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

MAPK/JNK signaling pathway

" in MedChemExpress (MCE) Product Catalog:

61

Inhibitors & Agonists

1

Screening Libraries

5

Peptides

2

Inhibitory Antibodies

34

Natural
Products

5

Isotope-Labeled Compounds

Targets Recommended:
Cat. No. Product Name Target Research Areas Chemical Structure
  • HY-N0484
    Liensinine
    Maximum Cited Publications
    20 Publications Verification

    		 Reactive Oxygen Species (ROS) Autophagy Apoptosis VEGFR JAK Amyloid-β p38 MAPK HIF/HIF Prolyl-Hydroxylase STAT PI3K JNK Akt Cardiovascular Disease Neurological Disease Inflammation/Immunology Cancer
    Liensinine is a bisbenzylisoquinoline alkaloid. By inhibiting the PI3K/AKT and JNK/p38-MAPK signaling pathways, Liensinine suppresses autophagy and apoptosis, clears Aβ, and exerts anti-inflammatory, antioxidant and neuroprotective effects. Liensinine activates AMPK and inhibits the expression of HIF-1α and VEGF, thereby suppressing angiogenesis. Liensinine exerts anti-tumor effects through ROS-mediated inhibition of the JAK2/STAT3 signaling pathway. Liensinine can be used for the research of diseases such as Alzheimer's disease, hepatocellular carcinoma, osteosarcoma, sepsis-induced organ injury and stroke .
    Liensinine
  • HY-113402
    Gamma-glutamylcysteine
    4 Publications Verification

    γ-Glu-Cys

    		 Endogenous Metabolite Interleukin Related TNF Receptor AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Gamma-glutamylcysteine (γ-Glu-Cys) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine activates AMPK, SIRT1, IL-4/STAT6, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, JAK1/STAT1/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease .
    Gamma-glutamylcysteine
  • HY-111431
    p-Cresyl sulfate
    5+ Cited Publications

    p-Tolyl sulfate

    		 JNK p38 MAPK Reactive Oxygen Species (ROS) Metabolic Disease
    p-Cresyl sulfate (p-Tolyl sulfate) is a uremic toxin, that can cause renal damage and dysfunction. p-Cresyl sulfate shows antiproliferation activity. p-Cresyl sulfate increases the protein expression of HIF-1α and VHL, decreases the protein expression of HIF-2α. p-Cresyl sulfate induces epithelial-mesenchymal transition (EMT). p-Cresyl sulfate activates the JNK and p38 MAPK signaling pathways .
    p-Cresyl sulfate
  • HY-111431A
    p-Cresyl sulfate potassium
    5+ Cited Publications

    p-Tolyl sulfate potassium

    		 Endogenous Metabolite JNK p38 MAPK Metabolic Disease Inflammation/Immunology
    p-Cresyl sulfate potassium is a uremic toxin that binds to a prototype protein. p-Cresyl sulfate potassium activates the JNK and p38 MAPK signaling pathways. p-Cresyl sulfate potassium has pro-inflammatory activity .
    p-Cresyl sulfate potassium
  • HY-158426
    2-APQC
    1 Publications Verification

    		 Sirtuin Cardiovascular Disease
    2-APQC is an orally active and selective agonist of Sirtuin-3 (SIRT3) (Kd=2.756 μM), antagonizes Isoproterenol/ISO (HY-B0468)-induced cytotoxicity. 2-APQC activates the SIRT3-PYCR1 axis to enhance mitochondrial proline metabolism and inhibit the ROS-p38MAPK pathway by inhibiting signaling pathways such as mTOR-p70S6K, JNK, and TGF-β/Smad3. 2-APQC also activates the AMPK-Parkin axis to alleviate myocardial hypertrophy and fibrosis and protect cardiac function. 2-APQC can be used in the study of heart failure .
    2-APQC
  • HY-N0826
    Corynoline
    5+ Cited Publications

    		 Cholinesterase (ChE) Keap1-Nrf2 Heme Oxygenase (HO) COX NO Synthase p38 MAPK JNK Apoptosis Bcl-2 Family Caspase STAT Interleukin Related Neurological Disease Inflammation/Immunology Cancer
    Corynoline is an orally active acetylcholinesterase (AChE) inhibitor with an IC50 of 30.6 μM. Corynoline exhibits multiple activities including anti-inflammatory, antinociceptive, antitumor and analgesic effects. Corynoline can be used in the research of diseases such as tumors and inflammatory pain .
    Corynoline
  • HY-N0481
    Roburic acid
    1 Publications Verification

    		 COX TNF Receptor NO Synthase Interleukin Related NF-κB Apoptosis p38 MAPK JNK ERK Keap1-Nrf2 RANKL/RANK Neurological Disease Inflammation/Immunology Cancer
    Roburic acid acts as an anti-inflammatory, anti-tumor and osteoclastogenesis inhibitor, with a Ki of 7.066 μM against human TNF, an IC50 of 9 μM against human COX-2, and an IC50 of 5 μM against ovine COX-1. Roburic acid reduces the production of inflammatory mediators such as NO and IL-6 in macrophages by inhibiting the NF-κB and MAPK (p38/JNK) pathways. By competitively inhibiting the TNF-TNF-R1 interaction, Roburic acid blocks the downstream NF-κB signaling pathway, thereby inducing cell cycle arrest and apoptosis in cancer cells. Roburic acid specifically inhibits osteoclastogenesis and bone resorption by suppressing the RANKL/TRAF6/NF-κB/NFATc1 axis. Roburic acid can be used in research related to osteolytic diseases such as osteoporosis, colorectal cancer and inflammatory diseases .
    Roburic acid
  • HY-N0763
    Angelicin
    10+ Cited Publications

