产品
编 号：F153821
分子式：C18H17N3O4S
分子量：371.41
分子式：C18H17N3O4S
分子量：371.41
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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25mg
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50mg
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100mg
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结构图
CAS No: 141430-65-1
产品详情
生物活性：
ABT-751 (E7010) is a novel, highly orally bioavailable sulfonamides antimitotic compound and tubulin binder. It prevents tubulin aggregation by binding to the colchicine site on β-tubulin, leading to cell cycle arrest in G2/M phase and inducing apoptosis, thus effectively preventing cell division. ABT-751 induces autophagy by inhibiting the AKT/MTOR signaling pathway. ABT-751 showed significant inhibition against various types of cancer cells, including lung, gastric, colon, and breast cancer.
体内研究：
ABT-751 (100 mg/kg/day, 口服, 5 days on, 5 days off x2, 21天) 在神经母细胞瘤模型中具有明显的抑制效果，在横纹肌肉瘤和肾母细胞瘤模型中，可以引发肿瘤体积的显著减小或消退。ABT-751 对 Vincristine 与 Paclitaxel (HY-B0015) 有协同作用。ABT-751 (100 mg/kg/day, 口服, 5 days on, 5 days off x2) 在小鼠前列腺、非小细胞肺癌和乳腺肿瘤异种移植模型中都对 Docetaxel (HY-B0011) 具有协同作用，提高对肿瘤的抑制作用。Animal Model:xenograft models of neuroblastoma, osteosarcoma, Ewing sarcoma rhabdomyosarcoma, medulloblastoma and eight kidney cancer lines (six Wilms tumors, two rhabdoid)
Dosage:100 mg/kg
Administration:Oral gavage (p.o.)
Result:Had obvious inhibitory effect in neuroblastoma model.Induced significant reduction or regression of tumor volume in rhabdomyosarcoma and nephroblastoma models.Had a synergistic effect on vincristine or Paclitaxel (HY-B0015).
Animal Model:PC-3 prostate, Calu-6 NSCLC, and breast MDA-MB-468 tumor xenografts in mice
Dosage:75, 100 mg/kg
Administration:Oral gavage (p.o.)
Result:与 Docetaxel 具有协同作用，提高对肿瘤的抑制作用。
体外研究：
ABT-751 (2 μM; 4, 8 , 24h) 在肝细胞癌衍生的 Hep-3B 细胞中具有破坏有丝分裂，破坏线粒体膜电位，诱导 ROS 生成和 DNA 损伤的作用。ABT-751 (2 μM; 4, 8 , 24h) 在 Hep-3B 细胞中能造成 DNA 损伤，抑制细胞增殖和诱导 G2/M 细胞周期阻滞。ABT-751 (2 μM; 4, 8 , 24h) 通过抑制 AKT/MTOR 信号通路来诱导 TP53 缺失的 Hep-3B 细胞自噬，以及通过 caspase 依赖性、外源性和内源性途径诱导凋亡。当外源性表达 TP53 基因时，会进一步增加 ABT-751 诱导的这些细胞的自噬和凋亡。
ABT-751 (E7010) is a novel, highly orally bioavailable sulfonamides antimitotic compound and tubulin binder. It prevents tubulin aggregation by binding to the colchicine site on β-tubulin, leading to cell cycle arrest in G2/M phase and inducing apoptosis, thus effectively preventing cell division. ABT-751 induces autophagy by inhibiting the AKT/MTOR signaling pathway. ABT-751 showed significant inhibition against various types of cancer cells, including lung, gastric, colon, and breast cancer.
体内研究：
ABT-751 (100 mg/kg/day, 口服, 5 days on, 5 days off x2, 21天) 在神经母细胞瘤模型中具有明显的抑制效果，在横纹肌肉瘤和肾母细胞瘤模型中，可以引发肿瘤体积的显著减小或消退。ABT-751 对 Vincristine 与 Paclitaxel (HY-B0015) 有协同作用。ABT-751 (100 mg/kg/day, 口服, 5 days on, 5 days off x2) 在小鼠前列腺、非小细胞肺癌和乳腺肿瘤异种移植模型中都对 Docetaxel (HY-B0011) 具有协同作用，提高对肿瘤的抑制作用。Animal Model:xenograft models of neuroblastoma, osteosarcoma, Ewing sarcoma rhabdomyosarcoma, medulloblastoma and eight kidney cancer lines (six Wilms tumors, two rhabdoid)
Dosage:100 mg/kg
Administration:Oral gavage (p.o.)
Result:Had obvious inhibitory effect in neuroblastoma model.Induced significant reduction or regression of tumor volume in rhabdomyosarcoma and nephroblastoma models.Had a synergistic effect on vincristine or Paclitaxel (HY-B0015).
Animal Model:PC-3 prostate, Calu-6 NSCLC, and breast MDA-MB-468 tumor xenografts in mice
Dosage:75, 100 mg/kg
Administration:Oral gavage (p.o.)
Result:与 Docetaxel 具有协同作用，提高对肿瘤的抑制作用。
体外研究：
ABT-751 (2 μM; 4, 8 , 24h) 在肝细胞癌衍生的 Hep-3B 细胞中具有破坏有丝分裂，破坏线粒体膜电位，诱导 ROS 生成和 DNA 损伤的作用。ABT-751 (2 μM; 4, 8 , 24h) 在 Hep-3B 细胞中能造成 DNA 损伤，抑制细胞增殖和诱导 G2/M 细胞周期阻滞。ABT-751 (2 μM; 4, 8 , 24h) 通过抑制 AKT/MTOR 信号通路来诱导 TP53 缺失的 Hep-3B 细胞自噬，以及通过 caspase 依赖性、外源性和内源性途径诱导凋亡。当外源性表达 TP53 基因时，会进一步增加 ABT-751 诱导的这些细胞的自噬和凋亡。
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