产品
编 号：F038025
分子式：C31H34F2N6O2
分子量：560.64
分子式：C31H34F2N6O2
分子量：560.64
产品类型
规格
价格
是否有货
10mM*1mL in DMSO
询价
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5mg
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10mg
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50mg
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100mg
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结构图
CAS No: 1108743-60-7
产品详情
生物活性：
Entrectinib (NMS-E628) is an orally active, BBB-penetrated and centrally active inhibitor of TrkA/B/C, ROS1 and ALK, with IC50 values of 1, 3, 5, 12 and 7 nM, respectively. Entrectinib induces apoptosis and cycle arrest in cancer cells, has antitumor activity, and attenuates bleomycin-induced lung fibrosis in mice.
体内研究：
Entrectinib (20, 40, 60 mg/kg; i.g.; single daily for 7 days) 减轻 Bleomycin 诱导的小鼠肺纤维化。Entrectinib (30, 60 mg/kg; p.o.; twice daily for 10 consecutive days) 可诱导荷瘤小鼠中异种移植肿瘤的消退，包括 TRKA 依赖性结直肠癌 KM12、ROS1 驱动的肿瘤和几种不同组织来源的 ALK 依赖性模型，包括脑局部肺模型癌转移。Animal Model:Male C57BL/6 mice (6-8 weeks old, 20-25 g; Bleomycin-induced pulmonary fibrosis model).
Dosage:20, 40, 60 mg/kg
Administration:Intragastric Administration; single daily for 7 days.
Result:Significantly improved lung function in the pulmonary fibrosis model mice.
体外研究：
Entrectinib (100, 200, 400 nM; 24 h) 缓解 TGF-β1 诱导的小鼠肺成纤维细胞的激活。Entrectinib(100, 200, 400 nM; 24 h) 抑制 TGF-β1 诱导的小鼠肺上皮细胞上皮间质转化。Entrectinib (10, 50, 250 nM; 2 h) 消除 KM12 细胞中 TPM3-TRKA 的自身磷酸化，同时完全抑制 PLCg1、AKT 和 MAPK 的磷酸化。Entrectinib (10, 50, 250 nM; 24, 48 h) 诱导 KM12 细胞周期停滞 (24 小时) 和凋亡 (48 小时)。
Entrectinib (NMS-E628) is an orally active, BBB-penetrated and centrally active inhibitor of TrkA/B/C, ROS1 and ALK, with IC50 values of 1, 3, 5, 12 and 7 nM, respectively. Entrectinib induces apoptosis and cycle arrest in cancer cells, has antitumor activity, and attenuates bleomycin-induced lung fibrosis in mice.
体内研究：
Entrectinib (20, 40, 60 mg/kg; i.g.; single daily for 7 days) 减轻 Bleomycin 诱导的小鼠肺纤维化。Entrectinib (30, 60 mg/kg; p.o.; twice daily for 10 consecutive days) 可诱导荷瘤小鼠中异种移植肿瘤的消退，包括 TRKA 依赖性结直肠癌 KM12、ROS1 驱动的肿瘤和几种不同组织来源的 ALK 依赖性模型，包括脑局部肺模型癌转移。Animal Model:Male C57BL/6 mice (6-8 weeks old, 20-25 g; Bleomycin-induced pulmonary fibrosis model).
Dosage:20, 40, 60 mg/kg
Administration:Intragastric Administration; single daily for 7 days.
Result:Significantly improved lung function in the pulmonary fibrosis model mice.
体外研究：
Entrectinib (100, 200, 400 nM; 24 h) 缓解 TGF-β1 诱导的小鼠肺成纤维细胞的激活。Entrectinib(100, 200, 400 nM; 24 h) 抑制 TGF-β1 诱导的小鼠肺上皮细胞上皮间质转化。Entrectinib (10, 50, 250 nM; 2 h) 消除 KM12 细胞中 TPM3-TRKA 的自身磷酸化，同时完全抑制 PLCg1、AKT 和 MAPK 的磷酸化。Entrectinib (10, 50, 250 nM; 24, 48 h) 诱导 KM12 细胞周期停滞 (24 小时) 和凋亡 (48 小时)。
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