Cytarabine

cytotoxic agent, blocks DNA synthesis CAS# 147-94-4

Cytarabine

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Quality Control of Cytarabine

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Chemical structure

Cytarabine

3D structure

Chemical Properties of Cytarabine

Cas No. 147-94-4 SDF Download SDF
PubChem ID 6253 Appearance Powder
Formula C9H13N3O5 M.Wt 243.2
Type of Compound N/A Storage Desiccate at -20°C
Synonyms Cytosine b-D-arabinofuranoside
Solubility H2O : 48 mg/mL (197.35 mM; Need ultrasonic)
DMSO : 17.3 mg/mL (71.13 mM; Need ultrasonic and warming)
Chemical Name 4-amino-1-[(2R,3S,4S,5R)-3,4-dihydroxy-5-(hydroxymethyl)oxolan-2-yl]pyrimidin-2-one
SMILES C1=CN(C(=O)N=C1N)C2C(C(C(O2)CO)O)O
Standard InChIKey UHDGCWIWMRVCDJ-CCXZUQQUSA-N
Standard InChI InChI=1S/C9H13N3O5/c10-5-1-2-12(9(16)11-5)8-7(15)6(14)4(3-13)17-8/h1-2,4,6-8,13-15H,3H2,(H2,10,11,16)/t4-,6-,7+,8-/m1/s1
General tips For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months.
We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months.
Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it.
About Packaging 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial.
2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial.
3. Try to avoid loss or contamination during the experiment.
Shipping Condition Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request.

Biological Activity of Cytarabine

DescriptionNucleoside analog of deoxycytidine; inhibits DNA replication by incorporating into DNA (IC50 = 0.04 μM in L1210 and CEM cell lines). Displays no inhibitory effects on RNA synthesis. Causes S phase cell cycle arrest in ML-1 cell lines; cytotoxic in L5817Y leukemia cells. Antineoplastic and antileukemic agent.

Cytarabine Dilution Calculator

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Cytarabine Molarity Calculator

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Preparing Stock Solutions of Cytarabine

1 mg 5 mg 10 mg 20 mg 25 mg
1 mM 4.1118 mL 20.5592 mL 41.1184 mL 82.2368 mL 102.7961 mL
5 mM 0.8224 mL 4.1118 mL 8.2237 mL 16.4474 mL 20.5592 mL
10 mM 0.4112 mL 2.0559 mL 4.1118 mL 8.2237 mL 10.2796 mL
50 mM 0.0822 mL 0.4112 mL 0.8224 mL 1.6447 mL 2.0559 mL
100 mM 0.0411 mL 0.2056 mL 0.4112 mL 0.8224 mL 1.028 mL
* Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations.

