cytarabine triphosphate

Cytarabine triphosphate (Ara-CTP), a competitive inhibitor of DNA synthesis and an active metabolite of Cytarabine, exhibits predictive potential for leukemic blasts' chemosensitivity to Cytarabine through intracellular levels.

Cytarabine triphosphate (Ara-CTP) trisodium, an active metabolite of Cytarabine, is a competitive inhibitor of DNA synthesis. Intracellular Cytarabine triphosphate trisodium levels can predict the chemosensitivity of leukemic blasts to Cytarabine [1].

Ancitabine hydrochloride (NSC 145668 HCl) is the hydrochloride salt of a cytarabine congener prodrug with antineoplastic activity. Upon administration, ancitabine is slowly hydrolyzed into cytarabine. Subsequently, cytarabine is converted to the triphosphate form within the cell and then competes with cytidine for incorporation into DNA. Because the arabinose sugar sterically hinders the rotation of the molecule within DNA, DNA replication ceases, specifically during the S phase of the cell cycle. Cytarabine agent also inhibits DNA polymerase, resulting in a decrease in DNA replication and repair. Compared to cytarabine, a more prolonged, consistent cytarabine-mediated therapeutic effect may be achieved with ancitabine because of the slow hydrolytic conversion of ancitabine to cytarabine.

Fazarabine, also known as Kymarabine, is an orally-active pyrimidine analogue of an aza-substituted cytidine in which the ribose moiety is replaced by an arabinose sugar. Similar in action to cytarabine, fazarabine is phosphorylated by deoxycytidine kinase to a triphosphate form which competes with thymidine for incorporation into DNA; its incorporation into DNA inhibits DNA synthesis, resulting in tumor cell death and tumor necrosis. The presence of deoxycytidine kinase in a tumor is a determinant of tumor sensitivity to this drug.