    Isopsoralen

    		 Apoptosis Virus Protease NF-κB p38 MAPK JNK Caspase Infection Inflammation/Immunology Cancer
    Angelicin is a furanocoumarin compound that functions as an inhibitor of NF-κB and MAPK signaling pathways, exhibiting anti-inflammatory, antiviral, and antitumor activities. It suppresses the lytic replication of γ-herpesviruses, such as MHV-68, early during viral infection, potentially inhibiting RTA gene expression (IC50=28.95 μM). Angelicin also mitigates inflammation by inhibiting the phosphorylation and nuclear translocation of NF-κB, and the phosphorylation of p38 and JNK. Furthermore, it induces apoptosis in neuroblastoma cells by downregulating anti-apoptotic proteins like Bcl-2, Bcl-xL, and Mcl-1, while activating caspase-9 and caspase-3.
    Angelicin
  • HY-113402A
    Gamma-glutamylcysteine TFA
    4 Publications Verification

    γ-Glu-Cys TFA

    		 Interleukin Related TNF Receptor Endogenous Metabolite AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Gamma-glutamylcysteine TFA (γ-Glu-Cys TFA) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine TFA activates AMPK, SIRT1, IL-4/STAT6, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, JAK1/STAT1/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine TFA regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine TFA is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease .
    Gamma-glutamylcysteine TFA
  • HY-N7046
    Silybin B

    Silibinin B

    		 Amyloid-β Apoptosis JNK p38 MAPK Neurological Disease Cancer
    Silybin B (Silibinin B) is an orally active amyloid-β aggregation inhibitor and ATR pathway activator that can cross the blood-brain barrier. Silybin B inhibits Aβ fibril formation and promotes amorphous aggregate formation, while activating the ATR-mediated DNA damage repair pathway and inhibiting JNK/p38 MAPK signaling. Silybin B can reduce Cisplatin (HY-17394)-induced neuronal DNA damage and apoptosis. Silybin B has anti-oxidative stress, cell cycle regulation and neuroprotective activities. Silybin B is mainly used in the study of Alzheimer's disease and Cisplatin chemotherapy-related neurotoxicity .
    Silybin B
  • HY-N0631
    Cornuside
    5+ Cited Publications

    		 p38 MAPK NF-κB JNK Cholinesterase (ChE) Acyltransferase NO Synthase Interleukin Related TNF Receptor Prostaglandin Receptor ERK COX Neurological Disease Inflammation/Immunology
    Cornuside is an iridoid glycoside with anti-allergic, anti-inflammatory, and neuroprotective activities. Cornuside exerts anti-allergic activity by downregulating the p38 MAPK, JNK, and NF-κB signaling pathways, and inhibits IgE-mediated histamine release from mast cells. Cornuside improves cognitive impairment in mice by inhibiting BACE1 activity (IC50 = 55.84 μg/mL) and enhancing ChAT activity. Cornuside inhibits LPS (HY-D1056)-induced inflammatory mediators, including iNOS, COX-2, PGE2, TNF-α, IL-6, and IL-1β, by suppressing NF-κB activation .
    Cornuside
  • HY-N0852
    Benzoylpaeoniflorin

    		p38 MAPK NF-κB Interleukin Related JNK PERK CXCR Cardiovascular Disease Inflammation/Immunology
    Benzoylpaeoniflorin is an orally active monoterpene glycoside compound. Benzoylpaeoniflorin exerts anti-inflammatory, anti-allergic, psoriasis-improving and sepsis-improving effects by inhibiting signaling pathways such as TNF/NF-κB and MAPK, as well as regulating immune homeostasis. Benzoylpaeoniflorin can be used in research related to immune, allergic and inflammatory diseases .
    Benzoylpaeoniflorin
  • 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-N0863
    Methyl protodioscin

    NSC-698790; Smilax saponin B

    		 Bcl-2 Family Apoptosis Akt c-Myc ERK p38 MAPK JNK FOXO Cancer
    Methyl protodioscin (NSC-698790; Smilax saponin B) is a multi-target, selective, steroidal diglycoside inhibitor with antitumor activity that induces cell cycle arrest. The mechanism of action of Methyl protodioscin is complex, involving the induction of G2/M cell cycle arrest, regulation of the Bcl-2/Bax apoptotic pathway, inhibition of the Akt1/c-Myc axis and MAPK/ERK signaling, while simultaneously downregulating ADAM15 and inducing FOXO1 to reduce cholesterol synthesis. It also inhibits the JNK/c-Jun pathway, reducing the production of inflammatory factors (IL-6, TNF-α). Methyl protodioscin exhibits significant antitumor (inhibiting proliferation, migration, invasion, and inducing apoptosis), anti-inflammatory, and anti-restenosis activities. Methyl protodioscin can be used in research on lung cancer, prostate cancer, pancreatic cancer, and other tumors, as well as inflammatory diseases such as airway inflammation and enteritis .
    Methyl protodioscin
  • HY-13703A
    Nimustine hydrochloride
    1 Publications Verification

    ACNU

    		 DNA Alkylator/Crosslinker DNA/RNA Synthesis Apoptosis p38 MAPK JNK AP-1 Cancer
    Nimustine hydrochloride (ACNU) is the hydrochloride salt form of Nimustine (HY-13703). Nimustine hydrochloride is an alkylating agent, which induces DNA double-strand breaks (DSBs) and inter-strand crosslinks (ICLs), thereby activating the DNA damage response (DDR) signaling pathway. Nimustine hydrochloride activates p38 MAPK/JNK signaling pathway, and exhibits antitumor activity .
    Nimustine hydrochloride
  • HY-B1014
    Acenocoumarol