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Background on Cytarabine

Cytarabine (AraC), an analogue of deoxycytidine, is the most effective cytotoxic agent in the treatment of acute myeloid leukemia (AML), which blocks DNA synthesis by inhibiting the function of DNA and RNA polymerases [1].
Cytarabine is incorporated into DNA, it blocks DNA synthesis by inhibiting the function of DNA and RNA polymerases. The most essential step in the AraC activation is phosphorylation into the monophosphate form, which is catalyzed by deoxycytidine kinase (dCK).
In AraC-sensitive rat leukemic cells, sole expression of inactive or spliced dCK forms make a cell resistant to the cytotoxic effects of AraC. It was reported that Ara-C also causes placental growth retardation, induce apoptosis and also impair cell proliferation in the zone of placental labyrinth. By injecting Ara-C into pregnant rats, the placentas were examined from 1 to 48h. the apoptosis of trophoblastic cells in the placental labyrinth zone increased from 3 h after the injecting and then peaked at 6 h and returned to control level at 48 h. Immunoreactivity of p53 protein in the placental labyrinth zone was significantly enhanced and peaked at 3 h after treatment, while no increase in p53 mRNA expression was detected by a reverse transcription polymerase chain reaction [1, 2].
A retrospective analysis was performed in 40 patients which treated with cytarabine 1000 mg/m2/day, mitoxantrone 8 mg/m2/day and etoposide 100 mg/m2/day for five days. 30% of remission rate and 11.2 months of median remission duration was got. In univariate analysis, compared to ≥second relapse (p = 0.02), patients in first relapse had improved overall survival [3].
References:
[1].Veuger MJT, Heemskerk MHM, Honders MW, et al. Functional role of alternatively spliced deoxycytidine kinase in sensitivity to cytarabine of acute myeloid leukemic cells. Blood, 2002, 99(4): 1373-1380.
[2].Yamauchi H, Katayama K, Ueno M, et al. Involvement of p53 in 1-beta-D-arabinofuranosylcytosine-induced trophoblastic cell apoptosis and impaired proliferation in rat placenta. Biology of Reproduction, 2004, 70(6): 1762-1767.
[3]. Liedtke M, Dunn T, Dinner S, et al. Salvage therapy with mitoxantrone, etoposide and cytarabine in relapsed or refractory acute lymphoblastic leukemia. Leukemia Research, 2014, 38(12): 1441-1445.

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References on Cytarabine

Phase II Study of Yttrium-90 Ibritumomab Tiuxetan Plus High-Dose BCNU, Etoposide, Cytarabine, and Melphalan for Non-Hodgkin Lymphoma: The Role of Histology.[Pubmed:28267593]

Biol Blood Marrow Transplant. 2017 Jun;23(6):922-929.

Standard-dose (90)yttrium-ibritumomab tiuxetan (.4 mci/kg) together with high-dose BEAM (BCNU, etoposide, Cytarabine, and melphalan) (Z-BEAM) has been shown to be a well-tolerated autologous hematopoietic stem cell transplantation preparative regimen for non-Hodgkin lymphoma. We report the outcomes of a single-center, single-arm phase II trial of Z-BEAM conditioning in high-risk CD20(+) non-Hodgkin lymphoma histologic strata: diffuse large B cell (DLBCL), mantle cell, follicular, and transformed. Robust overall survival and notably low nonrelapse mortality rates (.9% at day +100 for the entire cohort), with few short- and long-term toxicities, confirm the safety and tolerability of the regimen. In addition, despite a high proportion of induction failure patients (46%), the promising response and progression-free survival (PFS) rates seen in DLBCL (3-year PFS: 71%; 95% confidence interval, 55 to 82%), support the premise that the Z-BEAM regimen is particularly effective in this histologic subtype. The role of Z-BEAM in other strata is less clear in the context of the emergence of novel agents.

Exploring the Antitumor Mechanism of High-Dose Cytarabine through the Metabolic Perturbations of Ribonucleotide and Deoxyribonucleotide in Human Promyelocytic Leukemia HL-60 Cells.[Pubmed:28335578]

Molecules. 2017 Mar 21;22(3). pii: molecules22030499.

Despite the apparent clinical benefits of high-dose Cytarabine (Ara-C) over lower dose Ara-C in acute myeloid leukemia (AML) therapy, the mechanism behind high-dose Ara-C therapy remains uncertain. In this study, a LC-MS-based method was carried out to investigate the metabolic alteration of ribonucleotide and deoxyribonucleotide in human promyelocytic leukemia cells (HL-60) after treatment with Ara-C to reveal its antitumor mechanism. The metabolic results revealed that four nucleotides (ATP, ADP, CDP, and dCTP) could be used as potential biomarkers indicating the benefit of high-dose Ara-C over lower dose Ara-C treatment. Combining metabolic perturbation and cell cycle analysis, we conjectured that, apart from the acknowledged mechanism of Ara-C on tumor inhibition, high-dose Ara-C could present a specific action pathway. It was suggested that the pronounced rise in AMP/ATP ratio induced by high-dose Ara-C can trigger AMP-activated protein kinase (AMPK) and subsequently Forkhead Box, class O (FoxO), to promote cell cycle arrest. Moreover, the significant decrease in CDP pool induced by high-dose Ara-C might further accelerate the reduction of dCTP, which then aggravates DNA synthesis disturbance. As a result, all of these alterations led to heightened tumor inhibition. This study provides new insight in the investigation of potential mechanisms in the clinical benefits of high-dose Ara-C in therapy for AML.

