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Amsacrine HCl

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Chemical Structure| 54301-15-4 同义名 : 盐酸胺苯吖啶 ;m-AMSA hydrochloride;acridinyl anisidide hydrochloride;NSC 141549;AMSA;Amsacrine (hydrochloride);acridinyl anisidide;m-AMSA
CAS号 : 54301-15-4
货号 : A580248
分子式 : C21H20ClN3O3S
纯度 : 98+%
分子量 : 429.92
MDL号 : MFCD07799963
存储条件：

粉末 Keep in dark place,Inert atmosphere,Room temperature

液体 -20°C:3-6个月-80°C:12个月
溶解度 :

DMSO: 60 mg/mL(139.56 mM)，配合低频超声助溶，注意：DMSO长时间开封后，会吸水并导致溶解能力下降，请避免使用长期开封的DMSO
动物实验配方：
生物活性
描述 Amsacrine HCl is an inhibitor of topoisomerase II, and acts as an antineoplastic agent which can intercalates into the DNA of tumor cells. Amsacrine blocked HERG currents in HEK 293 cells and Xenopus oocytes in a concentration-dependent manner, with IC50 values of 209.4 nm and 2.0 microm, respectively[3]. During chronic exposure at low concentrations, amsacrine causes cell and nuclear enlargement, lobulation of the nucleus, and nucleolar segregation[4]. In animals treated with different doses of amsacrine (0.5-12 mg kg(-1) ), the frequencies of micronucleated polychromatic erythrocytes increased significantly after treatment with 9 and 12 mg kg(-1) [5]. Amsacrine abolishes ERK- and Pin1-mediated stabilization of MCL1 and promotes GSK3β-mediated degradation of MCL1, leading to activate mitochondria-mediated apoptosis pathway in U937 cells[6].
临床研究
NCT号 适应症或疾病 临床期 招募状态 预计完成时间 地点
NCT00002719 Leukemia Neut... 展开 >>ropenia 收起 << Phase 3 Completed - Italy ... 展开 >> Azienda Policlinico Umberto Primo Rome, Italy, 00161 收起 <<
NCT00002658 Leukemia Neut... 展开 >>ropenia 收起 << Phase 3 Unknown - United Kingdom ... 展开 >> University of Wales College of Medicine Cardiff, Wales, United Kingdom, CF14 4XN 收起 <<
NCT01324063 Leukemia Phase 3 Completed - -
实验方案
1mg 5mg 10mg

1 mM

5 mM

10 mM

2.33mL

0.47mL

0.23mL

11.63mL

2.33mL

1.16mL

23.26mL

4.65mL

2.33mL
参考文献

[1]Attia SM. Molecular cytogenetic evaluation of the mechanism of genotoxic potential of amsacrine and nocodazole in mouse bone marrow cells. J Appl Toxicol. 2013 Jun;33(6):426-33.

[2]Thomas D, Hammerling BC, et al. Inhibition of cardiac HERG currents by the DNA topoisomerase II inhibitor amsacrine: mode of action. Br J Pharmacol. 2004 Jun;142(3):485-94.

[3]Thomas D, Hammerling BC, Wu K, Wimmer AB, Ficker EK, Kirsch GE, Kochan MC, Wible BA, Scholz EP, Zitron E, Kathöfer S, Kreye VA, Katus HA, Schoels W, Karle CA, Kiehn J. Inhibition of cardiac HERG currents by the DNA topoisomerase II inhibitor amsacrine: mode of action. Br J Pharmacol. 2004 Jun;142(3):485-94

[4]Jensen CG, Wilson WR, Bleumink AR. Effects of amsacrine and other DNA-intercalating drugs on nuclear and nucleolar structure in cultured V79 Chinese hamster cells and PtK2 rat kangaroo cells. Cancer Res. 1985 Feb;45(2):717-25

[5]Attia SM. Molecular cytogenetic evaluation of the mechanism of genotoxic potential of amsacrine and nocodazole in mouse bone marrow cells. J Appl Toxicol. 2013 Jun;33(6):426-33

[6]Lee YC, Chen YJ, Huang CH, Chang LS. Amsacrine-induced apoptosis of human leukemia U937 cells is mediated by the inhibition of AKT- and ERK-induced stabilization of MCL1. Apoptosis. 2017 Mar;22(3):406-420