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 5′-monophosphate (ara-CMP), an active metabolite of the nucleoside analog cytarabine formed by deoxycytidine kinase, is incorporated into DNA by DNA polymerase α, significantly slowing DNA synthesis. It inhibits nuclear and mitochondrial DNA replication in S. cerevisiae at 15 mM and improves survival in an L1210 murine leukemia model at 3.5-75.1 mg/kg.

Adamantoylcytarabine is abioactive chemical.

Cytarabine (Ara-C) is a nucleoside analog, an inhibitor of DNA synthesis (IC50=16 nM). Cytarabine inhibits DNA polymerase and induces cell cycle arrest, autophagy, and apoptosis. Cytarabine has antitumor activity.

Cytarabine hydrochloride (Ara-C hydrochloride) is a nucleoside analog that causes S phase cell cycle arrest and inhibits DNA polymerase. Cytarabine inhibits DNA synthesis with an IC 50 of 16 nM. Cytarabine hydrochloride has antiviral effects against HSV.

Elacytarabine (M7594 0037), a lipid-conjugated derivative of the nucleoside analog cytarabine, is an antineoplastic drug. It has cytotoxicity in solid tumors.

Fosteabine is an oral and prodrug analog of cytarabine. It is resistant to deoxycytidine deaminase.

CPX-351 is a Liposomal-encapsulated combination of daunorubicin and cytarabine for the treatment of newly diagnosed tAML or AML with myelodysplasia-related changes (AML-MRCs).

MBC-11 A coupling agent that targets cancer by concentrating cytarabine and etidronate at the site of disease.MBC-11 is used to study tumor-induced bone disease.

Flurocitabine HCl is a fluorinated anhydride analog of cytarabine, which is partially hydrolyzed in vivo to two active antitumor substances (arabinosyl-fluorouracil (ara-FC) and arabinosyl-fluorouracil (ara-FU)).Flurocitabine HCl has demonstrated antitumor activity in phase I studies in acute leukemia and solid tumors.

APcK110 is a novel Kit inhibitor . APcK110 inhibits proliferation of the mastocytosis cell line HMC1.2 and the SCF-responsive cell line OCI/AML3 in a dose-dependent manner . APcK110 is a more potent inhibitor of OCI/AML3 proliferation than the clinically used Kit inhibitors imatinib and dasatinib and at least as potent as cytarabine. APcK110 inhibits the phosphorylation of Kit, Stat3, Stat5, and Akt in a dose-dependent fashion, showing activity of APcK110 on Kit and its downstream signaling pathways . APcK110 may have potent application in AML.

Ancitabine, a congener of cyterabine, is metabolized to cytarabine, thereby maintains a more constant antineoplastic action.

MBC-11 triethylamine has potential to treat tumor-induced bone disease (TIBD), is a first-in-class conjugate of the bone-targeting bisphosphonate etidronate covalently linked to the antimetabolite cytarabine (araC).

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.

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.

Ara-SH, a derivative of Cytarabine with a mercaptopropionic acid substitution, serves as the initiator for the self-assembly of a smart, co-loaded Cytarabine and Venetoclax nanoparticle (AV-NP), demonstrating notable synergistic antileukemia effects both in vitro and in vivo [1].