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Pathways Recommended: NF-κB Neuronal Signaling JAK/STAT Signaling
Results for "

NF-κB/AP-1 signaling

" in MedChemExpress (MCE) Product Catalog:

24

Inhibitors & Agonists

1

Biochemical Assay Reagents

1

Peptides

10

Natural
Products

2

Isotope-Labeled Compounds

Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-B1272
    Desipramine hydrochloride
    Maximum Cited Publications
    15 Publications Verification

    		 Adrenergic Receptor ERK JNK p38 MAPK NF-κB AP-1 Apoptosis Reactive Oxygen Species (ROS) Mitochondrial Metabolism TNF Receptor Neurological Disease Inflammation/Immunology Cancer
    Desipramine hydrochloride is a first-generation tricyclic antidepressant. Desipramine hydrochloride selectively binds to norepinephrine transporter and blocks neuronal norepinephrine reuptake. Desipramine hydrochloride activates MAPK signaling via ERK1/2, JNK, and p38, represses NF-κB and AP-1 activity, and induces apoptosis via ROS elevation, mitochondrial membrane potential reduction, and intracellular calcium increase. Desipramine hydrochloride also shows anyi-inflammatory activity, inhibiting TNF-α production. Desipramine hydrochloride can be used for the research of hepatocellular cancer, inflammation, and neurological diseases .
    Desipramine hydrochloride
  • HY-N2593
    Isorhapontigenin
    4 Publications Verification

    		 Carnitine Palmitoyltransferase (CPT) Reactive Oxygen Species (ROS) Autophagy Apoptosis NF-κB PI3K Akt MMP Keap1-Nrf2 Metabolic Disease Inflammation/Immunology Cancer
    Isorhapontigenin is an orally active dietary polyphenol. Isorhapontigenin acts as a potent antioxidant that reduces the production of reactive oxygen species (ROS). Isorhapontigenin promotes the binding of JUN to the AP-1 site on the SESN2 promoter, induces SESN2 transcription, triggers MAPK8-dependent JUN activation, and upregulates the expression of PPAR-α, PGC-1α and CPT-1A to facilitate fatty acid oxidation. Isorhapontigenin induces autophagy, apoptosis and preadipocyte differentiation; it inhibits tumor growth, cell invasion, NF-κB transcriptional activity, the PI3K/Akt signaling pathway, STAT1 phosphorylation and MMP-2 expression. Isorhapontigenin alleviates oxidative stress, inflammatory cytokine release and triglyceride accumulation; it increases intracellular ATP levels and promotes Nrf2 nuclear translocation. Isorhapontigenin improves insulin sensitivity in adipose tissue and glucose tolerance, and reduces postprandial blood glucose, insulin and free fatty acid levels. Isorhapontigenin is applicable to research on bladder cancer, liver injury, chronic obstructive pulmonary disease, acute lung injury and type 2 diabetes .
    Isorhapontigenin
  • HY-107574
    TC-E 5003
    3 Publications Verification

    		 Histone Methyltransferase AP-1 NF-κB PKA Metabolic Disease Inflammation/Immunology Cancer
    TC-E 5003 is a selective protein arginine methyltransferase 1 (PRMT1) inhibitor with an IC50 of 1.5 µM against hPRMT1. TC-E 5003 modulates the lipopolysaccharide (LPS) (HY-D1056)-induced AP-1 and NF-κB signaling pathways with anti-inflammatory properties. TC-E 5003 also upregulates the expression of Ucp1 and Fgf21, activates protein kinase A signaling and lipolysis in primary subcutaneous adipocytes from both mouse and humans. TC-E 5003 is promising for research of obesity and associated metabolic disorders, oxidative stress, inflammation and cancers .
    TC-E 5003
  • HY-N0815
    Resibufogenin
    Maximum Cited Publications
    7 Publications Verification

