Class/mechanism: Purine analog, antimetabolite; fludarabine is converted to the active compound, 2-fluoro-ara-ATP, which inhibits DNA synthesis by inhibiting DNA polymerase alpha, ribonucleotide reductase, and DNA primase. Relatively resistant to deamination by adenosine deaminase. The mechanism of action is not completely characterized and may be multi-faceted.
Route: IV, PO Note: Oral fludarabine is no longer available in the US, at this time.
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.
Diseases for which it is used
- Acute myeloid leukemia
- B-cell acute lymphoblastic leukemia
- Chronic lymphocytic leukemia (CLL/SLL)
- Cold agglutinin disease
- Follicular lymphoma
- Hodgkin lymphoma
- Mantle cell lymphoma
- Marginal zone lymphoma
- Peripheral T-cell lymphoma
- Transformed lymphoma
- Transplant conditioning regimens
- Waldenström macroglobulinemia
Patient drug information
- Fludarabine (Fludara) patient drug information (Chemocare)
- Fludarabine (Fludara) patient drug information (UpToDate)
History of changes in FDA indication
- 4/18/1991: Initial FDA approval for the treatment of patients with B-cell chronic lymphocytic leukemia (CLL) who have not responded to or whose disease has progressed during treatment with at least one standard alkylating-agent containing regimen.
Also known as
- Generic names: FAMP, fludarabine phosphate
- Brand names: Beneflur, Fludabine, Fludara, Lymfuda, Oforta