Hornedo J, Van Echo D A
Pharmacotherapy. 1985 Mar-Apr;5(2):78-90. doi: 10.1002/j.1875-9114.1985.tb03406.x.
The synthetic aminoacridine derivative amsacrine (m-AMSA) is capable of preventing DNA from serving as a template in replication and DNA synthesis. This mechanism of action is similar to that of anthracyclines, but clinical evidence suggests the lack of cross-resistance. The recommended dosage in patients with solid tumors is 90-120 mg/m2 intravenously every 3-4 weeks. Despite the initial encouraging reports from experimental models, m-AMSA has shown no real impact in the treatment of patients with a wide variety of solid tumors. In relapsed acute nonlymphocytic leukemia, 20-30% of patients will achieve complete remission. An increased remission rate is obtained when m-AMSA is combined with other agents, especially with high-dose cytosine arabinoside, with a complete remission rate of 50-60% in relapsed patients. Currently, several phase III trials are evaluating m-AMSA combinations against daunorubicin-containing regimens in patients with previously untreated acute leukemia. The potential role of these regimens in this disease remains to be defined.
合成氨基吖啶衍生物安吖啶（m-AMSA）能够阻止DNA在复制和DNA合成过程中作为模板。这种作用机制与蒽环类药物相似，但临床证据表明不存在交叉耐药性。实体瘤患者的推荐剂量为每3-4周静脉注射90-120 mg/m²。尽管实验模型最初的报告令人鼓舞，但m-AMSA对多种实体瘤患者的治疗并未产生实际影响。在复发的急性非淋巴细胞白血病中，20%-30%的患者将实现完全缓解。当m-AMSA与其他药物联合使用时，缓解率会提高，尤其是与大剂量阿糖胞苷联合使用时，复发患者的完全缓解率可达50%-60%。目前，几项III期试验正在评估m-AMSA联合方案与含柔红霉素方案对既往未治疗的急性白血病患者的疗效。这些方案在该疾病中的潜在作用仍有待确定。
