产品
编 号：F271685
分子式：C24H16FN5O
分子量：409.42
分子式：C24H16FN5O
分子量：409.42
产品类型
规格
价格
是否有货
10mM*1mL in DMSO
询价
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1mg
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5mg
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10mg
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结构图
CAS No: 2123491-32-5
产品详情
生物活性：
CLK1-IN-1 is a potent and selective of Cdc2-like kinase 1 (CLK1) inhibitor, with an IC50 of 2 nM.
体内研究：
APAP exposure results in severe liver injury, and treatment with CLK1-IN-1 (ip, 30 mg/kg) imparts a significant hepatoprotective effect. The results show that treatment with CLK1-IN-1 decreases serum ALT and AST levels significantly such that both marker enzymes return to normal levels.
体外研究：
CLK1 is the most potently inhibited kinase (IC50: 2 nM). In addition to CLK1, only two kinases have an IC50 value less than 100 nM, namely CLK2 (IC50: 31 nM) and CLK4 (IC50: 8 nM), DYRK1A is the strongest off-target. The ability of CLK1-IN-1 to induce autophagy in BNL CL.2 and SKOV-3 (human ovarian cancer cell line) cells is also examined. The effects of CLK1-IN-1 on yellow LC3 puncta also displays obvious dose dependency, and a dose of 10 μM shows the best performance. In addition, in CLK1-IN-1-treated cells, the number of red LC3 puncta (mRFP signals only35) increases compared with that of DMSO-treated cells, indicating the formation of autolysosomes. Importantly, CLK1-IN-1 stimulats the degradation of SQSTM1/p62 and increases the ratio of red LC3 puncta to yellow LC3 puncta, both of which indicate an induction of autophagic flux by CLK1-IN-1.
CLK1-IN-1 is a potent and selective of Cdc2-like kinase 1 (CLK1) inhibitor, with an IC50 of 2 nM.
体内研究：
APAP exposure results in severe liver injury, and treatment with CLK1-IN-1 (ip, 30 mg/kg) imparts a significant hepatoprotective effect. The results show that treatment with CLK1-IN-1 decreases serum ALT and AST levels significantly such that both marker enzymes return to normal levels.
体外研究：
CLK1 is the most potently inhibited kinase (IC50: 2 nM). In addition to CLK1, only two kinases have an IC50 value less than 100 nM, namely CLK2 (IC50: 31 nM) and CLK4 (IC50: 8 nM), DYRK1A is the strongest off-target. The ability of CLK1-IN-1 to induce autophagy in BNL CL.2 and SKOV-3 (human ovarian cancer cell line) cells is also examined. The effects of CLK1-IN-1 on yellow LC3 puncta also displays obvious dose dependency, and a dose of 10 μM shows the best performance. In addition, in CLK1-IN-1-treated cells, the number of red LC3 puncta (mRFP signals only35) increases compared with that of DMSO-treated cells, indicating the formation of autolysosomes. Importantly, CLK1-IN-1 stimulats the degradation of SQSTM1/p62 and increases the ratio of red LC3 puncta to yellow LC3 puncta, both of which indicate an induction of autophagic flux by CLK1-IN-1.
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