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Amsacrine (m‐AMSA): A New Antineoplastic Agent Pharmacology, Clinical Activity and Toxicity
Author(s) -
Hornedo Javier,
Echo David A.
Publication year - 1985
Publication title -
pharmacotherapy: the journal of human pharmacology and drug therapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.227
H-Index - 109
eISSN - 1875-9114
pISSN - 0277-0008
DOI - 10.1002/j.1875-9114.1985.tb03406.x
Subject(s) - amsacrine , medicine , daunorubicin , cytosine , acute leukemia , leukemia , pharmacology , chemotherapy , antimetabolite , toxicity , dna , chemistry , etoposide , biochemistry
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/m 2 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.