    Bufogenin; Recibufogenin

    		 PI3K Akt NF-κB AP-1 GSK-3 CDK Neurological Disease Inflammation/Immunology Cancer
    Resibufogenin is an orally active anticancer agent. Resibufogenin can be extracted from toad venom. Resibufogenin blocks signaling pathways such as PI3K/Akt, NF-κB, AP-1, activates GSK-3β, and regulates cyclin D1. Resibufogenin can activate central neurons. Resibufogenin has anti-inflammatory activity. Resibufogenin has anti-tumor effects on a variety of tumors such as multiple myeloma, renal cancer, colorectal cancer, pancreatic cancer, and glioma .
    Resibufogenin
  • HY-13755A
    (R)-Sulforaphane
    2 Publications Verification

    L-SulforAPhane

    		 Keap1-Nrf2 Bcl-2 Family Caspase Reactive Oxygen Species (ROS) NF-κB Inflammation/Immunology Cancer
    (R)-Sulforaphane (L-Sulforaphane) is a orally active, potent inducer of the Keap1/Nrf2/ARE pathway, exhibiting antioxidant and anticancer activities. (R)-Sulforaphane primarily functions by upregulating phase II detoxifying enzymes in cells, aiding in the removal of carcinogens and combating oxidative stress. (R)-Sulforaphane is capable of modulating gene expression, influencing various signaling pathways, including Nrf2, NF-κB, and AP-1. (R)-Sulforaphane can be used in studies of tumor biology, antioxidant defense mechanisms, as well as inflammation and immune responses .
    (R)-Sulforaphane
  • HY-122808
    (-)-Camphoric acid

    		mGluR NF-κB AP-1 Metabolic Disease
    (-)-Camphoric acid is the less active enantiomer of Camphoric acid. Camphoric acid induces glutamate receptor expression. Camphoric acid also significantly induces the activation of NF-κB and AP-1. Camphoric acid significantly stimulates the differentiation of mouse osteoblastic MC3T3-E1 subclone 4 cells. Camphoric acid has weak regulatory function towards glutamate receptors. Camphoric acid can induce mRNA expression of glutamate signaling molecules and activate transcription factors, thereby stimulating osteoblast differentiation .
    (-)-Camphoric acid
  • HY-W016412
    Coenzyme Q0
    2 Publications Verification

    CoQ0

    		 Apoptosis Autophagy EGFR Akt mTOR Caspase Bcl-2 Family Reactive Oxygen Species (ROS) PARP COX NO Synthase TNF Receptor Interleukin Related MMP NF-κB Neurological Disease Inflammation/Immunology Cancer
    Coenzyme Q0 (CoQ0) is a potent, oral active ubiquinone compound can be derived from Antrodia cinnamomea. Coenzyme Q0 induces apoptosis and autophagy, suppresses of HER-2/AKT/mTOR signaling to potentiate the apoptosis and autophagy mechanisms. Coenzyme Q0 regulates NFκB/AP-1 activation and enhances Nrf2 stabilization in attenuation of inflammation and redox imbalance. Coenzyme Q0 has anti-angiogenic activity through downregulation of MMP-9/NF-κB and upregulation of HO-1 signaling .
    Coenzyme Q0
  • HY-P2036A
    FSL-1 TFA
    4 Publications Verification

    		 Toll-like Receptor (TLR) MMP HSV Antibiotic Infection
    FSL-1 TFA, a bacterial-derived toll-like receptor 2/6 (TLR2/6) agonist, enhances resistance to experimental HSV-2 infection . FSL-1 TFA induces MMP-9 production through TLR2 and NF-κB/AP-1 signaling pathways in monocytic THP-1 cells .
    FSL-1 TFA
  • HY-110398
    5,6,7-Trimethoxyflavone
    1 Publications Verification

    Baicalein trimethyl ether

    		 NF-κB AP-1 STAT HSV CMV Enterovirus Infection Inflammation/Immunology
    5,6,7-Trimethoxyflavone is a flavonoid compound that can be isolated from plants Callicarpa japonica. 5,6,7-Trimethoxyflavone exhibits antiviral and anti-inflammatory activities through inhibition of NF-κB/AP-1/STAT signaling pathway .
    5,6,7-Trimethoxyflavone
  • HY-115062
    MJ33 lithium salt

