ライフサイエンスコーパス: decitabine

1 ): 5-azacitidine and 5-aza-2'-deoxycitidine (decitabine).

2 tic target for hypomethylating agents (e.g., decitabine).

3 life and exposure than its active metabolite decitabine.

4 40 (35%) with azacitidine and 73 (65%) with decitabine.

5 d who also received serial 10-day courses of decitabine.

6 nce after receiving serial 10-day courses of decitabine.

7 fraction of TET1-CD-GFP after treatment with Decitabine.

8 following treatment with the DNMT inhibitor, decitabine.

9 nhibitor entinostat or hypomethylating agent decitabine.

10 hematology, with a focus on azacitidine and decitabine.

11 uced by the DNA methyltransferase inhibitor, decitabine.

12 by sensitivity of MPN-derived cell lines to decitabine.

13 relapsed cases were found to be sensitive to decitabine.

14 ry tumor cells treated with panobinostat and decitabine.

15 of three cycles (range, one to 25 cycles) of decitabine.

16 RRM2B) is a robust transcriptional target of decitabine.

17 loid differentiation agents such as ATRA and decitabine.

18 s at low doses and persists after removal of decitabine.

19 compared with that reported for intravenous decitabine.

20 onger in-vivo exposure time than intravenous decitabine.

21 At the decitabine 0.16 mg/kg dose, plasma concentrations peaked

22 able in patients who had previously received decitabine (1.1 vs 0.9 vs 3.1 months, respectively, P =

23 Oral cedazuridine/decitabine (100/35 mg) produced similar systemic decitab

24 re seen in two of four patients treated with decitabine 135 mg/m2 and carboplatin AUC 5.

25 The starting dose was decitabine 20 mg and cedazuridine 40 mg.

26 g/m(2) intravenously/subcutaneously daily or decitabine 20 mg/m(2) intravenously daily for 3 consecut

27 Patients received decitabine 20 mg/m(2) intravenously for 10 days with ora

28 ine on day -3, a 1-h intravenous infusion of decitabine 20 mg/m(2) on day 1, and cohort-defined doses

29 e exposure, DNA demethylation, and safety vs decitabine 20 mg/m2 IV in the first 2 cycles, with simil

30 zuridine 100 mg/decitabine 35 mg vs standard decitabine 20 mg/m2 IV.

31 Induction with decitabine (20 mg/m(2) intravenously on days 1-10) plus

32 or 1200 mg daily in combination with either decitabine (20 mg/m(2), days 1-5, intravenously [IV]) or

33 Decitabine 30 mg and 40 mg plus cedazuridine 100 mg prod

34 ean day-5 decitabine AUCs (146 ng x h/mL for decitabine 30 mg, and 221 ng x h/mL for decitabine 40 mg

35 the first 2 cycles with cedazuridine 100 mg/decitabine 35 mg vs standard decitabine 20 mg/m2 IV.

36 for decitabine 30 mg, and 221 ng x h/mL for decitabine 40 mg) closest to the mean intravenous-decita

37 4(+) cells but not normal CD34(+) cells with decitabine (5-aza-2'-deoxycytidine [5azaD]), followed by

38 treatment with the DNA hypomethylating drug decitabine (5-aza-dC; DAC) extended survival in the KPC-

39 a nonsignificant increase in median OS with decitabine (7.7 months; 95% CI, 6.2 to 9.2) versus TC (5

40 t) was seen in two of 10 patients treated at decitabine 90 mg/m2 and carboplatin AUC 6.

