor (NLR) Keap1-Nrf2 TNF Receptor Interleukin Related NO Synthase Heme Oxygenase (HO) Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology Endocrinology
    Necrosulfonamide is a MLKL and Gasdermin D (GSDMD) inhibitor, capable of separately inhibiting necroptosis and pyroptosis of cells. Necrosulfonamide does not affect the activation of upstream signals, but specifically inhibits the downstream executor oligomerization step. Necrosulfonamide reduces the expression of the key kinases NLRP3 and caspase-1 involved in necroptosis and pyroptosis, activate the Nrf2 pathway and the downstream antioxidant enzymes, and also downregulates a variety of inflammatory factors. Necrosulfonamide plays significant roles in various diseases such as neurodegenerative diseases (such as Parkinson’s disease), tissue damage and ischemia-reperfusion injury, inflammatory bowel disease, osteoarthritis and fracture repair, and hair loss by regulating two important programmed necrosis pathways .
    Necrosulfonamide
  • HY-116084
    Trimethylamine N-oxide
    10+ Cited Publications

    Drug Metabolite NOD-like Receptor (NLR) Reactive Oxygen Species (ROS) TGF-beta/Smad Endogenous Metabolite Cardiovascular Disease Inflammation/Immunology
    Trimethylamine N-oxide is a gut microbe-dependent metabolite of dietary choline and other trimethylamine-containing nutrients. Trimethylamine N-oxide induces inflammation by activating the ROS/NLRP3 inflammasome. Trimethylamine N-oxide also accelerates fibroblast-myofibroblast differentiation and induces cardiac fibrosis by activating the TGF-β/smad2 signaling pathway .
    Trimethylamine N-oxide
  • HY-N0131
    Stigmasterol
    10+ Cited Publications

    MMP Endogenous Metabolite Neurological Disease Inflammation/Immunology
    Stigmasterol is an orally acitve, immunomodulatory agent with anti-inflammatory and neuroprotective effect, as well as able to cross the blood-brain barrier. Stigmasterol activates AMPK, which in turn inhibits NF-κB and NLRP3 signaling pathways, reduces microglia-mediated neuroinflammation, and alleviates cognitive impairment and Alzheimer's disease. Stigmasterol regulates M1/M2 polarization of microglia through the TLR4/ NF-κB pathway, thereby reducing neuropathic pain. Stigmasterol can be used for neurodegenerative diseases, inflammatory diseases, and pain management, among others .
    Stigmasterol
  • HY-N0535
    (+)-Magnoflorine chloride
    1 Publications Verification

    Magnoflorine chloride; α-Magnoflorine chloride; Thalictrine chloride

    Fungal Autophagy Apoptosis PINK1/Parkin NOD-like Receptor (NLR) Caspase JNK NF-κB Sirtuin AMPK Reactive Oxygen Species (ROS) Infection Metabolic Disease
    (+)-Magnoflorine (α-Magnoflorine) chloride is an orally active aporphine alkaloid with multiple biological activities. (+)-Magnoflorine chloride promotes Parkin/PINK1-mediated mitochondrial autophagy, inhibits the activation of NLRP3/Caspase-1 pathway, regulates the intestinal microbiota, and exhibits significant anti-inflammatory and immunomodulatory activities. (+)-Magnoflorine chloride inhibits JNK and TLR4/NF-κB signaling pathways, activates Sirt1/AMPK pathway, alleviates neuronal oxidative stress and apoptosis. Magnoflorine chloride upregulates miR-410-3p, inhibits HMGB1/NF-κB pathway, and has anti-tumor activity. (+)-Magnoflorine chloride also has significant antifungal activity .
    (+)-Magnoflorine chloride
  • HY-N0373
    Licochalcone B
    10+ Cited Publications

    Amyloid-β Apoptosis NOD-like Receptor (NLR) Neurological Disease
    Licochalcone B is an extract from the root of Glycyrrhiza uralensis. Licochalcone B inhibits amyloid β (42) self-aggregation (IC50=2.16 μM) and disaggregate pre-formed Aβ42 fibrils, reduce metal-induced Aβ42 aggregation through chelating metal ionsLicochalcone B inhibits phosphorylation of NF-κB p65 in LPS signaling pathway. Licochalcone B inhibits growth and induces apoptosis of NSCLC cells. Licochalcone B specifically inhibits the NLRP3 inflammasome by disrupting NEK7‐NLRP3 interaction .
    Licochalcone B
  • 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-108915
    Trimethylamine N-oxide dihydrate
    10+ Cited Publications

    NOD-like Receptor (NLR) Reactive Oxygen Species (ROS) TGF-beta/Smad Endogenous Metabolite Cardiovascular Disease Metabolic Disease Inflammation/Immunology
    Trimethylamine N-oxide dihydrate is a gut microbe-dependent metabolite of dietary choline and other trimethylamine-containing nutrients. Trimethylamine N-oxide dihydrate induces inflammation by activating the ROS/NLRP3 inflammasome. Trimethylamine N-oxide dihydrate also accelerates fibroblast-myofibroblast differentiation and induces cardiac fibrosis by activating the TGF-β/smad2 signaling pathway .
    Trimethylamine N-oxide dihydrate
  • HY-116084S
    Trimethylamine N-oxide-d9
    1 Publications Verification

