CT-721
目录号 : GC35753CT-721 是一种有效的,时间依赖性的 Bcr-Abl 激酶抑制剂,抑制野生型 Bcr-Abl 激酶的 IC50 值为 21.3 nM,具有抗慢性骨髓白血病 (CML) 活性。
Cas No.:1388710-60-8
Sample solution is provided at 25 µL, 10mM.
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CT-721 is a potent and time-dependent Bcr-Abl kinase inhibitor with an IC50 of 21.3 nM for wild-type Bcr-Abl kinase, and possesses anti-chronic myeloid leukemia (CML) activities[1]. IC50: 21.3 nM (wild-type Bcr-Abl kinase)[1]
[1]. Sun Y, et al. CT-721, a Potent Bcr-Abl Inhibitor, Exhibits Excellent In Vitro and In Vivo Efficacy in the Treatment of Chronic Myeloid Leukemia. J Cancer. 2017 Aug 23;8(14):2774-2784.
Cas No. | 1388710-60-8 | SDF | |
Canonical SMILES | CC1=CC=C(NC(C2=CC=C([C@@H](N3CCN(C)CC3)CC4)C4=C2)=O)C=C1C#CC5=CN=C6N5N=C(Cl)C=C6 | ||
分子式 | C30H29ClN6O | 分子量 | 525.04 |
溶解度 | Soluble in DMSO | 储存条件 | Store at -20°C |
General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液;一旦配成溶液,请分装保存,避免反复冻融造成的产品失效。 储备液的保存方式和期限:-80°C 储存时,请在 6 个月内使用,-20°C 储存时,请在 1 个月内使用。 为了提高溶解度,请将管子加热至37℃,然后在超声波浴中震荡一段时间。 |
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1 mg | 5 mg | 10 mg | |
1 mM | 1.9046 mL | 9.5231 mL | 19.0462 mL |
5 mM | 0.3809 mL | 1.9046 mL | 3.8092 mL |
10 mM | 0.1905 mL | 0.9523 mL | 1.9046 mL |
第一步:请输入基本实验信息(考虑到实验过程中的损耗,建议多配一只动物的药量) | ||||||||||
给药剂量 | mg/kg | 动物平均体重 | g | 每只动物给药体积 | ul | 动物数量 | 只 | |||
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% DMSO % % Tween 80 % saline | ||||||||||
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工作液浓度: mg/ml;
DMSO母液配制方法: mg 药物溶于 μL DMSO溶液(母液浓度 mg/mL,
体内配方配制方法:取 μL DMSO母液,加入 μL PEG300,混匀澄清后加入μL Tween 80,混匀澄清后加入 μL saline,混匀澄清。
1. 首先保证母液是澄清的;
2.
一定要按照顺序依次将溶剂加入,进行下一步操作之前必须保证上一步操作得到的是澄清的溶液,可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
CT-721, a Potent Bcr-Abl Inhibitor, Exhibits Excellent In Vitro and In Vivo Efficacy in the Treatment of Chronic Myeloid Leukemia
J Cancer 2017 Aug 23;8(14):2774-2784.PMID:28928866DOI:PMC5604209
Kinase inhibitors that target Bcr-Abl are highly effective in the treatment of chronic myeloid leukemia (CML). However, these inhibitors are often invalidated due to the drug resistance. Therefore, the discovery and development of novel Bcr-Abl inhibitors is required to overwhelm the drug resistance in the treatment of CML resistant to the currently used first-line Bcr-Abl inhibitors. Herein we have described a newly developed Bcr-Abl inhibitor CT-721, which displayed potent inhibitory effects on wild-type and T315I mutant Bcr-Abl. It functioned as a typically ATP-competitive inhibitor, superior to other existing Bcr-Abl inhibitors. CT-721 also demonstrated time-dependent inhibition of Bcr-Abl activation and the resultant downstream signaling transduction pathways in Bcr-Abl positive cells. Furthermore, CT-721 induced cell apoptosis and cell cycle arrest, and efficaciously inhibited tumor growth in Bcr-Abl-expressed K562 and KU812 xenograft models in a mechanism-based manner. Further PK/PD studies revealed a positive in vivo correlation between the compound concentration and inhibition of Bcr-Abl activity. Taken together, CT-721 is a potent and time-dependent Bcr-Abl kinase inhibitor, and has shown strong in vitro and in vivo anti-CML activities with a favorable pharmacokinetic profile, differentiating it from other Bcr-Abl kinase inhibitors already approved and current in development for the treatment of CML.