    		VD/VDR p38 MAPK JNK ERK NF-κB Akt GSK-3 PKA Apoptosis Cardiovascular Disease Inflammation/Immunology Cancer
    Acenocoumarol is an anticoagulant that functions as a Vitamin K antagonist. Acenocoumarol inhibits MAPK/ERK/JNK signaling pathway, reduces the nuclear translocation of NF-κB p65, activates Akt/GSK3β signaling pathway. Acenocoumarol induces apoptosis in cell A549, arrests cell cycle at S phase .
    Acenocoumarol
  • HY-N2375
    L-Quebrachitol

    		Wnt β-catenin p38 MAPK Metabolic Disease
    L-Quebrachitol is a methoxy analog of inositol that can be isolated from plants. L-Quebrachitol has free-radical scavenging, gastroprotection, anti-platelet aggregation and anti-diabetic activity. L-Quebrachitol promotes osteoblastogenesis by uppregulation of BMP-2, runt-related transcription factor-2 (Runx2), MAPK (ERK, JNK, p38α), and Wnt/β-catenin signaling pathway .
    L-Quebrachitol
  • HY-N4322
    Decursinol angelate
    1 Publications Verification

    		 PKC Inflammation/Immunology Cancer
    Decursinol angelate acts as a PKC activator and GDH inhibitor, with an IC50 of 1.432 μM against human GDH. Decursinol angelate activates PKC, downregulates PKCα and PKCβII isoforms, and exerts cytotoxic activity against cancer cells. Decursinol angelate binds to GDH and inhibits its enzymatic activity. Decursinol angelate inhibits VEGF-induced autophosphorylation of VEGFR2, downstream p42/44 ERK and JNK-MAPK signaling pathways, as well as the angiogenesis process. Decursinol angelate is applicable to research related to cancer and leukemia .
    Decursinol angelate
  • HY-N1983
    Caudatin
    1 Publications Verification

    		 Apoptosis Autophagy Reactive Oxygen Species (ROS) Mitochondrial Metabolism PARP Caspase Bcl-2 Family VEGFR FAK WDR5 p38 MAPK JNK PPAR Neurological Disease Inflammation/Immunology Cancer
    Caudatin is an orally active and brain-penetrant C-21 steroidal found in Cynanchum bungei decne with a variety of biological activities. Caudatin can inhibit cell proliferation, migration, invasion, cause cell phase arrest, induce apoptosis, autophagy, ROS prodution and loss of mitochondrial membrane potential. Caudatin activates PARP, caspase-3, -7, -9, upregulates pro-apoptotic Bad and Bax and downregulates anti-apoptotic Bcl-2 and Bcl-XL. Caudatin suppresses VEGF, FAK phosphorylation, upregulates p21, p27, DR5 protein expression, activates the p38 MAPK, JNK and PPARα/TFEB-mediated autophagy-lysosomal signaling pathways. Caudatin can be used for the research of cancer, inflammation and neurological disease, such as glioma and Alzheimer's disease .
    Caudatin
  • HY-P991400
    GSK1995057

    		TNF Receptor Apoptosis Interleukin Related NF-κB JNK p38 MAPK Inflammation/Immunology
    GSK1995057 is a human monoclonal antibody (mAb) targeting TNFRSF1A. GSK1995057 selectively binds to TNFR1, blocks the binding of TNF-α and LT-α, and does not interfere with TNFR2 signaling. GSK1995057 inhibits the activation of NF-κB, JNK and MAPK pathways, alleviates apoptosis (apoptosis) and inflammatory responses (inhibiting IL-1β, IL-6, IL-10, TNF-α), and prevents viability loss of human nucleus pulposus cells. GSK1995057 inhibits the expression of cytokines and neutrophil adhesion molecules in human pulmonary microvascular endothelial cell monolayers, and reduces inflammatory responses and lung injury symptoms in non-human primates. GSK1995057 forms complexes with HAVH autoantibodies, thereby activating TNFR1 and triggering the release of cytokines and IL-8 in human cells. GSK1995057 can be used in research related to intervertebral disc degeneration and acute lung injury .
    GSK1995057
  • HY-N0363
    (+)-Columbianetin
    2 Publications Verification

    (S)-Columbianetin

    		 ERK JNK Collagen TGF-beta/Smad p38 MAPK Reactive Oxygen Species (ROS) Others
    (+)-Columbianetin ((S)-Columbianetin) acts as an inhibitor of JNK/ERK. (+)-Columbianetin inhibits UVA-induced phosphorylation of JNK and ERK, reduces the production of MMP-1, reverses UVA-induced Collagen (HY-NP003) degradation, and alleviates UVA-mediated inhibition of Smad2/3 phosphorylation and translocation. (+)-Columbianetin regulates the AP-1 and ASK1-MAPK signaling pathways, inhibits the production of ROS and blocks sub-G1 cell cycle arrest. (+)-Columbianetin is applicable to research related to skin aging .
    (+)-Columbianetin
  • HY-160469
    INY-05-040