    NOD-like Receptor (NLR) Reactive Oxygen Species (ROS) TGF-beta/Smad Endogenous Metabolite Cardiovascular Disease Inflammation/Immunology
    Trimethylamine N-oxide-d9 is the deuterium labeled Trimethylamine N-oxide. Trimethylamine N-oxide is a gut microbe-dependent metabolite of dietary choline and other trimethylamine-containing nutrients. Trimethylamine N-oxide induces inflammation by activating the ROS/NLRP3 inflammasome. Trimethylamine N-oxide also accelerates fibroblast-myofibroblast differentiation and induces cardiac fibrosis by activating the TGF-β/smad2 signaling pathway .
    Trimethylamine N-oxide-d9
  • HY-P10408

    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-N2909

    NF-κB RIP kinase Mixed Lineage Kinase Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Aurantiamide is a non-covalent, orally active, blood-brain-permeable GRPR selective antagonist with anti-inflammatory and neuroprotective effects. Aurantiamide reduces inflammation and oxidative stress in renal tissue by inhibiting GRPR-mediated renal necrosis pathways (such as RIPK3/MLKL signaling) and NF-κB inflammatory pathways, exerting anti-acute kidney injury and endothelial function activities. Aurantiamide also inhibits the M1 polarization of microglia and inhibits NLRP3 activation, thereby improving AD mouse models. Aurantiamide has in vivo inhibitory efficacy in acute kidney injury models such as ischemia/reperfusion, sepsis, and hypertension models .
    Aurantiamide
  • HY-N0559
    Kirenol
    1 Publications Verification

    Casein Kinase Apoptosis AMPK Akt NF-κB TGF-beta/Smad Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    Kirenol is a diterpenoid compound, an orally active apoptosis inducer and signaling pathway regulator, with a Kd value of 5.47 μM against the target CK2. Kirenol promotes the cleavage of Bid into tBid, regulates the protein levels/phosphorylation of Bax, Bcl-2, p53 and p21, and induces caspase-independent apoptosis, S-phase cell cycle arrest, ROS accumulation and cytotoxicity in cancer cells. Kirenol activates the CK2/AKT and AMPK-mTOR-ULK1 pathways, inhibits the signaling of NF-κB, TGF-β/Smads and NLRP3 inflammasome, and regulates the GSK3β, BMP and Wnt/β-catenin pathways. Kirenol induces autophagy, mitophagy and osteoblast differentiation, promotes mitochondrial fusion, and exerts antioxidant, anti-inflammatory, antifibrotic, renoprotective, cardioprotective, neuroprotective and analgesic effects. Kirenol is applicable to research related to chronic myeloid leukemia, ischemic stroke, diabetic nephropathy, heart failure, acute lung injury and osteoporosis .
    Kirenol
  • HY-N0743
    Senkyunolide A
    4 Publications Verification

    α-synuclein Neurological Disease Inflammation/Immunology Cancer
    Senkyunolide A is a phthalide, anti-tumor cell proliferation agent with anticancer activity. Senkyunolide A protects neurons from corticosterone (HY-B1618)-induced apoptosis by decreasing protein phosphatase PP2A and α-synuclein phosphorylation and protein level. Senkyunolide A also inhibits osteoarthritis through the NLRP3 signaling pathway and suppresses the expression of CD137, a diagnostic biomarker for atherosclerosis .
    Senkyunolide A
  • HY-N0334

    Magnoflorine; α-Magnoflorine; Thalictrine

    Fungal Autophagy Apoptosis PINK1/Parkin NOD-like Receptor (NLR) Caspase JNK NF-κB Sirtuin AMPK Reactive Oxygen Species (ROS) Cardiovascular Disease Infection Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    (+)-Magnoflorine (α-Magnoflorine) is an orally active aporphine alkaloid with multiple biological activities. (+)-Magnoflorine promotes Parkin/PINK1 -mediated mitochondrial autophagy, inhibits the activation of NLRP3/Caspase-1 pathway, regulates the intestinal microbiota, and exhibits significant anti-inflammatory and immunomodulatory activities. (+)-Magnoflorine inhibits JNK and TLR4/NF-κB signaling pathways, activates Sirt1/AMPK pathway, alleviates neuronal oxidative stress and apoptosis. Magnoflorine upregulates miR-410-3p, inhibits HMGB1/NF-κB pathway, and has anti-tumor activity. (+)-Magnoflorine also has significant antifungal activity .
    (+)-Magnoflorine
  • HY-N0671
    Rhapontin
    2 Publications Verification

    Rhaponiticin

    Apoptosis Cardiovascular Disease Metabolic Disease Inflammation/Immunology Cancer
    Rhapontin (Rhaponiticin) is an orally aactive SIRT1 agonist and AMPK activator with anti-inflammatory and anti-fibrotic activities. Rhapontin inhibits NLRP3 inflammasome activation by activating SIRT1 and inhibits TGF-β/Smad signaling via the AMPK pathway. Rhapontin reduces intestinal and lung inflammation, inhibits fibroblast differentiation and extracellular matrix deposition, and enhances tight junction protein expression to repair epithelial barriers. Rhapontin can be used in the study of inflammatory bowel diseases (such as ulcerative colitis) and pulmonary fibrosis .
    Rhapontin
  • HY-N0699
    Daphnoretin
    3 Publications Verification

