产品
编 号：F756900
分子式：C24H23FN6O
分子量：430.48
分子式：C24H23FN6O
分子量：430.48
产品类型
规格
价格
是否有货
1mg
询价
询价
5mg
询价
询价
10mg
询价
询价
结构图
CAS No: 2922550-28-3
产品详情
生物活性：
CLK1-IN-3 (compound 10ad) is a potent and selective Clk1 inhibitor, with an IC50 of 5 nM and over 300-fold selectivity for Dyrk1A. CLK1-IN-3 also shows a relatively potent inhibition against Clk2 and Clk4, with IC50 values of 42 and 108 nM, respectively. CLK1-IN-3 potently induces autophagy in vitro. CLK1-IN-3 can be used for acute liver injury (ALI) research.
体内研究：
CLK1-IN-3 (compound 10ad) (0-40 mg/kg, 腹腔注射, 一次) 在acetaminophen (HY-66005, APAP) 诱导的 ALI 模型，可显著抑制急性肝损伤 (ALI)，且没有明显的肝细胞死亡.CLK1-IN-3 (10 mg/kg; 静脉注射, 口服, 腹腔注射, 一次) 表现出可接受的药代动力学特征，具有相对较长的 T1/2，为 5.29 小时，口服生物利用度为 19.5%。Animal Model:Male C57BL/6 mice(8 weeks, injected acetaminophen (HY-66005) (500 mg/kg, ip))
Dosage:10, 20, and 40 mg/kg
Administration:IP, once
Result:Decreased serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels significantly in dose-dependent.
Animal Model:Male Balb/c mice (aged 8 weeks)
Dosage:10 mg/kg
Administration:IV, PO, IP, once (Pharmacokinetic Analysis)
Result:Pharmacokinetic Parameters of CLK1-IN-3 in male Balb/C mice.IV (10 mg/kg) PO (10 mg/kg) IP (10 mg/kg)
Cmax (ng/mL)13166.5±875.91457.4±177.34654.3±435.3
T1/2 (h)2.96±1.25.29±2.13.27 ±1.1
AUC0-t (ng/mL?h)9520.5±1011.31860.2±411.05010.4±987.2
CL (L/h/kg)1.05±0.105.51±1.003.58±0.82
F (%)19.5%
体外研究：
CLK1-IN-3 (compound 10ad) 由于对 Clk1 和 Clk2 具有双重抑制作用而显示出抗肿瘤潜力。CLK1-IN-3 (10 μM-1000 μM) 能有效结合Clk1蛋白并以剂量依赖的方式抑制其降解。CLK1-IN-3 (0-10 μM, 24 h) 在 Hela、BNLCL.2 和 HCT 116 细胞中诱导自噬。CLK1-IN-3 刺激 SQSTM1/p62（自溶酶体标志物）的降解。
CLK1-IN-3 (compound 10ad) is a potent and selective Clk1 inhibitor, with an IC50 of 5 nM and over 300-fold selectivity for Dyrk1A. CLK1-IN-3 also shows a relatively potent inhibition against Clk2 and Clk4, with IC50 values of 42 and 108 nM, respectively. CLK1-IN-3 potently induces autophagy in vitro. CLK1-IN-3 can be used for acute liver injury (ALI) research.
体内研究：
CLK1-IN-3 (compound 10ad) (0-40 mg/kg, 腹腔注射, 一次) 在acetaminophen (HY-66005, APAP) 诱导的 ALI 模型，可显著抑制急性肝损伤 (ALI)，且没有明显的肝细胞死亡.CLK1-IN-3 (10 mg/kg; 静脉注射, 口服, 腹腔注射, 一次) 表现出可接受的药代动力学特征，具有相对较长的 T1/2，为 5.29 小时，口服生物利用度为 19.5%。Animal Model:Male C57BL/6 mice(8 weeks, injected acetaminophen (HY-66005) (500 mg/kg, ip))
Dosage:10, 20, and 40 mg/kg
Administration:IP, once
Result:Decreased serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels significantly in dose-dependent.
Animal Model:Male Balb/c mice (aged 8 weeks)
Dosage:10 mg/kg
Administration:IV, PO, IP, once (Pharmacokinetic Analysis)
Result:Pharmacokinetic Parameters of CLK1-IN-3 in male Balb/C mice.IV (10 mg/kg) PO (10 mg/kg) IP (10 mg/kg)
Cmax (ng/mL)13166.5±875.91457.4±177.34654.3±435.3
T1/2 (h)2.96±1.25.29±2.13.27 ±1.1
AUC0-t (ng/mL?h)9520.5±1011.31860.2±411.05010.4±987.2
CL (L/h/kg)1.05±0.105.51±1.003.58±0.82
F (%)19.5%
体外研究：
CLK1-IN-3 (compound 10ad) 由于对 Clk1 和 Clk2 具有双重抑制作用而显示出抗肿瘤潜力。CLK1-IN-3 (10 μM-1000 μM) 能有效结合Clk1蛋白并以剂量依赖的方式抑制其降解。CLK1-IN-3 (0-10 μM, 24 h) 在 Hela、BNLCL.2 和 HCT 116 细胞中诱导自噬。CLK1-IN-3 刺激 SQSTM1/p62（自溶酶体标志物）的降解。
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