41 Furthermore, decitabine 90 mg/m2 induced demethylation of the MAGE1A

42 Decitabine, a cancer therapeutic that inhibits DNA methy

43 Co-administration of 7a with decitabine, a CDA substrate, boosted the plasma levels o

44 and primary AML xenografts were treated with decitabine, a DNA demethylating agent, and cytarabine, a

45 Epigenetic therapy using decitabine, a DNA hypomethylating agent, is clinically e

46 s, low-dose (20 mg/m(2) per day for 10 days) decitabine, a DNA hypomethylating azanucleoside, produce

47 Treatment with decitabine, a DNA methylation inhibitor, either during L

48 Decitabine, a DNA methyltransferase 1 inhibitor or DNA h

49 Decitabine, a DNA-targeted hypomethylating agent, is app

50 8 promoter hypermethylation, incubation with decitabine activated SLC5A8 expression.

51 e clinical and biologic activity of low-dose decitabine administered before carboplatin in platinum-r

52 -expression end point), 14 patients received decitabine alone for 10 days.

53 Enzyme-released decitabine along with other mononucleosides were separat

54 In parallel with these responses, decitabine also upregulated the proapoptotic BCL-2 famil

55 Decitabine also upregulates BNIP3 and Bik expression, wh

56 results of this study suggest that low-dose decitabine altered DNA methylation of genes and cancer p

57 We identified and validated decitabine, an FDA-approved drug, as a potent inhibitor

58 Treating neonatal rats with decitabine, an inhibitor of DNA methylation, during inte

59 The DNA hypomethylating agents decitabine and 5-azacytidine are the only two drugs appr

60 The DNA methylation inhibitors decitabine and azacitidine are efficacious for hematolog

61 Low-dose decitabine and azacitidine may have broad applicability

62 : 20 and 13 months for patients treated with decitabine and azacitidine, respectively (P = .1).

63 and 49% (P = .03) for patients treated with decitabine and azacitidine, respectively.

64 t may preferentially be reversed by the HMAs decitabine and azacitidine.

65 Hypomethylating agents decitabine and azacytidine are regarded as interchangeab

66 In cycles 2 and beyond, the oral decitabine and cedazuridine were given on days 1-5.

67 cohorts to receive escalating oral doses of decitabine and cedazuridine.

68 Sequential treatment with decitabine and cytarabine was found to be more effective

69 AEs were similar for decitabine and cytarabine, although patients received a

70 ) is a novel hypomethylating dinucleotide of decitabine and deoxyguanosine resistant to degradation b

71 nhibitors of DNA methyltransferases (DNMTs), decitabine and FdCyd, block mutant huntingtin (Htt)-indu

72 ombination of two clinically approved drugs, decitabine and gemcitabine, reduced HIV infectivity by 7

73 del of KRAS-mutant ovarian cancer, combining decitabine and navitoclax heightened antitumor activity

74 Ldb1 was more than double that observed with decitabine and pomalidomide; butyrate had an intermediat

75 Treatment with epigenetic compounds decitabine and trichostatin A rescued the BPA effects as

76 is mouse model, we further demonstrated that decitabine and vorinostat cooperate to suppress colon ca

77 , we demonstrated that epigenetic inhibitors decitabine and vorinostat cooperate to upregulate Fas ex

78 h their function in apoptosis sensitization, decitabine and vorinostat significantly increased the ef

79 mice, suggesting a critical role for FasL in decitabine and vorinostat-mediated tumor suppression in

80 infiltrating CD8(+) T cells are FasL(+), and decitabine and vorinostat-mediated tumor-suppression eff

81 patient blasts using 5-aza-2'-deoxycytidine (decitabine) and trichostatin A increased H3K4me3 and mai

82 ation for oral cedazuridine/decitabine vs IV decitabine, and clinical response.