    		Akt PROTACs Cancer
    INY-05-040 is an AKT degrader that can selectively and quickly degrade all three AKT isoforms. INY-05-040 exhibits anti-cancer activity. INY-05-040 can inhibit downstream signaling and cell proliferation in 288 cancer cell lines. INY-05-040 can suppress AKT signaling and induces the stress mitogen-activated protein kinase (MAPK) c-Jun N-terminal kinase (JNK). INY-05-040 is effective for breast cancer lines with a low-baseline activation of stress MAPK pathway. INY-05-040 can be studied for anti-cancer research .
    INY-05-040
  • HY-Y1322
    Triphenyl phosphate

    		Environmental Pollutants Mitophagy Apoptosis NF-κB p38 MAPK ERK JNK PI3K Akt Monoamine Oxidase Reactive Oxygen Species (ROS) PPAR Indoleamine 2,3-Dioxygenase (IDO) Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology Endocrinology
    Triphenyl phosphate is an orally active, blood-brain barrier-permeable aryl organophosphate flame retardant and endocrine disruptor. Triphenyl phosphate disrupts mitochondrial dynamic balance through oxidative stress, induces excessive mitophagy and apoptosis, and ultimately leads to myocardial fibrosis. In the brain, Triphenyl phosphate activates the NF-κB inflammatory pathway by disrupting the gut microbiota, alters tryptophan metabolism and elevates neurotoxins, thereby inducing anxiety- and depression-like behaviors. In the skeletal and reproductive systems, Triphenyl phosphate inhibits osteoblast differentiation and induces germ cell apoptosis by suppressing the MAPK/ERK pathway and activating the JNK signal, respectively. In adipose and placental tissues, Triphenyl phosphate promotes lipid accumulation by activating the PI3K/AKT-PPARγ axis, and disrupts placental metabolism via the MAOA/ROS/NF-κB cascade, impairing neurodevelopment of offspring .
    Triphenyl phosphate
  • HY-171705
    KMS99220

    		Keap1-Nrf2 AMPK JNK IKK p38 MAPK NO Synthase α-synuclein Interleukin Related Neurological Disease
    KMS99220 is an orally active, blood-brain barrier-permeable activator of the Nrf2 inhibitory protein Keap-1. KMS99220 enhances the activity of AMPK, activates the Nrf2 signaling pathway, and reduces the phosphorylation of IκB, nuclear translocation of NFκB, as well as the phosphorylation levels of JNK, IKK and p38 MAPK via HO-1. KMS99220 binds to Keap1 to trigger the nuclear translocation of Nrf2, induces the expression of HO-1, NQO1, GCLC, GCLM and proteasome subunits; enhances proteasomal enzymatic activity; inhibits iNOS expression, nitric oxide production and IL-1β generation; attenuates microglial activation; reduces α-synuclein aggregation; and prevents dopaminergic neuron degeneration and motor dysfunction. KMS99220 prevents the degeneration of dopaminergic neurons in the substantia nigra, induces the expression of Nrf2 downstream target genes, and effectively ameliorates associated motor dysfunction in a mouse model of Parkinson's disease. KMS99220 is applicable to research related to Parkinson's disease .
    KMS99220
  • HY-N5073
    Vitexin-4''-O-glucoside

    4''-O-Glucosylvitexin

    		 JNK p38 MAPK Interleukin Related TNF Receptor Caspase Lactate Dehydrogenase Apoptosis Cardiovascular Disease Metabolic Disease
    Vitexin-4''-O-glucoside (4''-O-Glucosylvitexin) is an orally active natural flavonoid component with multiple pharmacological effects including antioxidation, anti-inflammation, cytoprotection and anti-apoptosis. Vitexin-4''-O-glucoside regulates the MAPK signaling pathway by downregulating the phosphorylation levels of JNK and p38, thereby blocking endoplasmic reticulum stress responses. Vitexin-4''-O-glucoside alleviates oxidative stress by reducing MDA content and upregulating the activities of SOD and CAT, attenuates inflammation by downregulating the expressions of inflammatory factors TNF-α, IL-1β and IL-6, and also reduces LDH release and inhibits caspase-3 activation. Vitexin-4''-O-glucoside effectively improves drug-induced acute liver injury and exerts significant protective effects against myocardial hypoxia/reoxygenation injury. Vitexin-4''-O-glucoside can be used in studies on acute liver injury, cardiovascular diseases and myocardial hypoxia-reoxygenation injury .
    Vitexin-4''-O-glucoside
  • HY-126858
    Ambuic acid

    (+)-Ambuic acid

    		 ERK JNK NO Synthase COX Infection Inflammation/Immunology
    Ambuic acid exhibits antimicrobial activity against Staphylococcus aureus, with IC50 of 43.9 μM for strain ATCC 6538. Ambuic acid is an inhbitor for the biosynthesis of cyclic peptide quorum sensing molecules (quormones) in gram-positive bacteria. Ambuic acid exhibits anti-inflammatory activity through ERK/JNK/MAPK signaling pathway .
    Ambuic acid
  • HY-125953
    Ceramide (Egg)

    Ceramide (Egg, Chicken)

