Which medications in the drug class Antineoplastic Agents are used in the treatment of Acute Promyelocytic Leukemia?

Updated: May 03, 2019
  • Author: Sandy D Kotiah, MD; Chief Editor: Emmanuel C Besa, MD  more...
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Antineoplastic Agents

Antineoplastic agents inhibit cell growth and proliferation.

Arsenic trioxide (Trisenox)

May cause DNA fragmentation and damage or degrade the fusion protein PML-RAR alpha. Used in APL patients who have the presence of the t(15;17) translocation or PML/RAR-alpha gene expression. It is indicated also for induction of remission and consolidation in patients with APL who are refractory to, or have relapsed from, retinoid and anthracycline chemotherapy and in combination with tretinoin for treatment of adults with newly diagnosed low risk APL.

Idarubicin (Idamycin)

Used for induction or consolidation therapy. Topoisomerase-II inhibitor. Inhibits cell proliferation by inhibiting DNA and RNA polymerase.

Tretinoin (Vesanoid)

Induces maturation of acute promyelocytic leukemia cells in cultures. Used in both induction and maintenance phases for patients with acute promyelocytic leukemia.

Gemtuzumab ozogamicin (Mylotarg)

Withdrawn from United States market (June 21, 2010). A confirmatory, postapproval clinical trial was begun in 2004. The trial was designed to determine whether adding gemtuzumab to standard chemotherapy demonstrated an improvement in clinical benefit (survival time) to patients with AML. The trial was stopped early when no improvement in clinical benefit was observed and after a greater number of deaths occurred in the group of patients who received gemtuzumab compared with those receiving chemotherapy alone. At initial approval in 2000, gemtuzumab was associated with a serious liver condition called veno-occlusive disease, which can be fatal. This rate has increased in the postmarket setting.

Monoclonal antibody against CD33 antigen, which is expressed on leukemic blasts in >80% of patients with acute myeloid leukemia and normal myeloid cells. Antibody-antigen complex is then internalized and the calicheamicin derivative is released inside the myeloid cell where it binds to DNA, resulting in double-strand breaks and cell death. Nonhematopoietic and pluripotent cells are not affected.

For administration to patients >60 years (CD33 positive) in first relapse who are not considered candidates for cytotoxic chemotherapy.

Cytarabine (Cytosar-U)

Converted intracellularly to active compound cytarabine-5'-triphosphate, which inhibits DNA polymerase. Cell cycle S phase specific. Blocks the progression from G1 to S phase and in turn kills cells that undergo DNA synthesis in S phase of cell proliferation cycle.

Mitoxantrone (Novantrone)

Used for induction or consolidation therapy. Inhibits cell proliferation by intercalating DNA and inhibiting topoisomerase II.

Daunorubicin (Cerubidine)

Anthracycline antibiotic. Binds to nucleic acids by intercalation between base pairs of DNA, interfering with DNA synthesis. Causes inhibition of DNA topoisomerase II. Half-life is 14-20 h (23-40 h for active metabolite). Used in the induction phase of treatment.

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