Carboplatin instead of cisplatin in combination with dexamethasone, high-dose cytarabine with or without rituximab (DHAC+/-R) is an effective treatment with low toxicity in Hodgkin's and non-Hodgkin's lymphomas.[Pubmed:28374163]

Ann Hematol. 2017 Jun;96(6):943-950.

The DHAP regimen (high-dose Cytarabine in combination with dexamethasone and cisplatin) with or without rituximab (DHAP+/-R) is one of the most common regimens in daily practice. It is considered the standard treatment for relapse or refractory Hodgkin's and non-Hodgkin's lymphoma (NHL). Cisplatin nephrotoxicity is a major concern, and other platinum compounds are being tried. We performed a monocentric retrospective analysis to evaluate the use of carboplatin, so-called DHAC+/-R regimen. The purpose was to assess the toxicity of the DHAC+/-R regimen in real-life. The Dexamethasone, Cytarabine, Carboplatin (DHAC) regimen consisted of carboplatin AUC = 5 mg/ml/min (targeted area under the curve with Calvert's formula) on day 1, Cytarabine 2 g/m(2) twice a day on day 2 and IV dexamethasone 40 mg from days 1 to 4. Rituximab was administrated at 375 mg/m(2) on day 1 for CD20+ NHL. The interval between courses was 21 days. During the period considered, 199 patients received DHAC+/-R. For the entire cohort, median follow-up is 24 months (range, 2-82), median OS is not reached (NR), estimated 2-year OS is 75% (95% CI, 69-83) and median progression-free survival (PFS) is 46 months (95% CI, 22-NA). Of 144 patients scheduled for autologous stem cell transplantation (ASCT), 102 (71%, NA = 2) were in response after DHAC+/-R and all except 4 underwent ASCT. Grade >/= 3 haematological toxicities were mainly thrombocytopenia (n = 101) and anaemia (n = 95). Grade >/= 3 neutropenia occurred in 10 patients. No grade >/= 3 renal and one grade 3 neurological toxicity were reported. DHAC+/-R is feasible in daily practice, provides good response rates and jeopardises neither stem cell collection nor ASCT.

Vancomycin-resistant enterococci in acute myeloid leukemia and myelodysplastic syndrome patients undergoing induction chemotherapy with idarubicin and cytarabine.[Pubmed:28351179]

Leuk Lymphoma. 2017 Nov;58(11):2565-2572.

We conducted a retrospective study to determine the risk factors associated with vancomycin-resistant enterococci (VRE) acquisition/infection in newly diagnosed acute myeloid leukemia and myelodysplastic syndrome patients undergoing chemotherapy with the 7 + 3 regimen of Cytarabine and idarubicin. Although only 2.5% (6/235) patients were colonized with VRE on admission, 59% (134/229) of patients acquired VRE during their hospitalization. Multivariable analysis identified the use of intravenous vancomycin (p = .024; HR: 1.548) and cephalosporin (p = .009; HR: 1.596) as the risk factors for VRE acquisition. VRE infection developed in 14% (33/229) of patients, with bloodstream infections accounting for 82% (27/33) of cases. VRE infection occurred in 25/126 (20%) of the VRE-colonized patients, but only 8/103 (8%) of those who were not (p = .01). Our study provides the evidence for the role of intravenous cephalosporin and vancomycin in VRE acquisition and highlights the clinical significance of VRE colonization in these patients.

