产品
编 号：F600833
分子式：C23H31BrN8O3
分子量：547.45
分子式：C23H31BrN8O3
分子量：547.45
产品类型
规格
价格
是否有货
1mg
询价
询价
结构图
CAS No: 702676-93-5
产品详情
生物活性：
BX-320 is a selective, ATP-competitive, orally acitive, and direct PDK1 inhibitor with an IC50 of 30 nM in a direct kinase assay format. BX-320 also induces apoptosis. Anticancer effect.
体内研究：
BX-320 (oral dosing with 200 mg/kg, twice a day for 21 days) shows efficacy in a blood-borne metastasis model. BX-320 inhibits the growth of LOX melanoma tumors in the lungs of nude mice after injection of tumor cells into the tail vein. BX-320 has efficacy in an in vivo tumor model, which may reflect an inhibition of productive implantation of tumor cells in the lung or an inhibition of subsequent tumor growth.Animal Model:Athymic (nu/nu) female mice, 6-8 weeks old
Dosage:200 mg/kg; dose volume was 10 mL/kg
Administration:Oral gavage twice daily (12 h apart)
Result:Significantly inhibited the growth of lung tumors in this model.
体外研究：
BX-320 binds to the ATP binding site of PDK1. BX-320 also inhibits Chck1, c-Kit, KDR, PKA, CDK2b/cyclin E, GSK3β, PKC with IC50s of 0.82, 0.89, 1.4, 1.4, 1.5, 4.0, and 5.7 μM, respectively. BX-320 blocks PDK1/Akt signaling in tumor cells and inhibits the anchorage-dependent growth of a variety of tumor cell lines in culture or induces apoptosis. BX-320 inhibits the growth of MDA-468 breast cancer cells (IC50=0.6 μM) and induces apoptosis. BX-320 promotes a 12-fold induction of caspase-3/7 activity after 48 h of treatment (IC50=0.5 μm), indicating a strong proapoptotic response. BX-320 (0.3-10 μM; for 18 hours) greatly reduces the amount of both p-Thr308-Akt and p-Thr386-S6K1.
BX-320 is a selective, ATP-competitive, orally acitive, and direct PDK1 inhibitor with an IC50 of 30 nM in a direct kinase assay format. BX-320 also induces apoptosis. Anticancer effect.
体内研究：
BX-320 (oral dosing with 200 mg/kg, twice a day for 21 days) shows efficacy in a blood-borne metastasis model. BX-320 inhibits the growth of LOX melanoma tumors in the lungs of nude mice after injection of tumor cells into the tail vein. BX-320 has efficacy in an in vivo tumor model, which may reflect an inhibition of productive implantation of tumor cells in the lung or an inhibition of subsequent tumor growth.Animal Model:Athymic (nu/nu) female mice, 6-8 weeks old
Dosage:200 mg/kg; dose volume was 10 mL/kg
Administration:Oral gavage twice daily (12 h apart)
Result:Significantly inhibited the growth of lung tumors in this model.
体外研究：
BX-320 binds to the ATP binding site of PDK1. BX-320 also inhibits Chck1, c-Kit, KDR, PKA, CDK2b/cyclin E, GSK3β, PKC with IC50s of 0.82, 0.89, 1.4, 1.4, 1.5, 4.0, and 5.7 μM, respectively. BX-320 blocks PDK1/Akt signaling in tumor cells and inhibits the anchorage-dependent growth of a variety of tumor cell lines in culture or induces apoptosis. BX-320 inhibits the growth of MDA-468 breast cancer cells (IC50=0.6 μM) and induces apoptosis. BX-320 promotes a 12-fold induction of caspase-3/7 activity after 48 h of treatment (IC50=0.5 μm), indicating a strong proapoptotic response. BX-320 (0.3-10 μM; for 18 hours) greatly reduces the amount of both p-Thr308-Akt and p-Thr386-S6K1.
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