Difference between revisions of "Amsacrine (Amsidine)"
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<br>Extravasation: [[vesicant]] | <br>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 | + | 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 or the prescribing information.<ref name="insert"></ref> |
==Patient drug information== | ==Patient drug information== | ||
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Latest revision as of 01:02, 29 June 2024
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 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