Pharmacodynamics of cytarabine alone and in combination with 7-hydroxystaurosporine (UCN-01) in AML blasts in vitro and during a clinical trial.[Pubmed:16293603]

Blood. 2006 Mar 15;107(6):2517-24.

Chk1 and Akt signaling facilitate survival of cells treated with nucleoside analogues. Activation of Chk1 in response to Cytarabine (ara-C) induced an S-phase checkpoint characterized by the inhibition of Cdk2, cell cycle arrest, no change in constitutively active Akt, or low-stress kinase signaling in ML-1 cells. However, inhibition of Chk1 by UCN-01 in S-phase-arrested cells resulted in an abrogation of the checkpoint, inhibition of Akt, activation of JNK, and a rapid induction of apoptosis. Similarly, primary acute myelogenous leukemia (AML) blasts exposed to ara-C and UCN-01 demonstrated a selective loss in cloning potential when compared with normal progenitors. Therefore, we evaluated a pilot clinical trial of ara-C in combination with UCN-01 in patients with relapsed AML. Blasts from some patients demonstrated a previously activated Chk1-Cdk2 DNA damage response pathway that decreased during therapy. Constitutively phosphorylated Akt kinase declined on addition of UCN-01 to the ara-C infusion, an action accompanied by an activation of JNK and reduction in absolute AML blast counts. Thus, use of UCN-01 in combination with ara-C decreases Chk1 phosphorylation, inhibits the Akt survival pathway, and activates JNK during the course of therapy, offering a rationale for the cytotoxic action of this combination during AML treatment.

Antitumor activity of P-4055 (elaidic acid-cytarabine) compared to cytarabine in metastatic and s.c. human tumor xenograft models.[Pubmed:10383159]

Cancer Res. 1999 Jun 15;59(12):2944-9.

The antineoplastic efficacy of P-4055, a 5'-elaidic acid (C18:1, unsaturated fatty acid) ester of Cytarabine, a nucleoside antimetabolite frequently used in the treatment of hematological malignancies, was examined in several in vivo models for human cancer. In initial dose-finding studies in nude mice, the efficacy of P-4055 was highest when using schedules with repeated daily doses. In a Raji Burkitt's lymphoma leptomeningeal carcinomatosis model in nude rats, the control Cytarabine- and saline-treated animals (five in each group) had a mean survival time of 13.2 days, whereas treatment with P-4055 resulted in three of five long-time survivors (>70 days). In a systemic Raji leukemia model in nude mice, 8 of 10 of the P-4055-treated animals survived (>80 days), compared with none of the Cytarabine-treated animals (mean survival time, 34.2 days). In s.c. xenograft models, the effects of maximum tolerated doses of P-4055 and Cytarabine, given in four weekly cycles of daily bolus i.v. injections for 5 subsequent days, against seven tumors (three melanomas, one lung adenocarcinoma, one breast cancer, and two osteogenic sarcomas) were investigated. P-4055 induced partial or complete tumor regression of the lung carcinoma, as well as of all three malignant melanomas. In two of the melanomas the activity was highly superior to that of Cytarabine, and both P-4055 and Cytarabine were, in general, more effective than several clinically established drugs previously tested in the same tumor models. In in vitro studies, inhibitors of nucleoside carrier-dependent transport, nitrobenzylmercaptopurine riboside and dipyridamol, reduced strongly the cellular sensitivity to Cytarabine, but not to P-4055, indicating that P-4055 uses an alternative/additional mechanism of internalization into the cell compared with Cytarabine. The results explain, at least in part, the observed differences between the two compounds in in vivo efficacy, and together the data strongly support the evaluation of P-4055 in clinical studies.

Description

Cytarabine, a nucleoside analog, causes S phase cell cycle arrest and inhibits DNA polymerase. Cytarabine inhibits DNA synthesis with an IC50 of 16 nM. Cytarabine has antiviral effects against HSV.

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