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编 号：F742109
分子式：C65H110N10O16
分子量：1287.63
分子式：C65H110N10O16
分子量：1287.63
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CAS No: 1029227-48-2
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生物活性：
Coibamide A, an N-methyl-stabilized cytotoxic depsipeptide, shows potent antiproliferative activity. Coibamide A induces autophagosome accumulation via an mTOR-independent mechanism. Coibamide A induces apoptosis. Coibamide A inhibits VEGFA/VEGFR2 expression and suppresses tumor growth in glioblastoma xenografts.
体内研究：
Coibamide A (300 μg/kg; 瘤内注射; 前两天, 之后每 48 小时注射一次, 持续 35 天) 抑制胶质母细胞瘤皮下小鼠模型的肿瘤生长。 Animal Model:8-week old female nude athymic mice with U87-MG cells
Dosage:300 μg/kg
Administration:Intratumoral injections; for the first two days, and then every 48 h afterward for 35 days
Result:Remained stable at 200-300 mm3 without significant growth over 4 weeks of treatmen, whereas the tumors of vehicle-treated animals continued to grow at a steady rate consistent with this aggressive cancer cell type
体外研究：
Coibamide A (0.3-1 nM; 3-60 小时) 抑制 MDA-MB-231 乳腺癌细胞的增殖。 Coibamide A (2.3-230 nM; 3 天) 在人 U87-MG 和 SF-295 胶质母细胞瘤细胞中产生浓度和时间依赖性细胞毒性死亡。 Coibamide A (10-300 nM; 72 小时) 以细胞类型特异性的方式诱导 caspase-3/7 的激活和细胞凋亡。 Coibamide A (20 nM; 48 小时) 在抗凋亡的 U87-MG 细胞中诱导自噬体积累。
Coibamide A, an N-methyl-stabilized cytotoxic depsipeptide, shows potent antiproliferative activity. Coibamide A induces autophagosome accumulation via an mTOR-independent mechanism. Coibamide A induces apoptosis. Coibamide A inhibits VEGFA/VEGFR2 expression and suppresses tumor growth in glioblastoma xenografts.
体内研究：
Coibamide A (300 μg/kg; 瘤内注射; 前两天, 之后每 48 小时注射一次, 持续 35 天) 抑制胶质母细胞瘤皮下小鼠模型的肿瘤生长。 Animal Model:8-week old female nude athymic mice with U87-MG cells
Dosage:300 μg/kg
Administration:Intratumoral injections; for the first two days, and then every 48 h afterward for 35 days
Result:Remained stable at 200-300 mm3 without significant growth over 4 weeks of treatmen, whereas the tumors of vehicle-treated animals continued to grow at a steady rate consistent with this aggressive cancer cell type
体外研究：
Coibamide A (0.3-1 nM; 3-60 小时) 抑制 MDA-MB-231 乳腺癌细胞的增殖。 Coibamide A (2.3-230 nM; 3 天) 在人 U87-MG 和 SF-295 胶质母细胞瘤细胞中产生浓度和时间依赖性细胞毒性死亡。 Coibamide A (10-300 nM; 72 小时) 以细胞类型特异性的方式诱导 caspase-3/7 的激活和细胞凋亡。 Coibamide A (20 nM; 48 小时) 在抗凋亡的 U87-MG 细胞中诱导自噬体积累。
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