83 US regulatory approval of azacitidine, decitabine, and lenalidomide between 2004 and 2006 seeme

84 Lenalidomide, azacitidine, and decitabine are all FDA-approved agents to treat MDS; how

85 Hypomethylating agents (HMA) azacitidine and decitabine are standard of care for myelodysplastic synd

86 Hypomethylating agents, including decitabine are used to treat elderly AML patients with r

87 gues azacytidine and 5-aza-2'-deoxycytidine (decitabine) are commonly used to treat myelodysplastic s

88 Hypomethylating agents, such as decitabine, are the standard of care for older patients

89 The drug dose was escalated if mean decitabine area under the curve (AUC) of the oral drug w

90 igenetic drugs: 5-aza-2'-deoxycytidine (DAC; decitabine), arsenic trioxide (ATO), and MS-275 [entinos

91 sing a high-throughput screen, we identified decitabine as a potent inducer of immunogenic EBV antige

92 Responding patients received decitabine as consolidation therapy on a 5-day schedule

93 cy and toxicity of the hypomethylating agent decitabine as initial therapy in older patients with AML

94 uding the inhibitor of DNA methyltransferase decitabine as well as the inhibitors of histone deacetyl

95 Subjects received low-dose decitabine at 20 mg/m(2) i.v. over 1 h on days 1 to 10.

96 abine 40 mg) closest to the mean intravenous-decitabine AUC (164 ng x h/mL).

97 Dose-dependent increases in decitabine AUC and peak plasma concentration occurred wi

98 Once the decitabine AUC target range set as the primary endpoint,

99 plus cedazuridine 100 mg produced mean day-5 decitabine AUCs (146 ng x h/mL for decitabine 30 mg, and

100 ve chemotherapy (n = 557) or azacitidine- or decitabine-based therapy (n = 114).

101 Thirty-two percent of patients treated with decitabine became transfusion independent compared with

102 biologic activity of epigenetic priming with decitabine before standard induction chemotherapy in pat

103 e novel CDA inhibitor cedazuridine increases decitabine bioavailability for the treatment of myelodys

104 Decitabine, but not 5-azacytidine, also produced a G(2)/

105 versely correlates with clinical response to decitabine, but not to azacytidine.

106 This suggests that decitabine can be administered in an outpatient setting

107 lton et al show that epigenetic therapy with decitabine can upregulate immunogenic Epstein-Barr virus

108 n of 2.5 to 5 micromol/L (similar to that of decitabine), complete degradation of DNMT1 protein was a

109 We hypothesised that venetoclax with 10-day decitabine could have improved activity in patients with

110 ies have suggested that a 10-day schedule of decitabine cycles leads to better outcomes than the usua

111 Decitabine (DAC) and 5-azacitidine have recently been ap

112 t clinical studies on combination therapy of decitabine (DAC) and arsenic trioxide (ATO) have demonst

113 At low doses, the cytosine analogue decitabine (DAC) can be used to deplete DNA methyl-trans

114 The deoxycytidine analog decitabine (DAC) can deplete DNA methyl-transferase 1 (D

115 MT with the DNA methyltransferease inhibitor decitabine (DAC) decreased MDSC accumulation and increas

116 g agents (DHAs) like 5-azacytidine (5AC) and decitabine (DAC) demonstrate efficacy in the treatment o

117 a comparative study of azacitidine (AZA) and decitabine (DAC) in combination with allogeneic NK cells

118 patients who were responsive or resistant to decitabine (DAC) in order to develop a molecular means o

119 In vitro treatment of AML blasts with decitabine (DAC) or 5-azacytidine, 2 hypomethylating age

120 The DNA hypomethylating drug decitabine (DAC) reactivates silenced gene expression in

121 omplexes combined with gemcitabine (GEM) and decitabine (DAC) to improve the efficiency and reduce th

122 treated with hypomethylating agents, such as decitabine (DAC), although the mechanisms by which it in

123 at treatment of 143B osteosarcoma cells with decitabine (DAC, 5-Aza-2'-deoxycytidine) induces express

124 hat the FDA-approved hypomethylating agents, decitabine (Dec) and azacitidine (AzaC), induce FOXP3 ex

125 d before treatment with azacitidine (AZA) or decitabine (DEC).

