Molecular Weight(MW): 243.22
Cytarabine is an antimetabolic agent and DNA synthesis inhibitor with IC50 of 16 nM in wild-type CCRF-CEM cells.
3 Customer Reviews
Viability and CI vs Fa after 24-h exposure to cytarabine alone or in combination with ABT-199 in Riva, U2932 and VavP-Bcl2/c-MYC murine tumor cells. Viability shown at 500 nM (500 ng/ml for cytarabine; quadruplicates±s.e.m.).
Leukemia, 2015, 29(8): 1702–1712. Cytarabine purchased from Selleck.
Cell cycle was analyzed using propidium iodide (PI) staining and flow cytometry. The plots show PI staining at the x-axis and cell counts at the y-axis. The graphs were prepared using ModFit LT™ software (Verity Software House). Nd: not detected, Ara-c:Cytarabine
J Exp Clin Cancer Res, 2017, 36(1):22. Cytarabine purchased from Selleck.
Flow cytometry analysis for cell surface expression of CD11b shows time- and dose-dependent upregulation of the marker CD11b in MLL-rearranged leukemia cells treated with EPZ-5676 and Cytarabine(Ara-C) as single agents and in combination.
J Pharmacol Exp Ther, 2014, 350(3): 646-56. Cytarabine purchased from Selleck.
Purity & Quality Control
Choose Selective DNA/RNA Synthesis Inhibitors
|Description||Cytarabine is an antimetabolic agent and DNA synthesis inhibitor with IC50 of 16 nM in wild-type CCRF-CEM cells.|
|Features||The 1st of a series of cancer drugs that alters the sugar component of nucleosides.|
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.  Cytarabine apparently induces apoptosis of rat sympathetic neurons at 10 μM, of which 100 μM 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. 
|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. |
In Vitro Growth Inhibition 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 vitro||Water||48 mg/mL (197.35 mM)|
|DMSO||1 mg/mL (4.11 mM)|
|In vivo||Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
For best results, use promptly after mixing.
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
Calculate the mass, volume or concentration required for a solution. The Selleck molarity calculator is based on the following equation:
Mass (g) = Concentration (mol/L) × Volume (L) × Molecular Weight (g/mol)
*When preparing stock solutions, please always use the batch-specific molecular weight of the product found on the via label and MSDS / COA (available on product pages).
Calculate the dilution required to prepare a stock solution. The Selleck dilution calculator is based on the following equation:
Concentration (start) x Volume (start) = Concentration (final) x Volume (final)
This equation is commonly abbreviated as: C1V1 = C2V2 ( Input Output )
* When preparing stock solutions always use the batch-specific molecular weight of the product found on the vial label and MSDS / COA (available online).
Molecular Weight Calculator
Enter the chemical formula of a compound to calculate its molar mass and elemental composition:
Tip: Chemical formula is case sensitive. C10H16N2O2 c10h16n2o2
Instructions to calculate molar mass (molecular weight) of a chemical compound:
To calculate molar mass of a chemical compound, please enter its chemical formula and click 'Calculate'.
Definitions of molecular mass, molecular weight, molar mass and molar weight:
Molecular mass (molecular weight) is the mass of one molecule of a substance and is expressed in the unified atomic mass units (u). (1 u is equal to 1/12 the mass of one atom of carbon-12)
Molar mass (molar weight) is the mass of one mole of a substance and is expressed in g/mol.
Clinical Trial Information
|NCT Number||Recruitment||Conditions||Sponsor/Collaborators||Start Date||Phases|
|NCT03571321||Not yet recruiting||Acute Lymphoblastic Leukemia|ALL Childhood|ALL||University of Chicago|Incyte Corporation||September 5 2019||Phase 1|
|NCT03719560||Not yet recruiting||Diffuse Large B Cell Lymphoma||Brown University||July 1 2019||Phase 2|
|NCT03634228||Not yet recruiting||Acute Myeloid Leukemia Arising From Previous Myelodysplastic Syndrome|Recurrent Acute Myeloid Leukemia|Refractory Acute Myeloid Leukemia|TP53 Gene Mutation Negative||M.D. Anderson Cancer Center|National Cancer Institute (NCI)||January 31 2019||Phase 1|Phase 2|
|NCT03724084||Not yet recruiting||Acute Myeloid Leukemia|KMT2A Gene Rearrangement||National Cancer Institute (NCI)||January 25 2019||Phase 1|Phase 2|
|NCT03710772||Not yet recruiting||CD20 Positive|Mantle Cell Lymphoma||M.D. Anderson Cancer Center|National Cancer Institute (NCI)||January 31 2019||Phase 2|
|NCT03701308||Not yet recruiting||Acute Myeloid Leukemia||National Cancer Institute (NCI)||January 16 2019||Phase 2|Phase 3|
Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.
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