产品
编 号：F762879
分子式：C20H25FN4O2
分子量：372.44
分子式：C20H25FN4O2
分子量：372.44
产品类型
规格
价格
是否有货
10mM*1mL in DMSO
询价
询价
1mg
询价
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5mg
询价
询价
10mg
询价
询价
25mg
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询价
结构图
CAS No: 2573071-18-6
产品详情
生物活性：
Rho-Kinase-IN-2 (Compound 23) is an orally active, selective, and central nervous system (CNS)-penetrant Rho Kinase (ROCK) inhibitor (ROCK2 IC50=3 nM). Rho-Kinase-IN-2 can be used in Huntington’s research.
体内研究：
Rho-Kinase-IN-2 (oral adiministration; 10 mg/kg; 6 times; 0.5, 1, 2, 4, 8, and 12 h) treatment shows dose- and time-dependent ROCK1 and ROCK2 target engagement.Rho-Kinase-IN-2 (oral adiministration; 10 or 20 mg/kg; QD or BID; 2 weeks) treatment shows excellent tolerability assessment.Rho-Kinase-IN-2 (oral adiministration; 1-20 mg/kg; once) treatment shows a direct dose- and time-dependent relationship between brain exposure and MYPT1 phosphorylation status.Rho-Kinase-IN-2 (oral adiministration; 10 or 20 mg/kg; once) treatment decreases in the mean arterial, systolic, diastolic blood pressure, and heart rate.Rho-Kinase-IN-2 (oral adiministration; 10 mg/kg; twice a day; 90 days) treatment leads to lower-than-expected brain concentrations.Animal Model:Male C57BL/6 mice
Dosage:10 mg/kg
Administration:Oral adiministration; 10 mg/kg; 6 times; 0.5, 1, 2, 4, 8, and 12 h
Result:Observed dose- and time-dependent ROCK1 and ROCK2 TE, with a free brain KiNativ ROCK1 and ROCK2 IC50=～6 nM.
Animal Model:3?4 months old heterozygote Q175DN KI and wild-type littermate mice
Dosage:10 or 20 mg/kg
Administration:Oral adiministration; 10 or 20 mg/kg; once a day or twice a day; 2 weeks
Result:Scored neurological index normally at all doses although a slight loss in bodyweight (～2%) in the 20 mg/kg treatment group.
Animal Model:Heterozygote HTT zQ175DN knock-in mice
Dosage:1-20 mg/kg
Administration:Oral adiministration; 1-20 mg/kg; once
Result:Remained over MYPT1 IC50 for over 2 h of the free brain at 10 mg/kg, and observed the dose- and time-dependent inhibition of MYPT1 phosphorylation in the striatum following acute in vivo dosing.
Animal Model:CD1 mice
Dosage:10 and 20 mg/kg
Administration:Oral adiministration; 10 or 20 mg/kg; once
Result:Observed the decreases in the mean arterial (maximum change of 61.0 ± 8.5 mmHg from baseline), systolic (maximum change of 59.5 ± 8.4 mmHg from baseline), diastolic blood pressure (maximum change of 56.4 ± 9.0 mmHg from baseline), and heart rate (maximum change from predose of 107 bpm) when compared to the control group from ～0.5 to 2 h post dose.
Animal Model:Heterozygote Q175DN KI mouse model of HD
Dosage:10 mg/kg
Administration:Oral adiministration; 10 mg/kg; twice a day; 90 days
Result:Led to lower-than-expected brain concentrations compared to single dosing.
体外研究：
Rho-Kinase-IN-2 (0-10 mM, 1 hour) treatment shows an increase in AKT phosphorylation and a decrease in MYPT1 phosphorylation.
Rho-Kinase-IN-2 (Compound 23) is an orally active, selective, and central nervous system (CNS)-penetrant Rho Kinase (ROCK) inhibitor (ROCK2 IC50=3 nM). Rho-Kinase-IN-2 can be used in Huntington’s research.
体内研究：
Rho-Kinase-IN-2 (oral adiministration; 10 mg/kg; 6 times; 0.5, 1, 2, 4, 8, and 12 h) treatment shows dose- and time-dependent ROCK1 and ROCK2 target engagement.Rho-Kinase-IN-2 (oral adiministration; 10 or 20 mg/kg; QD or BID; 2 weeks) treatment shows excellent tolerability assessment.Rho-Kinase-IN-2 (oral adiministration; 1-20 mg/kg; once) treatment shows a direct dose- and time-dependent relationship between brain exposure and MYPT1 phosphorylation status.Rho-Kinase-IN-2 (oral adiministration; 10 or 20 mg/kg; once) treatment decreases in the mean arterial, systolic, diastolic blood pressure, and heart rate.Rho-Kinase-IN-2 (oral adiministration; 10 mg/kg; twice a day; 90 days) treatment leads to lower-than-expected brain concentrations.Animal Model:Male C57BL/6 mice
Dosage:10 mg/kg
Administration:Oral adiministration; 10 mg/kg; 6 times; 0.5, 1, 2, 4, 8, and 12 h
Result:Observed dose- and time-dependent ROCK1 and ROCK2 TE, with a free brain KiNativ ROCK1 and ROCK2 IC50=～6 nM.
Animal Model:3?4 months old heterozygote Q175DN KI and wild-type littermate mice
Dosage:10 or 20 mg/kg
Administration:Oral adiministration; 10 or 20 mg/kg; once a day or twice a day; 2 weeks
Result:Scored neurological index normally at all doses although a slight loss in bodyweight (～2%) in the 20 mg/kg treatment group.
Animal Model:Heterozygote HTT zQ175DN knock-in mice
Dosage:1-20 mg/kg
Administration:Oral adiministration; 1-20 mg/kg; once
Result:Remained over MYPT1 IC50 for over 2 h of the free brain at 10 mg/kg, and observed the dose- and time-dependent inhibition of MYPT1 phosphorylation in the striatum following acute in vivo dosing.
Animal Model:CD1 mice
Dosage:10 and 20 mg/kg
Administration:Oral adiministration; 10 or 20 mg/kg; once
Result:Observed the decreases in the mean arterial (maximum change of 61.0 ± 8.5 mmHg from baseline), systolic (maximum change of 59.5 ± 8.4 mmHg from baseline), diastolic blood pressure (maximum change of 56.4 ± 9.0 mmHg from baseline), and heart rate (maximum change from predose of 107 bpm) when compared to the control group from ～0.5 to 2 h post dose.
Animal Model:Heterozygote Q175DN KI mouse model of HD
Dosage:10 mg/kg
Administration:Oral adiministration; 10 mg/kg; twice a day; 90 days
Result:Led to lower-than-expected brain concentrations compared to single dosing.
体外研究：
Rho-Kinase-IN-2 (0-10 mM, 1 hour) treatment shows an increase in AKT phosphorylation and a decrease in MYPT1 phosphorylation.
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