    Dephnoretin; Thymelol

    PKC Influenza Virus NOD-like Receptor (NLR) Apoptosis HBV JNK PI3K Akt CDK Caspase Bcl-2 Family Infection Inflammation/Immunology Cancer
    Daphnoretin (Dephnoretin; Thymelol) is a protein kinase C (PKC) activator that inhibits the expression of hepatitis B virus (HBV) surface antigen (HBsAg) and exhibits antiviral activity. Daphnoretin exerts its antitumor effects by inhibiting the activation of the PI3K/AKT signaling pathway and triggers the mitochondrial apoptosis pathway. Daphnoretin alleviates chondrocyte apoptosis and inflammatory responses by inhibiting endoplasmic reticulum stress and activation of the NLRP3 inflammasome. Daphnoretin regulates the differentiation and maturation of dendritic cells, inhibits their immunostimulatory function by downregulating the phosphorylation level of JNK, and thus exerts a protective effect in skin graft rejection .
    Daphnoretin
  • HY-N1990
    Gypenoside XLIX
    2 Publications Verification

    PPAR Sirtuin Keap1-Nrf2 Toll-like Receptor (TLR) NF-κB Reactive Oxygen Species (ROS) NOD-like Receptor (NLR) Apoptosis Pyroptosis Autophagy Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology
    Gypenoside XLIX is a multifunctional bioactive compound that can be isolated from Gynostemma pentaphyllum, with a Ka value of 1.58 μM for its binding to SIRT1. Gypenoside XLIX acts as a PPAR-α agonist. It inhibits the activation of TLR4-mediated NF-κB signaling pathway by activating the Sirt1/Nrf2 signaling pathway, reduces ROS accumulation, and alleviates hepatic inflammatory injury in mice with sepsis-induced liver disease. Gypenoside XLIX targets SIRT1 to block YAP-NLRP3 activation and improve sepsis-induced cardiomyopathy. Gypenoside XLIX inhibits apoptosis (Apoptosis), pyroptosis (Pyroptosis), autophagy (Autophagy), lipid peroxidation, pro-inflammatory cytokines and anti-inflammatory cytokines. Gypenoside XLIX alleviates sepsis-induced splenic injury by inhibiting inflammation and oxidative stress, and mitigates sepsis-associated encephalopathy by targeting PPAR-α. Gypenoside XLIX prevents acute kidney injury by inhibiting IGFBP7/IGF1R-mediated programmed cell death and inflammation. Gypenoside XLIX inhibits the expression and activity of vascular cell adhesion molecule-1 in cytokine-induced human endothelial cells. Gypenoside XLIX is applicable to research related to acute liver injury, lung injury, cardiomyopathy, acute splenic injury, sepsis-associated encephalopathy, acute kidney injury, atherosclerosis and chronic inflammation .
    Gypenoside XLIX
  • 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-N0819
    Raddeanin A
    1 Publications Verification

    Apoptosis PI3K Akt ERK mTOR Wnt β-catenin Wee1 JNK VEGFR CDK Neurological Disease Inflammation/Immunology Cancer
    Raddeanin A is an oleanane-type triterpenoid saponin with oral activity. Raddeanin A inhibits SRC, mTOR, JNK, VEGFR2, NLRP3 inflammasome, Wnt/β-catenin, Wee1, PI3K/AKT signaling pathway, MAPK/ERK signaling pathway, AR-FL, AR-Vs, and downregulates the expression of p-PI3K and p-AKT. Raddeanin A inhibits osteoclast formation, bone resorption, osteolysis, cancer cell invasion, migration, proliferation, angiogenesis and epithelial-mesenchymal transition, while induces apoptosis, cell cycle arrest, ROS production, immunogenic cell death and dendritic cell maturation. Raddeanin A improves blood-retinal barrier function, alleviates inflammation, regulates the tumor microenvironment, and enhances the activity of anti-PD-1 antibody. Raddeanin A is applicable to the research of breast cancer-associated osteolysis, human osteosarcoma, colorectal cancer, glioblastoma, Alzheimer's disease, cholangiocarcinoma, melanoma, non-small cell lung cancer, castration-resistant prostate cancer and multiple myeloma .
    Raddeanin A
  • HY-N0334A
    (+)-Magnoflorine iodide
    1 Publications Verification

    Magnoflorine iodide; α-Magnoflorine iodide; Thalictrine iodide

    Fungal Autophagy Apoptosis PINK1/Parkin NOD-like Receptor (NLR) Caspase JNK NF-κB Sirtuin AMPK Reactive Oxygen Species (ROS) Cardiovascular Disease Infection Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    (+)-Magnoflorine (α-Magnoflorine) iodide is an orally active aporphine alkaloid with multiple biological activities. (+)-Magnoflorine iodide promotes Parkin/PINK1 -mediated mitochondrial autophagy, inhibits the activation of NLRP3/Caspase-1 pathway, regulates the intestinal microbiota, and exhibits significant anti-inflammatory and immunomodulatory activities. (+)-Magnoflorine iodide inhibits JNK and TLR4/NF-κB signaling pathways, activates Sirt1/AMPK pathway, alleviates neuronal oxidative stress and apoptosis. Magnoflorine upregulates miR-410-3p, inhibits HMGB1/NF-κB pathway, and has anti-tumor activity. (+)-Magnoflorine iodide also has significant antifungal activity .
    (+)-Magnoflorine iodide
  • HY-N5063
    Plantainoside D
    2 Publications Verification