    		Phospholipase NADPH Oxidase p38 MAPK Akt NF-κB AP-1 Reactive Oxygen Species (ROS) Cardiovascular Disease Inflammation/Immunology Cancer
    MJ-33 lithium salt is a competitive phospholipase A2 (PLA2) inhibitor with an IC50 of 0.3 μM. MJ-33 lithium salt inhibits NOX2 activation and reduces ROS production by blocking the PLA2 activity of Prdx6. MJ-33 lithium salt effectively inhibits the activity of acidic PLA2 (pH 4.0) and reduces the degradation of alveolar surfactant phosphatidylcholine (PC), but exerts no effect on alkaline PLA2 (pH 8.5). MJ-33 lithium salt significantly alleviates lung oxidative injury induced by ischemia-reperfusion (I/R). MJ-33 lithium salt significantly inhibits the invasion, migration and adhesion abilities of prostate cancer cells by suppressing the MAPK, AKT, NF-κB and AP-1 signaling pathways. MJ-33 lithium salt can be used for the research of ROS-related diseases and prostate cancer .
    MJ33 lithium salt
  • HY-141645
    IMM-H007

    WS070117

    		 AMPK TGF-β Receptor NF-κB JNK AP-1 Cardiovascular Disease Metabolic Disease Inflammation/Immunology
    IMM-H007 (WS070117) is an orally active and potent AMPK (AMP-activated protein kinase) activator and TGFβ1 (transforming growth factor β1) antagonist. IMM-H007 has protective effects in cardiovascular diseases via activation of AMPK. IMM-H007 negatively regulates endothelium inflammation through inactivating NF-κB and JNK/AP1 signaling. IMM-H007 inhibits ABCA1 degradation. IMM-H007 resolves hepatic steatosis in HFD-fed hamsters by the regulation of lipid metabolism. IMM-H007 can be used for the research of nonalcoholic fatty liver disease (NAFLD) and inflammatory atherosclerosis .
    IMM-H007
  • HY-101318
    β-Funaltrexamine hydrochloride
    2 Publications Verification

    β-FNA hydrochloride

    		 Opioid Receptor p38 MAPK STAT NF-κB NO Synthase Toll-like Receptor (TLR) Cardiovascular Disease Neurological Disease
    β-Funaltrexamine (β-FNA) hydrochloride is a blood-brain barrier-permeable, selective and irreversible μ-opioid receptor antagonist with immunomodulatory, anti-inflammatory and neuroprotective activities. β-Funaltrexamine hydrochloride inhibits p38 MAPK and TLR4 signaling by blocking μ-opioid receptors, and reduces the transcriptional activities of NF-κB, AP-1, CREB and Stat. Furthermore, β-Funaltrexamine hydrochloride inhibits iNOS activation and pro-inflammatory microglial polarization, converting microglia to an anti-inflammatory phenotype, thereby downregulating neuroinflammation and ameliorating neuronal degeneration. β-Funaltrexamine hydrochloride is widely applicable to research related to stroke, cerebral ischemia/reperfusion injury and neurodegenerative diseases .
    β-Funaltrexamine hydrochloride
  • HY-B1272A
    Desipramine

    		Adrenergic Receptor ERK JNK p38 MAPK NF-κB AP-1 Apoptosis Reactive Oxygen Species (ROS) Mitochondrial Metabolism TNF Receptor Neurological Disease Inflammation/Immunology Cancer
    Desipramine is a first-generation tricyclic antidepressant. Desipramine selectively binds to norepinephrine transporter and blocks neuronal norepinephrine reuptake. Desipramine activates MAPK signaling via ERK1/2, JNK, and p38, represses NF-κB and AP-1 activity, and induces apoptosis via ROS elevation, mitochondrial membrane potential reduction, and intracellular calcium increase. Desipramine also shows anyi-inflammatory activity, inhibiting TNF-α production. Desipramine can be used for the research of hepatocellular cancer, inflammation, and neurological diseases .
    Desipramine
  • HY-N1326
    Santamarine

