产品
编 号：F142345
分子式：C24H30N8O
分子量：446.55
分子式：C24H30N8O
分子量：446.55
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
50mg
询价
询价
100mg
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询价
结构图
CAS No: 1374743-00-6
产品详情
生物活性：
Trilaciclib (G1T28) is an orally active CDK4/6 inhibitor with IC50 values of 1 nM and 4 nM for CDK4 and CDK6, respectively. . Trilaciclib can effectively inhibit tumor cell proliferation and reduce the hematological toxicity caused by chemotherapy. Trilaciclib attenuates apoptosis and myelosuppression induced by 5FU (HY-90006) chemotherapy.
体内研究：
Trilaciclib (50-150 mg/kg；口服；单剂量) 可保护小鼠骨髓细胞免受化疗诱导的细胞凋亡，并以剂量依赖性减轻体内化疗诱导的骨髓抑制。Trilaciclib 在 150 mg/kg 剂量下，可以减少 5FU (HY-90006) (150 mg/kg; ip) 化疗引起的 HSPC 损伤，从而加速化疗后血细胞计数的恢复。Animal Model:FVB/n female C57Bl6 mice
Dosage:50, 100, 150 mg/kg
Administration:Po; single dose; treated followed 11 or 23 hours later by a single injection of EdU (HY-118411) (100 μg; ip); mouse were euthanized 1 hour after EdU injection.
Result:Showed a dose-dependent decrease in caspase 3/7 activation.Attenuated chemotherapy-induced myelosuppression in mice.
体外研究：
Trilaciclib (10-1000 nM; 24 h) 可逆地调节小鼠和犬骨髓造血干细胞和祖细胞的增殖。Trilaciclib (10-1000 nM; 24 h) 可将 CDK4/6 依赖性细胞的细胞周期阻滞在 G1 期，对HS68的EC50为 30 nM。Trilaciclib (300 nM；16 或 48 h) 可保护 CDK4/6 依赖性细胞（HS68、WM2664）免受化疗引起的损伤，并减弱化疗引起的细胞凋亡。
Trilaciclib (G1T28) is an orally active CDK4/6 inhibitor with IC50 values of 1 nM and 4 nM for CDK4 and CDK6, respectively. . Trilaciclib can effectively inhibit tumor cell proliferation and reduce the hematological toxicity caused by chemotherapy. Trilaciclib attenuates apoptosis and myelosuppression induced by 5FU (HY-90006) chemotherapy.
体内研究：
Trilaciclib (50-150 mg/kg；口服；单剂量) 可保护小鼠骨髓细胞免受化疗诱导的细胞凋亡，并以剂量依赖性减轻体内化疗诱导的骨髓抑制。Trilaciclib 在 150 mg/kg 剂量下，可以减少 5FU (HY-90006) (150 mg/kg; ip) 化疗引起的 HSPC 损伤，从而加速化疗后血细胞计数的恢复。Animal Model:FVB/n female C57Bl6 mice
Dosage:50, 100, 150 mg/kg
Administration:Po; single dose; treated followed 11 or 23 hours later by a single injection of EdU (HY-118411) (100 μg; ip); mouse were euthanized 1 hour after EdU injection.
Result:Showed a dose-dependent decrease in caspase 3/7 activation.Attenuated chemotherapy-induced myelosuppression in mice.
体外研究：
Trilaciclib (10-1000 nM; 24 h) 可逆地调节小鼠和犬骨髓造血干细胞和祖细胞的增殖。Trilaciclib (10-1000 nM; 24 h) 可将 CDK4/6 依赖性细胞的细胞周期阻滞在 G1 期，对HS68的EC50为 30 nM。Trilaciclib (300 nM；16 或 48 h) 可保护 CDK4/6 依赖性细胞（HS68、WM2664）免受化疗引起的损伤，并减弱化疗引起的细胞凋亡。
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