    Angiotensin-converting Enzyme (ACE) IKK Calcium Channel PKC Reactive Oxygen Species (ROS) NF-κB Apoptosis Sirtuin NOD-like Receptor (NLR) Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Plantainoside D, a phenylethanoid glycosides, is a IKK-β inhibitor with diverse biological activities. Plantainoside D shows inhibitory activity of angiotensin-converting enzyme (ACE) with an IC50 of 2.17 mM. Plantainoside D significantly reduces the release of glutamate from nerve terminals in the cerebral cortex of rats by inhibiting the voltage-dependent calcium channel (VDCCs) and protein kinase C (PKC) signaling cascade. Plantainoside D significantly alleviates cell apoptosis by inhibiting the generation of ROS and the activation of NF-κB. Plantainoside D significantly improves acute lung injury (ALI) induced by sepsis by regulating the Sirt3/NLRP3 signaling pathway. Plantainoside D can be used for the study of neuroprotection, antioxidant, anti-inflammation, antihypertension .
    Plantainoside D
  • HY-W923189

    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-N2157
    Pteryxin
    1 Publications Verification

    (+)-Pteryxin

    Cholinesterase (ChE) NF-κB NOD-like Receptor (NLR) Keap1-Nrf2 Reactive Oxygen Species (ROS) Nuclear Factor of activated T Cells (NFAT) p38 MAPK Neurological Disease Metabolic Disease Inflammation/Immunology
    Pteryxin ((+)-Pteryxin) is an orally active multi-target inhibitor that targets NF-κB, MAPK, NLRP3 inflammasome, and Nrf2/ARE pathways. Pteryxin is also a BChE inhibitor (IC50=12.96 μg/mL) with a low inhibitory efficiency on AChE. Pteryxin inhibits the Ca 2+-calcineurin-NFATc1 pathway by blocking NF-κB/MAPK signaling, inhibiting NLRP3 inflammasome activation, and reducing ROS generation, and activates Nrf2-mediated antioxidant enzyme expression. Pteryxin has anti-inflammatory, antioxidant, and osteoclastogenesis inhibitory activities. Pteryxin can be used in the study of inflammatory diseases, osteoporosis, diabetes, and Alzheimer's disease .
    Pteryxin
  • HY-N0772
    Isomangiferin
    4 Publications Verification

    VEGFR NOD-like Receptor (NLR) NF-κB Bacterial AMPK Acetyl-CoA Carboxylase Apoptosis Reactive Oxygen Species (ROS) HSV Drug Derivative Infection Metabolic Disease Inflammation/Immunology Cancer
    Isomangiferin is an orally active xanthone C-glucoside, and its chemical structure is similar to Mangiferin (HY-N0290). Isomangiferin is an effective VEGFR-2 kinase inhibitor, which can induces cell apoptosis, inhibit the growth, metastasis and angiogenesis of breast cancer. Isomangiferin exerts anti-inflammatory effects by inhibiting the HMGB1/NLRP3/NF-κB signaling pathway, thereby improving the renal function indicators of diabetic mice. Isomangiferin exhibits inhibitory effects on various bacteria and herpes simplex virus type 1 (HSV-1). Isomangiferin promotes the migration and osteogenic differentiation of bone marrow mesenchymal stem cells (BMSCs) and reduces cell apoptosis and the production of ROS by activating the AMPK/ACC pathway, thereby facilitating fracture healing .
    Isomangiferin
  • HY-N8599
    Cichoriin
    2 Publications Verification

    Amylases Glycosidase Lipase Dipeptidyl Peptidase p38 MAPK PPAR P2Y Receptor NOD-like Receptor (NLR) SARS-CoV Pyroptosis GLUT Angiotensin-converting Enzyme (ACE) NF-κB Infection Metabolic Disease Inflammation/Immunology
    Cichoriin is an orally active coumarin glycoside with broad biological activities. Cichoriin exhibits inhibitory activities against α-amylase, α-glucosidase, pancreatic lipase and DPP-IV, with IC50 values of 5.76, 2.94, 16.83 and 9.16 μg/mL, respectively. Cichoriin significantly improves metabolic dysfunction-associated steatohepatitis (MASH) in mice by activating the AMPK signaling pathway. Cichoriin upregulates PPAR-γ in adipose tissue and alleviates obesity and associated cardiorenal injury in rats. Cichoriin blocks monosodium urate crystal-induced activation of the NLRP3 inflammasome and cell pyroptosis by inhibiting P2Y14R (IC50 = 8.47 nM). In silico virtual screening reveals that Cichoriin has a strong binding affinity for SARS-CoV-2 .
    Cichoriin
  • HY-N0442