    		 JNK p38 MAPK Phosphatase Akt Survivin CDK mTOR Apoptosis Autophagy Reactive Oxygen Species (ROS) Neurological Disease Cancer
    Ceramide (Egg) (Ceramide (Egg, Chicken)) is a ceramide from chicken. Ceramide (Egg) is a sphingomyelin signaling pathway second messenger. Ceramide (Egg) activates PP2A, JNK, p38 MAPK, CAPK, ceramide-activated protein phosphatase, Vav, PKCζ, and SAPK/JNK cascade. Ceramide (Egg) downregulates or inhibits AKT, survivin, CDK2, mTOR, and FLIP. Ceramide (Egg) mediates apoptosis, autophagy, cell cycle arrest, mitochondrial dysfunction, redox state shifts, and ROS generation. Ceramide (Egg) can be used for the research of cancer and neurological disease .
    Ceramide (Egg)
  • HY-N6576
    Hellebrigenin

    		p38 MAPK ERK JNK IAP PARP Apoptosis Caspase Cancer
    Hellebrigenin is an inhibitor that selectively targets the MAPK signaling pathway (ERK, p38, JNK) and XIAP, and can inhibit Akt expression and phosphorylation. Hellebrigenin can activate endogenous apoptosis pathways (such as mitochondrial membrane potential disruption, Caspase family activation, PARP cleavage), downregulate anti-apoptotic proteins (Bcl-2, Bcl-xL) and upregulate pro-apoptotic proteins (Bax, Bak). Hellebrigenin can also induce DNA double-strand breaks to activate the ATM pathway. Hellebrigenin can inhibit tumor cell proliferation and clone formation, and is mainly used in the study of oral squamous cell carcinoma, liver cancer and other cancers .
    Hellebrigenin
  • HY-N5014
    Liensinine perchlorate
    Maximum Cited Publications
    20 Publications Verification

    		 Reactive Oxygen Species (ROS) Autophagy Apoptosis VEGFR JAK Amyloid-β p38 MAPK HIF/HIF Prolyl-Hydroxylase STAT PI3K JNK Akt Cardiovascular Disease Neurological Disease Inflammation/Immunology Cancer
    Liensinine perchlorate is a bisbenzylisoquinoline alkaloid. By inhibiting the PI3K/AKT and JNK/p38-MAPK signaling pathways, Liensinine perchlorate suppresses autophagy and apoptosis, clears Aβ, and exerts anti-inflammatory, antioxidant and neuroprotective effects. Liensinine perchlorate activates AMPK and inhibits the expression of HIF-1α and VEGF, thereby suppressing angiogenesis. Liensinine perchlorate exerts anti-tumor effects through ROS-mediated inhibition of the JAK2/STAT3 signaling pathway. Liensinine perchlorate can be used for the research of diseases such as Alzheimer's disease, hepatocellular carcinoma, osteosarcoma, sepsis-induced organ injury and stroke .
    Liensinine perchlorate
  • HY-113402R
    Gamma-glutamylcysteine (Standard)

    γ-Glu-Cys (Standard)

    		 Reference Standards Endogenous Metabolite Interleukin Related TNF Receptor AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis Inflammation/Immunology
    Gamma-glutamylcysteine (Standard) is the analytical standard of Gamma-glutamylcysteine. This product is intended for research and analytical applications. Gamma-glutamylcysteine (γ-Glu-Cys) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine activates AMPK, SIRT1, IL-4/STAT6, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, JAK1/STAT1/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease.
    Gamma-glutamylcysteine (Standard)
  • HY-111431AR
    p-Cresyl sulfate potassium (Standard)

    p-Tolyl sulfate potassium (Standard)

    		 JNK p38 MAPK Reactive Oxygen Species (ROS) Reference Standards Metabolic Disease
    p-Cresyl sulfate (potassium) (Standard) is the analytical standard of p-Cresyl sulfate (potassium). This product is intended for research and analytical applications. p-Cresyl sulfate (p-Tolyl sulfate) potassium is a uremic toxin, that can cause renal damage and dysfunction. p-Cresyl sulfate potassium shows antiproliferation activity. p-Cresyl sulfate potassium increases the protein expression of HIF-1α and VHL, decreases the protein expression of HIF-2α. p-Cresyl sulfate potassium induces epithelial-mesenchymal transition (EMT). p-Cresyl sulfate potassium activates the JNK and p38 MAPK signaling pathways .
    p-Cresyl sulfate potassium (Standard)
  • HY-Y1322S
    Triphenyl phosphate-d15

    Celluflex TPP-d15; DHPF 005-d15; Disflamol TP-d15; Disflamoll TP-d15; NSC 57868-d15; Phenyl phosphate ((PhO)3PO)-d15; Phoscon FR 903N-d15

    		 Isotope-Labeled Compounds Environmental Pollutants ERK Indoleamine 2,3-Dioxygenase (IDO) p38 MAPK NF-κB Akt Monoamine Oxidase Mitophagy Reactive Oxygen Species (ROS) JNK PI3K PPAR Apoptosis Cardiovascular Disease Neurological Disease Metabolic Disease Inflammation/Immunology Endocrinology
    Triphenyl phosphate-d15 is the deuterium labeled Triphenyl phosphate. Triphenyl phosphate is an orally active, blood-brain barrier-permeable aryl organophosphate flame retardant and endocrine disruptor. Triphenyl phosphate disrupts mitochondrial dynamic balance through oxidative stress, induces excessive mitophagy and apoptosis, and ultimately leads to myocardial fibrosis. In the brain, Triphenyl phosphate activates the NF-κB inflammatory pathway by disrupting the gut microbiota, alters tryptophan metabolism and elevates neurotoxins, thereby inducing anxiety- and depression-like behaviors. In the skeletal and reproductive systems, Triphenyl phosphate inhibits osteoblast differentiation and induces germ cell apoptosis by suppressing the MAPK/ERK pathway and activating the JNK signal, respectively. In adipose and placental tissues, Triphenyl phosphate promotes lipid accumulation by activating the PI3K/AKT-PPARγ axis, and disrupts placental metabolism via the MAOA/ROS/NF-κB cascade, impairing neurodevelopment of offspring.
    Triphenyl phosphate-d15
  • HY-N1983R
    Caudatin (Standard)

