Cytarabine hydrochloride - CAS 69-74-9
Catalog number: 69-74-9
Category: Inhibitor
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
Molecular Weight:
Nucleoside Antimetabolite/Analog
Cytarabine, an antimetabolite analogue of cytidine with a modified sugar moiety, is an antimetabolic agent and DNA synthesis inhibitor.
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White powder
Cytosine arabinoside hydrochloride; 4-amino-1-[(2R,3S,4S,5R)-3,4-dihydroxy-5-(hydroxymethyl)oxolan-2-yl]pyrimidin-2-one;hydrochloride;
Soluble in DMSO
Store at -20 °C
An antimetabolic agent and DNA synthesis inhibitor.
Quality Standard:
Enterprise Standard
Shelf Life:
As supplied, 2 years from the QC date provided on the Certificate of Analysis, when stored properly
Melting Point:
197-198 °C(lit.)
Canonical SMILES:
Current Developer:
SkyePharma Inc
1.Progressive Multifocal Leukoencephalopathy and Systemic Lupus Erythematosus: Focus on Etiology.
Berntsson SG1, Katsarogiannis E1, Lourenço F2, Moraes-Fontes MF2. Case Rep Neurol. 2016 Mar 16;8(1):59-65. doi: 10.1159/000444874.
Progressive multifocal leukoencephalopathy (PML) caused by reactivation of the JC virus (JCV), a human polyomavirus, occurs in autoimmune disorders, most frequently in systemic lupus erythematosus (SLE). We describe a HIV-negative 34-year-old female with SLE who had been treated with immunosuppressant therapy (IST; steroids and azathioprine) since 2004. In 2011, she developed decreased sensation and weakness of the right hand, followed by vertigo and gait instability. The diagnosis of PML was made on the basis of brain MRI findings (posterior fossa lesions) and JCV isolation from the cerebrospinal fluid (700 copies/ml). IST was immediately discontinued. Cidofovir, mirtazapine, mefloquine and cycles of cytarabine were sequentially added, but there was progressive deterioration with a fatal outcome 1 year after disease onset. This report discusses current therapeutic choices for PML and the importance of early infection screening when SLE patients present with neurological symptoms.
2.HIF-1α inhibition by 2-methoxyestradiol induces cell death via activation of the mitochondrial apoptotic pathway in acute myeloid leukemia.
Zhe N1, Chen S1,2, Zhou Z1,3, Liu P1, Lin X1, Yu M1, Cheng B1,2, Zhang Y4,5, Wang J4,5. Cancer Biol Ther. 2016 Apr 15:0. [Epub ahead of print]
The bone marrow microenvironment plays an important role in the development and progression of AML. Leukemia stem cells are in a hypoxic condition, which induces the expression of HIF-1α. Aberrant activation of HIF-1α is implicated in the poor prognosis of patients with acute myeloid leukemia (AML). Herein, we investigated the expression of HIF-1α in AML and tested 2-methoxyestradiol (2ME2) as a candidate HIF-1α inhibitor for the treatment of AML. We found that HIF-1α was overexpressed in AML. HIF-1α suppression by 2ME2 significantly induced apoptosis of AML cells, and it outperformed traditional chemotherapy drugs such as cytarabine. At the same time, 2ME2 downregulated the transcriptional levels of VEGF, GLUT1 and HO-1 in cellular assays. Additionally, 2ME2 displayed antileukemia activity in bone marrow blasts from AML patients, but showed little effect on normal cells. 2ME2-induced activation of mitochondrial apoptotic pathway is mediated by reactive oxygen species (ROS), which decreased the slight effect of drug on normal cells.
3.Treatment of Acute Myeloid Leukemia in Elderly Patients-A Therapeutic Dilemma.
Mamdani H1, Santos CD2, Konig H3. J Am Med Dir Assoc. 2016 Apr 9. pii: S1525-8610(16)30005-6. doi: 10.1016/j.jamda.2016.03.001. [Epub ahead of print]
Older adults represent the majority of approximately 20,000 new patients diagnosed with acute myeloid leukemia (AML) in the United States each year. While the treatment goal for younger patients is to achieve a cure with intensive therapeutic protocols, including standard chemotherapy and hematopoietic stem cell transplantation, these goals are less well defined in the elderly population. This is in part due to the continuous decline in treatment outcomes with increasing age secondary to a number of patient-related and disease-specific factors, ranging from the presence of comorbid conditions to the higher frequency of adverse cytogenetic and unfavorable molecular markers. Although best supportive care, low-dose cytarabine, and epigenetic drugs represent well recognized treatment concepts, no universally accepted strategy for the management of elderly patients with AML exists. Therapeutic decisions are widely based on the patient's age, general health, the disease features, as well as the patient's personal wishes.
4.A randomized, double-blind trial of pegfilgrastim versus filgrastim for the management of neutropenia during CHASE(R) chemotherapy for malignant lymphoma.
Kubo K1, Miyazaki Y2, Murayama T3, Shimazaki R4, Usui N5, Urabe A6, Hotta T7, Tamura K8. Br J Haematol. 2016 Apr 12. doi: 10.1111/bjh.14088. [Epub ahead of print]
Pegfilgrastim is a pegylated form of the granulocyte-colony stimulating factor, filgrastim. Herein, we report the results of a multicentre, randomized, double-blind phase III trial comparing the efficacy and safety of pegfilgrastim with filgrastim in patients with malignant lymphoma. Patients were randomized to receive either a single subcutaneous dose of pegfilgrastim or daily subcutaneous doses of filgrastim on day 4 after the completion of cyclophosphamide, cytarabine, etoposide and dexamethasone ± rituximab (CHASE(R); day 1-3) chemotherapy. The primary endpoint was the duration of severe neutropenia (DSN), defined as the number of days with neutrophil count <0·5 × 109 /l in the first cycle of chemotherapy. A total of 111 lymphoma patients were randomized to either the pegfilgrastim or filgrastim group. 109 patients received either pegfilgrastim (n = 54) or filgrastim (n = 55). Efficacy data were available for 107 patients (pegfilgrastim: n = 53, filgrastim: n = 54).
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CAS 69-74-9 Cytarabine hydrochloride

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