    4'-O-β-D-Glucosyl-5-O-methylvisamminol

    NF-κB p38 MAPK JNK Src TNF Receptor NOD-like Receptor (NLR) Amyloid-β MEK ERK Ferroptosis VEGFR Anaplastic lymphoma kinase (ALK) Reactive Oxygen Species (ROS) Neurological Disease Metabolic Disease Inflammation/Immunology Cancer
    5-O-Methylvisammioside (4'-O-β-D-Glucosyl-5-O-methylvisamminol) is an orally active natural chromone glycoside and multiple biological activities. 5-O-Methylvisammioside inhibits ferroptosis by activating the Nrf2/HO-1 signaling axis. 5-O-Methylvisammioside alleviates intestinal barrier damage by inhibiting the ROS/NF-κB/NLRP3 pathway. 5-O-Methylvisammioside exerts a protective effect against acute liver injury by reducing ALT/AST, decreasing inflammatory infiltration, and inhibiting IκB-α phosphorylation and NF-κB nuclear translocation. 5-O-Methylvisammioside blocks the HMGB1/RAGE/MEK/ERK signaling axis to exert anti-tumor and anti-angiogenic effects. 5-O-Methylvisammioside improves depression-like behaviors by inhibiting Src kinase and the NF-κB pathway .
    5-O-Methylvisammioside
  • HY-160229

    R-1075 sodium

    Toll-like Receptor (TLR) MyD88 Caspase Reactive Oxygen Species (ROS) Autophagy Pyroptosis HIV Infection Neurological Disease
    ssRNA40 sodium (R-1075 sodium) is a single-stranded RNA40 derived from HIV-1. ssRNA40 sodium activates the TLR7, TLR8, TLR2, RIG-I, MDA5, MyD88, Caspase-3, IRE1α, NLRP3 inflammasome and IRF7 signaling pathways. ssRNA40 sodium alters mRNA expression in neutrophils, induces pro-inflammatory cytokines, ROS, autophagy (autophagy), pyroptosis (pyroptosis), neuronal death, neurodegeneration, aggregate formation and NK cell activation. ssRNA40 sodium activates the expression of CD62L, CD11b, CD69, MX1, OAS1, ATG7, LC3B and XBP1 in immune cell and neuronal populations. ssRNA40 sodium causes cortical neuron loss and axonal damage in mice in a TLR7-dependent manner. ssRNA40 sodium can be used in research on HIV-1 infection, neurodegeneration, COVID-19 and HIV-associated neurological disorders .
    ssRNA40 sodium
  • HY-N2485
    4'-Methoxyresveratrol
    1 Publications Verification

    4'-O-Methylresveratrol

    NF-κB NOD-like Receptor (NLR) Inflammation/Immunology
    4'-Methoxyresveratrol (4'-O-Methylresveratrol) is a polyphenol derived from Dipterocarpaceae, with antiandrogenic, antifungal and anti-inflammatory activities. 4'-Methoxyresveratrol alleviates AGE-induced inflammation through suppressing RAGE-mediated MAPK/NF-κB signaling pathway and NLRP3 inflammasome activation .
    4'-Methoxyresveratrol
  • HY-119684

    NOD-like Receptor (NLR) Interleukin Related Neurological Disease Inflammation/Immunology
    Maresin 2 is an anti-inflammatory and pro-resolving mediator. Maresin 2 drives intestinal epithelial cell migration by activating the focal cell-matrix adhesion signaling pathway in primary human intestinal epithelial cells, thereby promoting mucosal wound repair. Maresin 2 alleviates nociceptive and anxiety-like behaviors in rats with type 1 diabetes by inhibiting IL-1β in the spinal cord and prefrontal cortex. Maresin 2 attenuates allergic airway inflammation in mice by inhibiting the activation of the NLRP3 inflammasome, Th2-type immune responses, and oxidative stress. Maresin 2 inhibits inflammatory and neuropathic trigeminal neuralgia and reduces neuronal activation in the trigeminal ganglion. Maresin 2 promotes inflammation resolution and mucosal repair after DSS-induced colitis or biopsy-induced colonic mucosal injury .
    Maresin 2
  • HY-N1510

    Glycosidase Notch Toll-like Receptor (TLR) NF-κB Mucin Reactive Oxygen Species (ROS) Bacterial TGF-beta/Smad Anaplastic lymphoma kinase (ALK) Infection Inflammation/Immunology Cancer
    Kaempferol 3-O-gentiobioside is an orally active flavonoid, with a Ka value of 57 µM against human NOTCH1 and an IC50 value of 50 μM against α-glucosidase. Kaempferol 3-O-gentiobioside inhibits the NOTCH signaling pathway. It downregulates the expression of TLR4 and NLRP3, and suppresses the activation and nuclear translocation of NF-κB. Kaempferol 3-O-gentiobioside inhibits the expression of MUC5AC, reduces nitrite and ROS levels, and attenuates excessive mucus secretion. It exhibits antibacterial activity, reducing the formation and growth of MRSA biofilms. Kaempferol 3-O-gentiobioside blocks the TGF-β/ALK5/Smad signaling pathway and inhibits epithelial-mesenchymal transition. It suppresses the proliferation, migration, invasion and metastatic growth of tumor cells. Kaempferol 3-O-gentiobioside alleviates airway inflammation and mucus hypersecretion in mice with allergic asthma . It reduces the volume of ovarian cancer xenografts in mice. Kaempferol 3-O-gentiobioside can be used in research related to allergic asthma, diabetes, MRSA infection, breast cancer, gastric cancer and ovarian cancer .
    Kaempferol 3-O-gentiobioside
  • HY-150270A

