Decitabine - CAS 2353-33-5
Catalog number:
2353-33-5
Category:
Inhibitor
Not Intended for Therapeutic Use. For research use only.
Molecular Formula:
C8H12N4O4
Molecular Weight:
228.21
COA:
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Targets:
DNMT
Description:
Decitabine is a potent inhibitor of DNA methylation, used to treat myelodysplastic syndrome (MDS).
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Purity:
>98%
Synonyms:
Deoxycytidine, 5-aza-2'-deoxycytidine
MSDS:
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1.Low-dose DNA-demethylating agent enhances the chemosensitivity of cancer cells by targeting cancer stem cells via the upregulation of microRNA-497.
Liu L1, Chen L1, Wu X2, Li X2, Song Y3, Mei Q2, Nie J4, Han W5. J Cancer Res Clin Oncol. 2016 Apr 13. [Epub ahead of print]
PURPOSE: The DNA-demethylating agent decitabine has shown clinical response for the treatment of hematological malignancies and solid tumors, while the mechanisms underlying its antitumor capacity are not fully understood.
2.The risk of infections in patients with Myelodysplastic syndromes in 2016.
Caira M1, Latagliata R2, Girmenia C2. Expert Rev Hematol. 2016 Apr 21. [Epub ahead of print]
INTRODUCTION: The medical treatment of patients suffering from myelodysplastic syndromes has significantly changed during the last ten years, and this may have impacted the epidemiology of infectious complications. Some "real world" experiences raised the issue of infections in this setting and the possible negative consequences for patients and health system: the higher the rate of hospitalizations and need for anti-infective therapies, the higher the treatment delays/withdrawal and consecutive the worse the outcome. Areas Covered: The main epidemiological data on myelodysplastic patients are reviewed. Potential risk factors are described, including those related to the disease itself, patient's characteristics, health conditions and the environment. Expert Review: The complexity of MDS treatment is expected to increase further, with the introduction of other drugs and combined therapies. Defining the level of risk at time of treatment prescription will become more and more important, in order to better manage the infectious risk and the febrile events eventually occurring.
3.Azacitidine versus decitabine in patients with refractory anemia with excess blast-Results of multicenter study.
Salim O1, Toptas T2, Avsar E3, Yucel OK3, Ozturk E4, Ferhanoglu B4, Geduk A5, Mehtap O5, Tombak A6, Tiftik EN6, Deveci B7, Kurtoglu E7, Kara O2, Atagunduz IK2, Tuglular TF2, Undar L3. Leuk Res. 2016 Apr 11;45:82-89. doi: 10.1016/j.leukres.2016.04.003. [Epub ahead of print]
The present study aimed to compare the efficacy and safety of azacitidine and decitabine in patients with myelodysplastic syndrome (MDS). A total of 88 patients diagnosed with refractory anemia with excess blast (RAEB) treated with azacitidine (n=57) or decitabine (n=31) were evaluated. Comparisons between azacitidine and decitabine groups were performed in the whole cohort, and in a 1:1 propensity score-matched cohort in order to reduce the simple selection bias. Patients who received azacitidine or decitabine had comparable overall response rates in both the unmatched (49.1% vs. 64.5%, p=0.166) and the propensity-matched cohorts (52% vs. 68%, p=0.248). The cumulative incidence of AML transformation at one year was comparable between azacitidine and decitabine in the unmatched (24.0% vs. 31.3%, p=0.26) and in the propensity-matched cohorts (18.7% vs. 31.5%, p=0.11). There was no difference in terms of transfusion requirement, febrile neutropenia episodes or the need for antifungal use during the treatment cycles in the propensity-matched cohort.
4.IDH mutant gliomas escape natural killer cell immune surveillance by downregulation of NKG2D ligand expression.
Zhang X1, Rao A1, Sette P1, Deibert C1, Pomerantz A1, Kim WJ1, Kohanbash G1, Chang Y1, Park Y1, Engh J1, Choi J1, Chan T1, Okada H1, Lotze M1, Grandi P1, Amankulor N1. Neuro Oncol. 2016 Apr 25. pii: now061. [Epub ahead of print]
BACKGROUND: Diffuse gliomas are poorly immunogenic, fatal brain tumors. The basis for insufficient antitumor immunity in diffuse gliomas is unknown. Gain-of-function mutations in isocitrate dehydrogenases (IDH1 and IDH2) promote diffuse glioma formation through epigenetic reprogramming of a number of genes, including immune-related genes. Here, we identify epigenetic dysregulation of natural killer (NK) cell ligand genes as significant contributors to immune escape in glioma.
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