cytarabine

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 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 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.

Adamantoylcytarabine is abioactive chemical.

CPX-351 (Vyxeos) is a liposomal encapsulant of cytarabine and Zoerythromycin with potential antitumor activity and can be used in the study of acute myeloid leukemia.

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

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.

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].

Cytarabine-D2 is the deuterated form of Cytarabine. Cytarabine (T1272) is a nucleoside analog that induces cell cycle arrest at the S phase and inhibits DNA polymerase. It has an IC50 of 16 nM for inhibiting DNA synthesis and exhibits antiviral activity against HSV.

Cytarabine (Standard) is a reference standard for research and analysis in studies involving Cytarabine. 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-[13C,15N2] (Standard) is a reference standard of Cytarabine-[13C,15N2] intended for quantitative analysis, quality control, and related biochemical research applications.

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.

Retinoic acid (Tretinoin), a metabolite of vitamin A, is a natural agonist of the retinoic acid receptor RAR and inhibits RARα/β/γ (IC50=14 nM). Retinoic acid induces cellular differentiation, reduces cellular proliferation, and inhibits tumorigenesis.

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.

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).

HDAC11-IN-3 (Compound A9) is a selective inhibitor of HDAC11, exhibiting an IC50 value of 4.1 nM. It demonstrates inhibitory effects on U937 and OCI-AML2 acute myeloid leukemia (AML) cell lines with an IC50 of 10 μM. This compound shows significant anti-AML activity by inducing apoptosis, cell cycle arrest, and differentiation. HDAC11-IN-3 upregulates the iron transport proteins transferrin (TF) and transferrin receptor (TFRC), and activates the p62-Keap1-Nrf2-HMOX1 pathway, which collectively increases intracellular iron levels and induces ferroptosis in AML cells. HDAC11-IN-3 can be utilized for AML research either alone or in combination with Cytarabine.

Ancitabine is an antitumour drug that improves Hailey-Hailey disease-related phenotypes in yeast models. It is metabolised to cytarabine in vivo and inhibits DNA synthesis, primarily used for treating acute leukaemia.

Prostratin (12-Deoxyphorbol-13-acetate) is an orally active protein kinase C (PKC) activator with a Ki value of 12.5 nM.As an NF-κB activator, Prostratin activates HIV gene expression in T cells.Prostratin inhibits the growth of acute myeloid leukemia (AML) cell lines and enhances cytarabine-induced AML cell differentiation. In addition, Prostratin induced KRAS phosphorylation and inhibited the growth of KRAS-mutated tumors.

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.

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.

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].