    P2X Receptor Prostaglandin Receptor NOD-like Receptor (NLR) Caspase Interleukin Related Inflammation/Immunology
    NP-1815-PX sodium is an orally active dual inhibitor of P2X4 and prostaglandin TP receptors, with an IC50 of 0.26 μM against human P2X4 receptors. NP-1815-PX sodium specifically inhibits ATP-mediated prostaglandin production, TP receptor-induced calcium elevation, and the canonical/non-canonical NLRP3 inflammasome signaling pathway. NP-1815-PX sodium selectively blocks smooth muscle contractions induced by ATP, U46619 (HY-108566) and prostaglandin F2α. NP-1815-PX sodium not only produces anti-allodynic effects in vivo, but also significantly alleviates symptoms of DNBS (HY-W324435)-induced colitis (such as weight loss and tissue damage). NP-1815-PX sodium exerts anti-inflammatory effects by downregulating IL-1β levels and Caspase-1 activity. NP-1815-PX sodium is used in studies related to asthma and inflammatory bowel disease (colitis) .
    NP-1815-PX sodium
  • HY-N6893
    Ergolide
    3 Publications Verification

    NF-κB NOD-like Receptor (NLR) Apoptosis Autophagy Neurological Disease Cancer
    Ergolide is an orally active dual inhibitor targeting NF-κB/p65 and NLRP3. Ergolide blocks the NF-κB signaling pathway and the nuclear translocation of p65, and irreversibly binds to the NACHT domain of NLRP3 to inhibit inflammasome assembly. Ergolide significantly reduces the production of inflammatory mediators (e.g., NO, PGE2) and cytokines, induces cancer cell apoptosis, autophagy and ROS generation. Ergolide also enhances the anti-tumor effect of vincristine. Ergolide alleviates acute lung injury via an NLRP3-dependent mechanism, and effectively improves the survival rate and behavioral function of septic mice and inflammatory zebrafish models. Ergolide is used in the research of metastatic uveal melanoma, neurodegenerative diseases (such as Alzheimer's disease, Parkinson's disease), sepsis and acute lymphoblastic leukemia .
    Ergolide
  • HY-P6084

    NOD-like Receptor (NLR) p38 MAPK Apoptosis Inflammation/Immunology
    RP-220 is a renalase peptide targeting NLRP3. RP220 has anti-inflammatory and anti-apoptotic activities. RP220 inhibits renal tubular epithelial cells apoptosis with alkaline insult by activating MAPK signaling pathway. RP220 significantly inhibits NLRP3 expression and reduces macrophage infiltration and kidney tissue damage in acute kidney injury (AKI) mice model. RP-220 can be uses for systemic lupus erythematosus (SLE) and its complication lupus nephritis (LN) research .
    RP-220
  • HY-100573A
    (E/Z)-Necrosulfonamide
    1 Publications Verification

    Mixed Lineage Kinase Necroptosis Pyroptosis Caspase NOD-like Receptor (NLR) Keap1-Nrf2 TNF Receptor Interleukin Related NO Synthase Heme Oxygenase (HO) Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology Endocrinology
    (E/Z)-Necrosulfonamide is a racemic compound of Necrosulfonamide (HY-100573). Necrosulfonamide is a MLKL and Gasdermin D (GSDMD) inhibitor, capable of separately inhibiting necroptosis and pyroptosis of cells. Necrosulfonamide does not affect the activation of upstream signals, but specifically inhibits the downstream executor oligomerization step. Necrosulfonamide reduces the expression of the key kinases NLRP3 and caspase-1 involved in necroptosis and pyroptosis, activate the Nrf2 pathway and the downstream antioxidant enzymes, and also downregulates a variety of inflammatory factors. Necrosulfonamide plays significant roles in various diseases such as neurodegenerative diseases (such as Parkinson’s disease), tissue damage and ischemia-reperfusion injury, inflammatory bowel disease, osteoarthritis and fracture repair, and hair loss by regulating two important programmed necrosis pathways.
    (E/Z)-Necrosulfonamide
  • HY-164853

    Pyroptosis NOD-like Receptor (NLR) ERK FGFR AMPK Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Kanglexin is an orally active and novel anthraquinone compound. Kanglexin inhibits NLRP3 inflammatory body activation and cell pyroptosis, and has a cardioprotective effect. Kanglexin promotes angiogenesis through FGFR1/ERK signaling pathway and accelerates diabetic wound healing. In addition, Kanglexin has the effect of lipid-lowering and inhibiting the dedifferentiation of vascular smooth muscle cells, and can be used in the study of hyperlipidemia, fatty liver and atherosclerosis .
    Kanglexin
  • HY-161727