    		Reference Standards Apoptosis Autophagy Reactive Oxygen Species (ROS) Mitochondrial Metabolism PARP Caspase Bcl-2 Family VEGFR FAK WDR5 p38 MAPK JNK PPAR Neurological Disease Inflammation/Immunology Cancer
    Caudatin (Standard) is the analytical standard of Caudatin (HY-N1983). This product is intended for research and analytical applications. Caudatin is an orally active and brain-penetrant C-21 steroidal found in Cynanchum bungei decne with a variety of biological activities. Caudatin can inhibit cell proliferation, migration, invasion, cause cell phase arrest, induce apoptosis, autophagy, ROS prodution and loss of mitochondrial membrane potential. Caudatin activates PARP, caspase-3, -7, -9, upregulates pro-apoptotic Bad and Bax and downregulates anti-apoptotic Bcl-2 and Bcl-XL. Caudatin suppresses VEGF, FAK phosphorylation, upregulates p21, p27, DR5 protein expression, activates the p38 MAPK, JNK and PPARα/TFEB-mediated autophagy-lysosomal signaling pathways. Caudatin can be used for the research of cancer, inflammation and neurological disease, such as glioma and Alzheimer's disease .
    Caudatin (Standard)
  • HY-119420
    Acetoxycycloheximide

    		Antibiotic Apoptosis Caspase JNK p38 MAPK TNF Receptor ERK NF-κB Mitochondrial Metabolism Inflammation/Immunology Cancer
    Acetoxycycloheximide is an antibiotic with antitumor activity. Acetoxycycloheximide a protein synthesis inhibitor. Acetoxycycloheximide significantly induces activation of procaspase-3 and subsequent apoptosis mediated by the Cytochrome c from mitochondria via activation of JNK pathway. Acetoxycycloheximide triggers the downregulation of cell surface TNF-R1 via the activation of ERK and p38 MAPK, thereby preventing activation of the NF-κB signaling pathway by TNF-α. Acetoxycycloheximide is much more toxic to female rats than to males. Acetoxycycloheximide can be used for inflammatory and immune diseases and cancers research .
    Acetoxycycloheximide
  • HY-13703
    Nimustine

    		Apoptosis DNA Alkylator/Crosslinker DNA/RNA Synthesis p38 MAPK JNK AP-1 Cancer
    Nimustine is an alkylating agent, which induces DNA double-strand breaks (DSBs) and inter-strand crosslinks (ICLs), thereby activating the DNA damage response (DDR) signaling pathway. Nimustine activates p38 MAPK/JNK signaling pathway, and exhibits antitumor activity .
    Nimustine
  • HY-149087
    MR2938

    		Cholinesterase (ChE) NF-κB Interleukin Related TNF Receptor CCR NOD-like Receptor (NLR) JNK NO Synthase Neurological Disease Inflammation/Immunology
    MR2938 is a potent AChE inhibitor, with an IC50 of 5.04 μM. MR2938 also suppresses NO production obviously (IC50 = 3.29 μM). MR2938 suppresses the neuroinflammation through blocking MAPK/JNK and NF-κB signaling pathways. MR2938 can be used for Alzheimer’s disease (AD) research .
    MR2938
  • HY-P11250
    HVF18-a3-d

    		Bacterial NO Synthase Interleukin Related Reactive Oxygen Species (ROS) Toll-like Receptor (TLR) ERK JNK p38 MAPK Infection Inflammation/Immunology
    HVF18-a3-d is an antimicrobial peptide. HVF18-a3-d reduces NO production. HVF18-a3-d inhibits the production of TNF-α and IL-6, reduces ROS production, and suppresses the TLR4 signaling pathway, as well as LPS-induced phosphorylation of ERK, JNK, and p38 MAPK. HVF18-a3-d exhibits antimicrobial activity against a variety of bacteria by disrupting their outer and inner membranes. HVF18-a3-d protects mice from fatal septic shock induced by Acinetobacter baumannii resistant to Carbapenem. HVF18-a3-d shows anti-inflammatory and antioxidant effects .
    HVF18-a3-d
  • HY-113402AR
    Gamma-glutamylcysteine TFA (Standard)

    γ-Glu-Cys TFA (Standard)

    		 Interleukin Related TNF Receptor Endogenous Metabolite Reference Standards AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Gamma-glutamylcysteine (TFA) (Standard) is the analytical standard of Gamma-glutamylcysteine (TFA). This product is intended for research and analytical applications. Gamma-glutamylcysteine TFA (γ-Glu-Cys TFA) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine TFA activates AMPK, SIRT1, IL-4/STAT6, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, JAK1/STAT1/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine TFA regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine TFA is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease.
    Gamma-glutamylcysteine TFA (Standard)
  • HY-B1014S1
    Acenocoumarol-d4

    		Isotope-Labeled Compounds VD/VDR Apoptosis ERK GSK-3 PKA Akt NF-κB p38 MAPK JNK Cardiovascular Disease Inflammation/Immunology Cancer
    Acenocoumarol-d4 is deuterium labeled Acenocoumarol (HY-B1014). Acenocoumarol is an anticoagulant that functions as a Vitamin K antagonist. Acenocoumarol inhibits MAPK/ERK/JNK signaling pathway, reduces the nuclear translocation of NF-κB p65, activates Akt/GSK3β signaling pathway. Acenocoumarol induces apoptosis in cell A549, arrests cell cycle at S phase .
    Acenocoumarol-d4
  • HY-B1014R
    Acenocoumarol (Standard)

