Cytarabine

Brown Norway rat with myelocytic leukaemia

4-amino-1-((2R, 3S, 4S, 5R)-3, 4-dihydroxy-5-(hydroxymethyl)-tetrahydrofuran-2-yl)pyrimidin-2(1H)-one

ca.100 uM

5 - 1000 mg/kg

Dissolved in phosphate-buffered saline (pH 7.0) just before use.

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. [1] Increasing concentrations of Cytarabine (IC50 of 0.69 uM) 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 uM) but not the inactive, alternatively spliced dCK forms. [2] Cytarabine apparently induces apoptosis of rat sympathetic neurons at 10 uM, of which 100 uM shows the highest toxicity and kills over 80% of the neurons by 84 hours, involving the release of mitochondrial cytochrome-c and the activation of caspase-3, and the toxicity can be attenuated by p53 knockdown and delayed by bax deletion. [3]

24, 48 and 72 hours

Cells are incubated in the presence of different concentrations of Cytarabine at 37 C for 24, 48, and 72 hours. At the time of 20-, 44-, or 68-hour incubation in the presence of Cytarabine, 10 mL of cell proliferation reagent WST-1 solution is added. After 2- and 4-hour incubation with WST-1, cell metabolic activity is assessed with colorimetric changes quantified by measuring the absorbance in a spectrophotometer at 450 nm. And cell division times are calculated from eosin counting in parallel with viability assays.

Cytarabine Chemical Structure

2 years -20CPowder, 2 weeks4Cin DMSO, 2 months-80Cin DMSO