    Santamarin; Balchanin

    		 JNK p38 MAPK MMP NF-κB COX TNF Receptor Interleukin Related Reactive Oxygen Species (ROS) Apoptosis Mitochondrial Metabolism DNA/RNA Synthesis Keap1-Nrf2 Bcl-2 Family Caspase PARP TGF-beta/Smad Metabolic Disease Inflammation/Immunology Cancer
    Santamarine (Santamarin; Balchanin) is a sesquiterpene lactone found in Artemisia scoparia. Santamarine shows anti-inflammatory, antioxidant, anticancer and anti-photoaging activities. Santamarine suppresses UVA-induced phosphorylation of JNK and p38 MAPK, nuclear translocation of phosphorylated c-Fos and c-Jun, and AP-1-mediated MMP-1 transcription and secretion. Santamarine suppresses NF-κB signaling, iNOS, COX-2, TNF-α, and IL-1β production. Santamarine inhibits thioredoxin reductase activity, induces ROS production, mitochondrial apoptosis, G2/M cell cycle arrest, and DNA damage, and reduces cancer cell growth. Santamarine can be used for the photoaging, inflammatory diseases and cancer .
    Santamarine
  • HY-B1272R
    Desipramine hydrochloride (Standard)

    		Reference Standards Adrenergic Receptor ERK JNK p38 MAPK NF-κB AP-1 Apoptosis Reactive Oxygen Species (ROS) Mitochondrial Metabolism TNF Receptor Neurological Disease Inflammation/Immunology Cancer
    Desipramine hydrochloride (Standard) is the analytical standard of Desipramine hydrochloride (HY-B1272). This product is intended for research and analytical applications. Desipramine hydrochloride is a first-generation tricyclic antidepressant. Desipramine hydrochloride selectively binds to norepinephrine transporter and blocks neuronal norepinephrine reuptake. Desipramine hydrochloride activates MAPK signaling via ERK1/2, JNK, and p38, represses NF-κB and AP-1 activity, and induces apoptosis via ROS elevation, mitochondrial membrane potential reduction, and intracellular calcium increase. Desipramine hydrochloride also shows anyi-inflammatory activity, inhibiting TNF-α production. Desipramine hydrochloride can be used for the research of hepatocellular cancer, inflammation, and neurological diseases .
    Desipramine hydrochloride (Standard)
  • HY-136271
    MJ33

    		Phospholipase NADPH Oxidase p38 MAPK Akt NF-κB AP-1 Reactive Oxygen Species (ROS) Cardiovascular Disease Inflammation/Immunology Cancer
    MJ-33 is a competitive phospholipase A₂ (PLA₂) inhibitor with an IC50 of 0.3 μM. MJ-33 inhibits the activation of NOX2 by blocking the PLA₂ activity of Prdx6, thereby reducing the production of ROS. MJ-33 effectively inhibits the activity of acidic PLA₂ (pH 4.0), reduces the degradation of pulmonary surfactant phosphatidylcholine (PC), but has no effect on alkaline PLA₂ (pH 8.5). MJ-33 significantly alleviates lung oxidative damage induced by ischemia-reperfusion (I/R). MJ-33 significantly inhibits the invasive, migratory and adhesive abilities of prostate cancer cells by suppressing the MAPK, AKT, NF-κB and AP-1 signaling pathways. MJ-33 can be used to study ROS-related diseases and prostate cancer .
    MJ33
  • HY-N6969A
    Dicentrine hydrochloride