    		VD/VDR p38 MAPK JNK ERK NF-κB Akt GSK-3 PKA Apoptosis Reference Standards Cardiovascular Disease Inflammation/Immunology Cancer
    Acenocoumarol (Standard) is the analytical standard of Acenocoumarol. This product is intended for research and analytical applications. Acenocoumarol is an anticoagulant that functions as a Vitamin K antagonist. Acenocoumarol inhibits MAPK/ERK/JNK signaling pathway, reduces the nuclear translocation of NF-κB p65, activates Akt/GSK3β signaling pathway. Acenocoumarol induces apoptosis in cell A549, arrests cell cycle at S phase .
    Acenocoumarol (Standard)
  • HY-B1014S
    Acenocoumarol-d5

    		Isotope-Labeled Compounds VD/VDR Apoptosis ERK GSK-3 PKA Akt NF-κB p38 MAPK JNK Cardiovascular Disease Inflammation/Immunology Cancer
    Acenocoumarol-d5 is the deuterium labeled Acenocoumarol (HY-B1014). Acenocoumarol is an anticoagulant that functions as a Vitamin K antagonist. Acenocoumarol inhibits MAPK/ERK/JNK signaling pathway, reduces the nuclear translocation of NF-κB p65, activates Akt/GSK3β signaling pathway. Acenocoumarol induces apoptosis in cell A549, arrests cell cycle at S phase .
    Acenocoumarol-d5
  • HY-W654121
    p-Cresol sulfate-d4 potassium

    p-Tolyl sulfate-d4 potassium

    		 Isotope-Labeled Compounds Endogenous Metabolite p38 MAPK JNK Inflammation/Immunology
    p-Cresol sulfate-d4 (potassium) is deuterium labeled p-Cresyl sulfate (potassium). p-Cresyl sulfate potassium is a uremic toxin that binds to a prototype protein. p-Cresyl sulfate potassium activates the JNK and p38 MAPK signaling pathways. p-Cresyl sulfate potassium has pro-inflammatory activity .
    p-Cresol sulfate-d4 potassium
  • HY-N2375R
    L-Quebrachitol (Standard)

    		Reference Standards Wnt β-catenin p38 MAPK Metabolic Disease
    L-Quebrachitol is a methoxy analog of inositol that can be isolated from plants. L-Quebrachitol has free-radical scavenging, gastroprotection, anti-platelet aggregation and anti-diabetic activity. L-Quebrachitol promotes osteoblastogenesis by uppregulation of BMP-2, runt-related transcription factor-2 (Runx2), MAPK (ERK, JNK, p38α), and Wnt/β-catenin signaling pathway .
    L-Quebrachitol (Standard)
  • HY-N0484R
    Liensinine (Standard)

    		Reference Standards Reactive Oxygen Species (ROS) Autophagy Apoptosis VEGFR JAK Amyloid-β p38 MAPK HIF/HIF Prolyl-Hydroxylase STAT PI3K JNK Akt Cardiovascular Disease Neurological Disease Cancer
    Liensinine (Standard) is the analytical standard of Liensinine (HY-N0484). This product is intended for research and analytical applications. Liensinine is a bisbenzylisoquinoline alkaloid. By inhibiting the PI3K/AKT and JNK/p38-MAPK signaling pathways, Liensinine suppresses autophagy and apoptosis, clears Aβ, and exerts anti-inflammatory, antioxidant and neuroprotective effects. Liensinine activates AMPK and inhibits the expression of HIF-1α and VEGF, thereby suppressing angiogenesis. Liensinine exerts anti-tumor effects through ROS-mediated inhibition of the JAK2/STAT3 signaling pathway. Liensinine can be used for the research of diseases such as Alzheimer's disease, hepatocellular carcinoma, osteosarcoma, sepsis-induced organ injury and stroke .
    Liensinine (Standard)
  • HY-169412
    MAPK-IN-3

    		MDM-2/p53 CDK Caspase Bcl-2 Family Reactive Oxygen Species (ROS) p38 MAPK ERK JNK Cancer
    MAPK-IN-3 (Compound 4a) is an anti-proliferative agent that shows particularly strong inhibitory effects on KYSE 30, HCT 116, and HGC 27, with IC50 values of 0.57 μM, 3.27 μM, and 2.28 μM, respectively. MAPK-IN-3 blocks the cell cycle via a p53-dependent mechanism and induces cell apoptosis through a p53-independent mechanism. MAPK-IN-3 downregulates the expression of cell cycle-related proteins like Cyclin D1 and cyclin B1, upregulates pro-apoptotic proteins such as cleaved PARP, cleaved caspase-7, and cleaved caspase-9, and reduces the expression of anti-apoptotic proteins like Bcl-2. Additionally, MAPK-IN-3 increases the intracellular level of ROS in KYSE 30 cells and upregulates the expression of members of the MAPK signaling pathway associated with ROS, such as p-ERK, p-p38 and p-JNK .
    MAPK-IN-3
  • HY-N0481R
    Roburic acid (Standard)

