Difference between revisions of "Amsacrine (Amsidine)"

From HemOnc.org - A Hematology Oncology Wiki
Jump to navigation Jump to search
m
Line 28: Line 28:
  
 
[[Category:Human DNA synthesis inhibitors]]
 
[[Category:Human DNA synthesis inhibitors]]
[[Category:Topoisomerase inhibitors]]
+
[[Category:Topoisomerase II inhibitors]]
  
 
[[Category:Acute myeloid leukemia medications (historic)]]
 
[[Category:Acute myeloid leukemia medications (historic)]]

Revision as of 00:21, 23 September 2023

General information

Class/mechanism: Synthetic acridine-derivate. Exact mechanism unclear; amsacrine binds to DNA by intercalation and external electrostatic binding, which inhibits DNA synthesis and causes DNA fragmentation.[1][2]
Route: IV
Extravasation: vesicant

For conciseness and simplicity, HemOnc.org currently will focus on treatment regimens and not list information such as: renal/hepatic dose adjustments, metabolism (including CYP450), excretion, monitoring parameters (although this will be considered for checklists), or manufacturer. Instead, for the most current information, please refer to your preferred pharmacopeias such as Micromedex, Lexicomp, UpToDate (courtesy of Lexicomp), or the prescribing information.[1]

Patient drug information

Diseases for which it is used

History of changes in EMA indication

  • 1982-04-23: EURD

Also known as

  • Code names: CI-880, SN-11841
  • Generic names: acridinyl anisidide, AMSA, Cain's acridine, m-AMSA
  • Brand names: Amekrin, Amsa P-D, Amsidine, Amsidyl, Lamasine

References