    		Adrenergic Receptor Cancer
    Dicentrine hydrochloride is a drug with anti-inflammatory and anti-cancer activity. Dicentrine hydrochloride exerts its effects by enhancing TNF-α-induced apoptosis in A549 lung adenocarcinoma cells. Dicentrine hydrochloride increases caspase-8, -9, -3 and poly(ADP-ribose) polymerase (PARP) activities. Dicentrine hydrochloride inhibits TNF-α-induced invasion and migration of A549 cells. Dicentrine hydrochloride significantly inhibited the TNF-α-activated TAK1, p38, JNK and Akt signaling pathways, and reduced the transcriptional activities of NF-κB and AP-1 .
    Dicentrine hydrochloride
  • HY-B1272AS
    Desipramine-d4

    		Adrenergic Receptor ERK JNK p38 MAPK NF-κB AP-1 Apoptosis Reactive Oxygen Species (ROS) Mitochondrial Metabolism TNF Receptor Neurological Disease Inflammation/Immunology Cancer
    Desipramine-d4 is the deuterium labeled Desipramine (HY-B1272A). Desipramine is a first-generation tricyclic antidepressant. Desipramine selectively binds to norepinephrine transporter and blocks neuronal norepinephrine reuptake. Desipramine activates MAPK signaling via ERK1/2, JNK, and p38, represses NF-κB and AP-1 activity, and induces apoptosis via ROS elevation, mitochondrial membrane potential reduction, and intracellular calcium increase. Desipramine also shows anyi-inflammatory activity, inhibiting TNF-α production. Desipramine can be used for the research of hepatocellular cancer, inflammation, and neurological diseases .
    Desipramine-d4
  • HY-B1272AS1
    Desipramine-d3

    		Isotope-Labeled Compounds Adrenergic Receptor ERK JNK p38 MAPK NF-κB AP-1 Apoptosis Reactive Oxygen Species (ROS) Mitochondrial Metabolism TNF Receptor Neurological Disease Inflammation/Immunology Cancer
    Desipramine-d3 is the deuterium labeled Desipramine (HY-B1272A). Desipramine is a first-generation tricyclic antidepressant. Desipramine selectively binds to norepinephrine transporter and blocks neuronal norepinephrine reuptake. Desipramine activates MAPK signaling via ERK1/2, JNK, and p38, represses NF-κB and AP-1 activity, and induces apoptosis via ROS elevation, mitochondrial membrane potential reduction, and intracellular calcium increase. Desipramine also shows anyi-inflammatory activity, inhibiting TNF-α production. Desipramine can be used for the research of hepatocellular cancer, inflammation, and neurological diseases .
    Desipramine-d3
  • HY-N0815R
    Resibufogenin (Standard)

    Bufogenin (Standard); Recibufogenin (Standard)

    		 Reference Standards Others Cancer
    Resibufogenin (Standard) is the analytical standard of Resibufogenin. This product is intended for research and analytical applications. Resibufogenin is an orally active anticancer agent. Resibufogenin can be extracted from toad venom. Resibufogenin blocks signaling pathways such as PI3K/Akt, NF-κB, AP-1, activates GSK-3β, and regulates cyclin D1. Resibufogenin can activate central neurons. Resibufogenin has anti-inflammatory activity. Resibufogenin has anti-tumor effects on a variety of tumors such as multiple myeloma, renal cancer, colorectal cancer, pancreatic cancer, and glioma .
    Resibufogenin (Standard)
  • HY-N2593R
    Isorhapontigenin (Standard)

