Brands, Medical Use, Clinical Data
- Immunosuppressive Agents
- Antineoplastic Agents
Brands / Synonyms
Alexan; AR3; Ara-C; Arabinocytidine; Arabinofuranosylcytosine; Arabinosylcytosine; Arabitin; AraC; Aracytidine; Aracytin; Aracytine; Arafcyt; beta-Arabinosylcytosine; Beta-cytosine arabinoside; beta-D-Arabinosylcytosine
; Citarabina [INN-Spanish]; Cytarabin; Cytarabina; Cytarabine; Cytarabine (JP14/USP); Cytarabine [USAN:BAN:INN:JAN]; Cytarabine(USAN); Cytarabinoside; Cytarabinum [INN-Latin]; Cytarbel; Cytosar; Cytosar-U; Cytosine 1-beta-D-arabinofuranoside; Cytosine arabinofuranoside; Cytosine arabinose; Cytosine arabinoside; Cytosine arabinoside (VAN); Cytosine beta-D-arabinoside; Cytosine, 1-beta-D-arabinosyl-; Cytosine, beta-D-arabinoside; Cytosine-1-beta-D-arabinofuranoside; Cytosine-beta-arabinoside; Cytosine-beta-D-arabinofuranoside; Depocyt; Depocyt (liposomal); Depocyt (TN); Erpalfa; Iretin; Spongocytidine; Tarabine; Udicil
For the treatment of acute non-lymphocytic leukemia, acute lymphocytic leukemia and blast phase of chronic myelocytic leukemia.
Cytarabine is an antineoplastic anti-metabolite used in the treatment of several forms of leukemia including acute myelogenous leukemia and meningeal leukemia. Anti-metabolites masquerade as purine or pyrimidine - which become the building blocks of DNA. They prevent these substances becoming incorporated in to DNA during the "S" phase (of the cell cycle), stopping normal development and division. Cytarabine is metabolized intracellularly into its active triphosphate form (cytosine arabinoside triphosphate). This metabolite then damages DNA by multiple mechanisms, including the inhibition of alpha-DNA polymerase, inhibition of DNA repair through an effect on beta-DNA polymerase, and incorporation into DNA. The latter mechanism is probably the most important. Cytotoxicity is highly specific for the S phase of the cell cycle.
Mechanism of Action
Cytarabine acts through direct DNA damage and incorporation into DNA. Cytarabine is cytotoxic to a wide variety of proliferating mammalian cells in culture. It exhibits cell phase specificity, primarily killing cells undergoing DNA synthesis (S-phase) and under certain conditions blocking the progression of cells from the G1 phase to the S-phase. Although the mechanism of action is not completely understood, it appears that cytarabine acts through the inhibition of DNA polymerase. A limited, but significant, incorporation of cytarabine into both DNA and RNA has also been reported.
Less than 20% of the orally administered dose is absorbed from the gastrointestinal tract.
Cytarabine syndrome may develop - it is characterized by fever, myalgia, bone pain, occasionally chest pain, maculopapular rash, conjunctivitis, and malaise.
Biotrnasformation / Drug Metabolism
Cytarabine is contraindicated in those patients who are hypersensitive to the drug.
Reversible decreases in steady-state plasma digoxin concentrations and
renal glycoside excretion were observed in patients receiving beta-acetyl
digoxin and chemotherapy regimens containing cyclophosphamide, vincristine,
and prednisone with or without cytarabine or procarbazine. Steady state
plasma digitoxin concentrations did not appear to change. Therefore,
monitoring of plasma digoxin levels may be indicated in patients receiving
similar combination chemotherapy regimens. The utilization of digitoxin for
such patients may be considered as an alternative. Also flucytosine.