Rho-Kinase-IN-2 |
Catalog No.GC66050 |
Rho-Kinase-IN-2(화합물 23)는 경구 활성, 선택적 및 중추신경계(CNS) 침투성 Rho Kinase(ROCK) 억제제(ROCK2 IC50=3 nM)입니다. 821d96072c2d58d8970e76f526b0f6b8Rho-Kinase-IN-2는 Huntington'의 연구에 사용될 수 있습니다.821d96072c2d58d8970e76f526b0f6b8
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.: 2573071-18-6
Sample solution is provided at 25 µL, 10mM.
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[1].
Rho-Kinase-IN-2 (0-10 mM, 1 hour) treatment shows an increase in AKT phosphorylation and a decrease in MYPT1 phosphorylation[1].
Western Blot Analysis[1]
Cell Line: | A7r5 and PANC1 cells |
Concentration: | 0-10 mM |
Incubation Time: | 1 hour |
Result: | Showed concentration-dependent effects, leading to an increase in AKT phosphorylation (EC50=28 nM) and a decrease in MYPT1 phosphorylation (IC50=14 nM). |
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[1].
Rho-Kinase-IN-2 (oral adiministration; 10 or 20 mg/kg; QD or BID; 2 weeks) treatment shows excellent tolerability assessment[1].
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[1].
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[1].
Rho-Kinase-IN-2 (oral adiministration; 10 mg/kg; twice a day; 90 days) treatment leads to lower-than-expected brain concentrations[1].
Animal Model: | Male C57BL/6 mice[1] |
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[1] |
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[1] |
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[1] |
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[1] |
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. |
Average Rating: 5
(Based on Reviews and 30 reference(s) in Google Scholar.)GLPBIO products are for RESEARCH USE ONLY. Please make sure your review or question is research based.
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