    		Reference Standards Carnitine Palmitoyltransferase (CPT) Reactive Oxygen Species (ROS) Autophagy Apoptosis NF-κB PI3K Akt MMP Keap1-Nrf2 Inflammation/Immunology Cancer
    Isorhapontigenin (Standard) is the analytical standard of Isorhapontigenin (HY-N2593). This product is intended for research and analytical applications. Isorhapontigenin is an orally active dietary polyphenol. Isorhapontigenin acts as a potent antioxidant that reduces the production of reactive oxygen species (ROS). Isorhapontigenin promotes the binding of JUN to the AP-1 site on the SESN2 promoter, induces SESN2 transcription, triggers MAPK8-dependent JUN activation, and upregulates the expression of PPAR-α, PGC-1α and CPT-1A to facilitate fatty acid oxidation. Isorhapontigenin induces autophagy, apoptosis and preadipocyte differentiation; it inhibits tumor growth, cell invasion, NF-κB transcriptional activity, the PI3K/Akt signaling pathway, STAT1 phosphorylation and MMP-2 expression. Isorhapontigenin alleviates oxidative stress, inflammatory cytokine release and triglyceride accumulation; it increases intracellular ATP levels and promotes Nrf2 nuclear translocation. Isorhapontigenin improves insulin sensitivity in adipose tissue and glucose tolerance, and reduces postprandial blood glucose, insulin and free fatty acid levels. Isorhapontigenin is applicable to research on bladder cancer, liver injury, chronic obstructive pulmonary disease, acute lung injury and type 2 diabetes.
    Isorhapontigenin (Standard)
  • HY-N17736
    Chikusetsusaponin IVa methyl ester

    CME

    		 NF-κB COX Interleukin Related TNF Receptor NO Synthase Prostaglandin Receptor CDK β-catenin Wnt Apoptosis Inflammation/Immunology Cancer
    Chikusetsusaponin IVa methyl ester (CME) is a natural triterpenoid saponin compound. Chikusetsusaponin IVa methyl ester induces G0/G1 cell cycle arrest and apoptosis in colon cancer cells by inhibiting the Wnt/β-catenin signaling pathway. By inhibiting the NF-κB and AP-1 signaling pathways, Chikusetsusaponin IVa methyl ester significantly reduces the production of NO, PGE₂ and pro-inflammatory cytokines (TNF-α, IL-6, IL-1β), and downregulates the levels of iNOS and COX-2. Chikusetsusaponin IVa methyl ester can be used in researches on colorectal cancer and inflammation .
    Chikusetsusaponin IVa methyl ester
  • HY-160938
    β-Funaltrexamine

    β-FNA

    		 Opioid Receptor STAT NF-κB Toll-like Receptor (TLR) NO Synthase p38 MAPK Cardiovascular Disease Neurological Disease
    β-Funaltrexamine (β-FNA) is a blood-brain barrier-permeable, selective and irreversible μ-opioid receptor antagonist with immunomodulatory, anti-inflammatory and neuroprotective activities. β-Funaltrexamine inhibits p38 MAPK and TLR4 signaling by blocking μ-opioid receptors, and reduces the transcriptional activities of NF-κB, AP-1, CREB and Stat. Furthermore, β-Funaltrexamine inhibits iNOS activation and pro-inflammatory microglial polarization, converting microglia to an anti-inflammatory phenotype, thereby downregulating neuroinflammation and ameliorating neuronal degeneration. β-Funaltrexamine is widely applicable to research related to stroke, cerebral ischemia/reperfusion injury and neurodegenerative diseases .
    β-Funaltrexamine
  • HY-107574R
    TC-E 5003 (Standard)

    		Reference Standards Histone Methyltransferase AP-1 NF-κB PKA Metabolic Disease Inflammation/Immunology Cancer
    TC-E 5003 (Standard) is the analytical standard of TC-E 5003 (HY-107574). This product is intended for research and analytical applications. TC-E 5003 is a selective protein arginine methyltransferase 1 (PRMT1) inhibitor with an IC50 of 1.5 µM against hPRMT1. TC-E 5003 modulates the lipopolysaccharide (LPS) (HY-D1056)-induced AP-1 and NF-κB signaling pathways with anti-inflammatory properties. TC-E 5003 also upregulates the expression of Ucp1 and Fgf21, activates protein Kinase A signaling and lipolysis in primary subcutaneous adipocytes from both mouse and humans. TC-E 5003 is promising for research of obesity and associated metabolic disorders, oxidative stress, inflammation and cancers .
    TC-E 5003 (Standard)

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