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MAPK-p38

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11

阻害剤およびアゴニスト

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製品番号 製品名 Target 研究分野 構造式
  • 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-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-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-N2406
    Dihydrocaffeic acid
    2 Publications Verification

    3,4-Dihydroxy-benzenepropanoic acid

    		 p38 MAPK Endogenous Metabolite Reactive Oxygen Species (ROS) NO Synthase Inflammation/Immunology
    Dihydrocaffeic acid is a microbial metabolite of flavonoids. Dihydrocaffeic acid scavenges intracellular ROS and increases nitric oxide synthase activity. Dihydrocaffeic acid reduces phosphorylation of MAPK p38 and prevent UVB-induced skin damage. Dihydrocaffeic acid has antioxidant, anti-inflammatory and anti-cartilage degradation activities .
    Dihydrocaffeic acid
  • HY-116626
    SM-7368

    		NF-κB p38 MAPK MMP Cancer
    SM-7368 is a potent NF-kB inhibitor that targets downstream of MAPK p38 activation . SM-7368 inhibits TNF-α-induced MMP-9 upregulation. SM-7368 can be used for the research of chemotherapies targeting TNF-α-mediated tumor invasion and metastasis .
    SM-7368
  • HY-12144
    CP-99994

    		Neurokinin Receptor p38 MAPK Neurological Disease
    CP-99994 is a Tachykinin neurokinin 1 (NK-1) receptor antagonist with a Ki of 0.25 nM. CP-99994 prevents colorectal sensitization in the context of visceral hypersensitivity. CP-99994 reduces colorectal hypersensitivity induced by acetic acid injections in a model of bladder-colon cross-sensitization. CP-99994 hydrochloride attenuates the neuroglial interactions and MAPK-p38 phosphorylation associated with visceral hypersensitivity .
    CP-99994
  • 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-N10009
    Cudraflavone B

    		NF-κB TNF Receptor COX ERK p38 MAPK Sirtuin Inflammation/Immunology
    Cudraflavone B is a prenylated flavonoid with anti-inflammatory and anti-tumor properties. Cudraflavone B is also a dual inhibitor of COX-1 and COX-2. Cudraflavone B blocks the translocation of nuclear factor κB (NF-κB) from the cytoplasm to the nucleus in macrophages. Thus, Cudraflavone B inhibits tumor necrosis factor α (TNFα) gene expression and secretion. Cudraflavone B also triggers the mitochondrial apoptotic pathway, activates NF-κB, the MAPK p38, and ERK, and induced the expression of SIRT1. Thus Cudraflavone B inhibits the growth of human oral squamous cell carcinoma cells .
    Cudraflavone B
  • HY-12145
    CP-99994 hydrochloride

    		Endogenous Metabolite Neurokinin Receptor p38 MAPK Neurological Disease
    CP-99994 hydrochloride is a Tachykinin neurokinin 1 (NK-1) receptor antagonist with a Ki of 0.25 nM. CP-99994 hydrochloride prevents colorectal sensitization in the context of visceral hypersensitivity. CP-99994 hydrochloride reduces colorectal hypersensitivity induced by acetic acid injections in a model of bladder-colon cross-sensitization. CP-99994 hydrochloride attenuates the neuroglial interactions and MAPK-p38 phosphorylation associated with visceral hypersensitivity .
    CP-99994 hydrochloride
  • 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-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)

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