    P2Y Receptor NOD-like Receptor (NLR) Inflammation/Immunology
    P2Y14R antagonist 1 (compound I-17) is a selective P2Y14R antagonist with an IC50 of 0.6 nM. It exhibits potent P2Y14R antagonistic activity, both in vitro and in vivo efficacy, and favorable pharmacokinetic profiles. P2Y14R antagonist 1 reduces the release of inflammatory factors and cell pyroptosis through the NOD-like receptor family pyrin domain-containing 3 (NLRP3)/gasdermin D (GSDMD) signaling pathway. P2Y14R antagonist 1 holds promise for research in the field of acute gouty arthritis .
    P2Y14R antagonist 1
  • HY-N0671R
    Rhapontin (Standard)
    2 Publications Verification

    Rhaponiticin (Standard)

    Reference Standards Apoptosis Cardiovascular Disease Metabolic Disease Inflammation/Immunology Cancer
    Rhapontin (Standard) is the analytical standard of Rhapontin (HY-N0671). This product is intended for research and analytical applications. Rhapontin (Rhaponiticin) is an orally aactive SIRT1 agonist and AMPK activator with anti-inflammatory and anti-fibrotic activities. Rhapontin inhibits NLRP3 inflammasome activation by activating SIRT1 and inhibits TGF-β/Smad signaling via the AMPK pathway. Rhapontin reduces intestinal and lung inflammation, inhibits fibroblast differentiation and extracellular matrix deposition, and enhances tight junction protein expression to repair epithelial barriers. Rhapontin can be used in the study of inflammatory bowel diseases (such as ulcerative colitis) and pulmonary fibrosis .
    Rhapontin (Standard)
  • HY-126941

    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
  • HY-116084S1

    Isotope-Labeled Compounds NOD-like Receptor (NLR) Reactive Oxygen Species (ROS) TGF-beta/Smad Endogenous Metabolite Cardiovascular Disease Inflammation/Immunology
    Trimethylamine-N-oxide- 13C3 is the 13C-labeled Trimethylamine N-oxide. Trimethylamine N-oxide is a gut microbe-dependent metabolite of dietary choline and other trimethylamine-containing nutrients. Trimethylamine N-oxide induces inflammation by activating the ROS/NLRP3 inflammasome. Trimethylamine N-oxide also accelerates fibroblast-myofibroblast differentiation and induces cardiac fibrosis by activating the TGF-β/smad2 signaling pathway .
    Trimethylamine-N-oxide-13C3
  • HY-100573S

    Isotope-Labeled Compounds Mixed Lineage Kinase Necroptosis Pyroptosis Caspase NOD-like Receptor (NLR) Keap1-Nrf2 TNF Receptor Integrin NO Synthase Heme Oxygenase (HO) Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology Endocrinology
    Necrosulfonamide-d4 is the deuterium labeled Necrosulfonamide (HY-100573). Necrosulfonamide is a MLKL and Gasdermin D (GSDMD) inhibitor, capable of separately inhibiting necroptosis and pyroptosis of cells. Necrosulfonamide does not affect the activation of upstream signals, but specifically inhibits the downstream executor oligomerization step. Necrosulfonamide reduces the expression of the key kinases NLRP3 and caspase-1 involved in necroptosis and pyroptosis, activate the Nrf2 pathway and the downstream antioxidant enzymes, and also downregulates a variety of inflammatory factors. Necrosulfonamide plays significant roles in various diseases such as neurodegenerative diseases (such as Parkinson’s disease), tissue damage and ischemia-reperfusion injury, inflammatory bowel disease, osteoarthritis and fracture repair, and hair loss by regulating two important programmed necrosis pathways.
    Necrosulfonamide-d4
  • HY-175814

    NOD-like Receptor (NLR) Pyroptosis Interleukin Related Inflammation/Immunology
    NLRP3-IN-83 is a selective and orally active NLRP3 inflammasome activation inhibitor. NLRP3-IN-83 exhibits good inhibitory IL-1β activity with an IC50 of 1.4 μM by blocking NLRP3, independent of NF-κB signaling. NLRP3-IN-83 only slightly inhibits AIM2 inflammasome pathway, but has no effect on NLRC4 inflammasome. NLRP3-IN-83 prevent cell pyroptosis and exhibits significant anti-inflammatory efficacy in ulcerative colitis model. NLRP3-IN-83 can be used for the study of inflammatory bowel disease (IBD) .
    NLRP3-IN-83
  • HY-179387

    CXCR Autophagy NOD-like Receptor (NLR) Reactive Oxygen Species (ROS) Apoptosis Cancer
    CXCR2-IN-3 is a CXCR2 inhibitor with an IC50 of 11.37 μM. CXCR2-IN-3 mediates CXCR2-Ca 2+ signalling inhibition halted autophagic flux, subsequently facilitating ROS-mediated apoptotic cell death. CXCR2-IN-3 suppresses the CXCR2-NLRP3 canonical pathway, suppressing pre-tumorigenic markers. CXCR2-IN-3 causes autophagy-dependent cell death in polyploid giant cancer cells (PGCCs). CXCR2-IN-3 can be used for the research of oral squamous cell carcinoma (OSCC) .
    CXCR2-IN-3
  • HY-150270