    		Reference Standards COX TNF Receptor NO Synthase Interleukin Related NF-κB Apoptosis p38 MAPK JNK ERK Keap1-Nrf2 RANKL/RANK Inflammation/Immunology
    Roburic acid (Standard) is the analytical standard of Roburic acid. This product is intended for research and analytical applications. Roburic acid acts as an anti-inflammatory, anti-tumor and osteoclastogenesis inhibitor, with a Ki of 7.066 μM against human TNF, an IC50 of 9 μM against human COX-2, and an IC50 of 5 μM against ovine COX-1. Roburic acid reduces the production of inflammatory mediators such as NO and IL-6 in macrophages by inhibiting the NF-κB and MAPK (p38/JNK) pathways. By competitively inhibiting the TNF-TNF-R1 interaction, Roburic acid blocks the downstream NF-κB signaling pathway, thereby inducing cell cycle arrest and apoptosis in cancer cells. Roburic acid specifically inhibits osteoclastogenesis and bone resorption by suppressing the RANKL/TRAF6/NF-κB/NFATc1 axis. Roburic acid can be used in research related to osteolytic diseases such as osteoporosis, colorectal cancer and inflammatory diseases.
    Roburic acid (Standard)
  • HY-N7046R
    Silybin B (Standard)

    Silibinin B (Standard)

    		 Reference Standards JNK Amyloid-β p38 MAPK Apoptosis Neurological Disease Cancer
    Silybin (Silibinin B) (Standard) is the analytical standard of Silybin B (HY-N7046). This product is intended for research and analytical applications. Silybin B (Silibinin B) is an orally active amyloid-β aggregation inhibitor and ATR pathway activator, that can cross the blood-brain barrier. Silybin B inhibits Aβ fibril formation and promotes amorphous aggregate formation, while activating the ATR-mediated DNA damage repair pathway and inhibiting JNK/p38 MAPK signaling. Silybin B can reduce Cisplatin (HY-17394)-induced neuronal DNA damage and apoptosis. Silybin B has anti-oxidative stress, cell cycle regulation and neuroprotective activities. Silybin B is mainly used in the study of Alzheimer's disease and Cisplatin chemotherapy-related neurotoxicity .
    Silybin B (Standard)
  • HY-N7046S
    Silybin B-d3

    Silibinin B-d3

    		 Isotope-Labeled Compounds Amyloid-β Apoptosis JNK p38 MAPK Neurological Disease Cancer
    Silybin B-d3 (Silibinin B-d3) is a deuterated Silybin B (HY-N7046). Silybin B (Silibinin B) is an orally active amyloid-β aggregation inhibitor and ATR pathway activator, that can cross the blood-brain barrier. Silybin B inhibits Aβ fibril formation and promotes amorphous aggregate formation, while activating the ATR-mediated DNA damage repair pathway and inhibiting JNK/p38 MAPK signaling. Silybin B can reduce Cisplatin (HY-17394)-induced neuronal DNA damage and apoptosis. Silybin B has anti-oxidative stress, cell cycle regulation and neuroprotective activities. Silybin B is mainly used in the study of Alzheimer's disease and Cisplatin chemotherapy-related neurotoxicity .
    Silybin B-d3
  • HY-N0631R
    Cornuside (Standard)

    		Reference Standards Prostaglandin Receptor ERK p38 MAPK Acyltransferase TNF Receptor COX Cholinesterase (ChE) Interleukin Related JNK NO Synthase NF-κB Neurological Disease Inflammation/Immunology
    Cornuside (Standard) is the analytical standard of Cornuside (HY-N0631). This product is intended for research and analytical applications. Cornuside is an iridoid glycoside with anti-allergic, anti-inflammatory, and neuroprotective activities. Cornuside exerts anti-allergic activity by downregulating the p38 MAPK, JNK, and NF-κB signaling pathways, and inhibits IgE-mediated histamine release from mast cells. Cornuside improves cognitive impairment in mice by inhibiting BACE1 activity (IC50 = 55.84 μg/mL) and enhancing ChAT activity. Cornuside inhibits LPS (HY-D1056)-induced inflammatory mediators, including iNOS, COX-2, PGE2, TNF-α, IL-6, and IL-1β, by suppressing NF-κB activation.
    Cornuside (Standard)
  • HY-113402B
    Gamma-glutamylcysteine ammonium

    γ-Glu-Cys ammonium

    		 Interleukin Related TNF Receptor Endogenous Metabolite AMPK Sirtuin STAT PI3K NF-κB JAK p38 MAPK JNK Akt Apoptosis Ferroptosis Cardiovascular Disease Neurological Disease Inflammation/Immunology
    Gamma-glutamylcysteine ammonium (γ-Glu-Cys ammonium) is an orally active, blood-brain barrier permeable dipeptide . Gamma-glutamylcysteine ammonium activates AMPK, SIRT1, IL-4/STAT6, AC/cAMP/PI3K, IGF-1R/IRS1/PI3K, and Nrf2 signaling pathways; it inhibits NF-κB, JAK1/STAT1/3, MAPKs, cadmium-induced p38 MAPK, JNK, and PI3K/Akt signaling pathways. Gamma-glutamylcysteine ammonium regulates macrophage polarization, modulates the trafficking of CD36 and GLUT4, induces glutathione synthesis, improves metabolic dysfunction, reduces lipid deposition, ameliorates glucose homeostasis, inhibits apoptosis (Apoptosis), stabilizes mitochondria, suppresses lipid peroxidation, iron accumulation and ferroptosis (Ferroptosis), reduces ds-HMGB1 levels, reverses mechanical hyperalgesia, and alleviates hepatic lipid droplet formation. Gamma-glutamylcysteine ammonium is applicable to research related to inflammatory bowel disease, type 2 diabetes, cadmium-induced neurotoxicity, Alzheimer's disease, cerebral ischemia/reperfusion injury, neuropathy, and alcoholic liver disease .
    Gamma-glutamylcysteine ammonium

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