产品
编 号：F080345
分子式：C22H23N5O8
分子量：485.45
分子式：C22H23N5O8
分子量：485.45
产品类型
规格
价格
是否有货
1mg
询价
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5mg
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10mg
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25mg
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50mg
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100mg
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结构图
CAS No: 1221412-23-2
产品详情
生物活性：
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.
体内研究：
IMM-H007 inhibits fatty acid import into hepatocytes and liver lipogenesis, and concomitantly stimulates fatty acid oxidation, autophagy, and export of hepatic lipids.IMM-H007 (200?mg/kg, Orally, once per day for 10 days) inhibits ISO-induced cardiac fibrosis and diastolic dysfunction independently of AMPKα2 expression, reduces ISO-induced Smad2/3 phosphorylation downstream of TGFβ1 and cardiac fibrosis via an AMPKα2-independent pathway, but the inhibition of TGFβ1 expression is AMPKα2-dependent.
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.
体内研究：
IMM-H007 inhibits fatty acid import into hepatocytes and liver lipogenesis, and concomitantly stimulates fatty acid oxidation, autophagy, and export of hepatic lipids.IMM-H007 (200?mg/kg, Orally, once per day for 10 days) inhibits ISO-induced cardiac fibrosis and diastolic dysfunction independently of AMPKα2 expression, reduces ISO-induced Smad2/3 phosphorylation downstream of TGFβ1 and cardiac fibrosis via an AMPKα2-independent pathway, but the inhibition of TGFβ1 expression is AMPKα2-dependent.
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