    Prostaglandin Receptor P2X Receptor NOD-like Receptor (NLR) Caspase Interleukin Related Neurological Disease Inflammation/Immunology
    NP-1815-PX is an orally active dual inhibitor of P2X4 and prostaglandin TP receptors, with an IC50 of 0.26 μM against human P2X4 receptors. NP-1815-PX specifically inhibits ATP-mediated prostaglandin production, TP receptor-induced calcium elevation, and the canonical/non-canonical NLRP3 inflammasome signaling pathway. NP-1815-PX selectively blocks smooth muscle contractions induced by ATP, U46619 (HY-108566) and prostaglandin F2α. NP-1815-PX not only produces anti-allodynic effects in vivo, but also significantly alleviates symptoms of DNBS (HY-W324435)-induced colitis (such as weight loss and tissue damage). NP-1815-PX exerts anti-inflammatory effects by downregulating IL-1β levels and Caspase-1 activity. NP-1815-PX is used in studies related to asthma and inflammatory bowel disease (colitis) .
    NP-1815-PX
  • HY-116084R

    Drug Metabolite NOD-like Receptor (NLR) Reactive Oxygen Species (ROS) TGF-beta/Smad Endogenous Metabolite Reference Standards Cardiovascular Disease Inflammation/Immunology
    Trimethylamine N-oxide (Standard) is the analytical standard of Trimethylamine N-oxide. This product is intended for research and analytical applications. Trimethylamine N-oxide is a gut microbe-dependent metabolite of dietary choline and other trimethylamine-containing nutrients. Trimethylamine N-oxide induces inflammation by activating the ROS/NLRP3 inflammasome. Trimethylamine N-oxide also accelerates fibroblast-myofibroblast differentiation and induces cardiac fibrosis by activating the TGF-β/smad2 signaling pathway .
    Trimethylamine N-oxide (Standard)
  • HY-161266

    COX NOD-like Receptor (NLR) NF-κB Inflammation/Immunology
    COX-2/NLRP3-IN-1 (Compound 6k) is a COX-2/NLRP3 inhibitor with a IC50 of 1.53 μM for COX-2. COX-2/NLRP3-IN-1 exerts anti-inflammatory effects by inhibiting the NF-κB/NLRP3 signaling pathway .
    COX-2/NLRP3-IN-1
  • HY-170218

    NOD-like Receptor (NLR) Interleukin Related NF-κB NO Synthase Inflammation/Immunology
    NLRP3-IN-76 is an orally active NLRP3 inhibitor. NLRP3-IN-76 inhibits the production of NO, and the mRNA levels of proinflammatory cytokines (iNOS, IL-6, IL-1β and TNFα). NLRP3-IN-76 shows anti-inflammatory effects by inhibiting the activation of the NLRP3 inflammasome and NF-κB signaling pathway. NLRP3-IN-76 ameliorates DSS (HY-116282C)-induced colitis and can be used for research of inflammatory bowel diseases (IBD) .
    NLRP3-IN-76
  • HY-179421

    PROTACs HDAC NF-κB NOD-like Receptor (NLR) Interleukin Related TNF Receptor Inflammation/Immunology
    PROTAC HDAC6 degrader 7 is an orally active, highly efficient, and selective PROTAC degrader targeting histone deacetylase 6 (HDAC6) (IC50 = 118 nM). PROTAC HDAC6 degrader 7 can eliminate both the catalytic and zinc-finger ubiquitin-binding domain. PROTAC HDAC6 degrader 7 inhibits NLRP3 inflammasome assembly and activation, as well as blocks NF-κB signaling, thereby reducing the transcription and release of key inflammatory factors. PROTAC HDAC6 degrader 7 can reduce the mRNA levels of NLRP3, pro-IL-1β, TNF-α, and IL-6. PROTAC HDAC6 degrader 7 can be used for the study of inflammatory bowel disease (IBD) .
    PROTAC HDAC6 degrader 7
  • HY-179422

    Ligands for Target Protein for PROTAC HDAC Inflammation/Immunology
    HDAC6-IN-68 is an HDAC6 PROTAC ligand. HDAC6-IN-68 can be used to synthesize PROTAC HDAC6 degrader 7 (HY-179421) .
    HDAC6-IN-68
  • HY-N0373R

    Reference Standards Amyloid-β Apoptosis NOD-like Receptor (NLR) Neurological Disease
    Licochalcone B (Standard) is the analytical standard of Licochalcone B. This product is intended for research and analytical applications. Licochalcone B is an extract from the root of Glycyrrhiza uralensis. Licochalcone B inhibits amyloid β (42) self-aggregation (IC50=2.16 μM) and disaggregate pre-formed Aβ42 fibrils, reduce metal-induced Aβ42 aggregation through chelating metal ionsLicochalcone B inhibits phosphorylation of NF-κB p65 in LPS signaling pathway. Licochalcone B inhibits growth and induces apoptosis of NSCLC cells. Licochalcone B specifically inhibits the NLRP3 inflammasome by disrupting NEK7‐NLRP3 interaction .
    Licochalcone B (Standard)
  • HY-155753

    NF-κB COX Inflammation/Immunology
    Anti-inflammatory agent 50 (compound a1) is a Fusidic acid derivative with anti-inflammatory effects. Anti-inflammatory agent 50 inhibits inflammatory factor NO, IL-6 and TNF-α. Anti-inflammatory agent 50 alleviates acute lung injury by regulating inflammatory mediators and suppressing the MAPK, NF-κB and NLRP3 inflammasome signaling pathways .
    Anti-inflammatory agent 50

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