| CAS NO: | 147-94-4 |
| 规格: | ≥98% |
| 包装 | 价格(元) |
| 250mg | 电议 |
| 500mg | 电议 |
| 1g | 电议 |
| 2g | 电议 |
| 5g | 电议 |
| 10g | 电议 |
| Molecular Weight (MW) | 243.22 |
|---|---|
| Formula | C9H13N3O5 |
| CAS No. | 147-94-4 (free base); |
| Storage | -20℃ for 3 years in powder form |
| -80℃ for 2 years in solvent | |
| Solubility (In vitro) | DMSO: <1 mg/mL |
| Water: 48 mg/mL (197.4 mM) | |
| Ethanol: <1 mg/mL | |
| Solubility (In vivo) | Saline: 30 mg/mL |
| Synonyms | Cytosine β-D-arabinofuranoside; Cytosine Arabinoside; Ara-C; MK-8242; SCH-900242; MK 8242; SCH900242; MK8242; SCH 900242; AC-1075; CHX 3311, MK 8242; NCI-C04728; NSC 287459; Cytosine arabinose; Arabitin; Aracytidine |
| In Vitro | In vitro activity: Cytarabine (AraC) is phosphorylated into a triphosphate form (Ara-CTP) involving deoxycytidine kinase (dCK), which competes with dCTP for incorporation into DNA, and then blocks DNA synthesis by inhibiting the function of DNA and RNA polymerases. Cytarabine displays a higher growth inhibitory activity towards wild-type CCRF-CEM cells compared to other acute myelogenous leukemia (AML) cells with IC50 of 16 NM. Increasing concentrations of Cytarabine (IC50 of 0.69 μM) results in decreased metabolic activity of sensitive rat leukemic cell line RO/1, and the cell toxity can be highly enhanced by transfection with human wt dCK (IC50 of 0.037 μM) but not the inactive, alternatively spliced dCK forms. Kinase Assay: Stock solution of Cytarabine is prepared in absolute ethanol, and serial dilutions of Cytarabine are prepared. CCRF-CEM cells are suspended in RPMI medium supplemented with 10% FBS, 0.1% gentamicin, and 1% sodium pyruvate. The cells are suspended in their respective media to give 10 mL volumes of cell suspension at a final density of 3-6 × 104 cells/mL. Appropriate volumes of Cytarabine solution are transferred to the cell suspensions, and incubation is continued for 72 hours. The cells are spun down and resuspended in fresh Cytarabine -free medium, and final cell counts are determined. The data are analyzed by sigmoidal curve fitting of the cell count versus Cytarabine concentration, and the results are expressed as the IC50 (Cytarabine concentration that inhibits cell growth to 50% of the control value). Cell Assay: Stock solution of Cytarabine is prepared in absolute ethanol, and serial dilutions of Cytarabine are prepared. CCRF-CEM cells are suspended in RPMI medium supplemented with 10% FBS, 0.1% gentamicin, and 1% sodium pyruvate. The cells are suspended in their respective media to give 10 mL volumes of cell suspension at a final density of 3-6 × 104 cells/mL. Appropriate volumes of Cytarabine solution are transferred to the cell suspensions, and incubation is continued for 72 hours. The cells are spun down and resuspended in fresh Cytarabine -free medium, and final cell counts are determined. The data are analyzed by sigmoidal curve fitting of the cell count versus Cytarabine concentration, and the results are expressed as the IC50 (Cytarabine concentration that inhibits cell growth to 50% of the control value). |
|---|---|
| In Vivo | Cytarabine is highly effective against acute leukaemias, which causes the characteristic G1/S blockage and synchronization, and increases the survival time for leukaemic Brown Norway rats in a weak dose-related fashion indicating that the use of higher dosages of Cytarabine does not contribute to its antileukaemic effectiveness in man. Cytarabine (250 mg/kg) also causes placental growth retardation and increases placental trophoblastic cells apoptosis in the placental labyrinth zone of the pregnant Slc:Wistar rats, which increases from 3 hour after the treatment and peaks at 6 hour before returning to control levels at 48 hour, with remarkably enhanced p53 protein, p53 trancriptional target genes such as p21, cyclinG1 and fas and caspase-3 activity |
| Animal model | Brown Norway rat with myelocytic leukaemia |
| Formulation & Dosage | Dissolved in phosphate-buffered saline (pH 7.0); 5 - 1000 mg/kg; i.v. injection |
| References | Mol Pharm. 2004 Mar-Apr;1(2):112-6; Br J Cancer. 1988 Dec;58(6):730-3. |
m.cnreagent.com