126 Here, we demonstrated that resistance to decitabine (decitabine(R)) or PKC412 (PKC412(R)) eventua

127 Pretreatment with decitabine decreased the cytotoxic activity of MEK inhib

128 clinical and DNA-hypomethylating activity of decitabine delivered at 20 mg/m(2) by either a 1-hour in

129 Treatment of CCA cells with decitabine (demethylating agent) or butyrate (histone de

130 ethod again demonstrated correlation between decitabine DNA-incorporation and DNA hypomethylation.

131 The mechanism of p53R2 gene induction by decitabine does not seem to be promoter DNA hypomethylat

132 odysplastic syndrome (n=25) received reduced decitabine dosages (0.1-0.2 mg/kg/day compared with the

133 Oral decitabine doses, administered after oral THU 10 mg/kg,

134 Mechanistically, decitabine efficacy was linked to KRAS-driven dependency

135 Treating rats with decitabine either during LT-IH or during recovery from L

136 Overall, the repurposing of decitabine emerged as an intriguing option for treating

137 Together, 5-azacytidine and decitabine exert growth-inhibitory and proapoptotic effe

138 The USFDA approved "epigenetic drug", Decitabine, exerts its effect by hypomethylating DNA, de

139 f each drug needed to achieve a mean AUC for decitabine exposure similar to that for intravenous deci

140 t that most closely approximated intravenous decitabine exposure was expanded to 18 evaluable patient

141 ase 2 study was designed to compare systemic decitabine exposure, demethylation activity, and safety

142 tabine (100/35 mg) produced similar systemic decitabine exposure, DNA demethylation, and safety vs de

143 ine exposure similar to that for intravenous decitabine exposure.

144 lanoma, and breast cancer cells treated with decitabine, finding that RAS/MEK/ERK pathway activation

145 In latency I BL xenografts, decitabine followed by EBV-CTLs results in T-cell homing

146 that sequential treatment of AML blasts with decitabine followed by selinexor (XPO1 inhibitor) enhanc

147 Sequential treatment of decitabine followed by selinexor in an MV4-11 xenograft

148 linical results, a phase 1 clinical trial of decitabine followed by selinexor in elderly patients wit

149 28 received decitabine for 5 days and 43 for 10 days, and all were a

150 clax 400 mg daily for induction, followed by decitabine for 5 days with daily venetoclax for consolid

151 Following exposure to 2.5 microM decitabine, GDM decreased to approximately 50% of the ba

152 p53R2 as a novel hypomethylation-independent decitabine gene target associated with clinical response

153 Decitabine given in a low-dose, 5-day regimen has activi

154 Decitabine given on a 5-day schedule provided meaningful

155 Decitabine globally reactivated multiple transposable el

156 ypomethylating agent whose active metabolite decitabine has a longer in-vivo exposure time than intra

157 Venetoclax with 10-day decitabine has a manageable safety profile and showed hi

158 treatment with the DNA methylation inhibitor decitabine has been shown to be applicable for the manag

159 za) and its congener 5-aza-2'-deoxycytidine (decitabine) has provided an alternate approach to cancer

160 The hypomethylating drugs azacitidine and decitabine have shown efficacy in myelodysplastic syndro

161 stem cells, and two of them (azacytidine and decitabine) have been approved for treatment of myelodys

162 In older patients with AML, decitabine improved response rates compared with standar

163 ation increases the antileukemic activity of decitabine in AML cell lines, primary leukemic blasts, a

164 Treatment with the DNA-hypomethylating agent decitabine in cultured melanoma cells induced transcript

165 o receive oral cedazuridine/decitabine or IV decitabine in cycle 1, followed by crossover to the othe

166 included 32 additional patients who received decitabine in different protocols.

167 gions, suggesting a differential activity of decitabine in distinct chromosome regions.

168 2; conversely, KIT depletion synergized with decitabine in eliminating decitabine(R).

169 ng clinical activity for a 10-day regimen of decitabine in older AML patients; high miR-29b expressio

170 f two low-dose regimens of subcutaneous (SC) decitabine in patients with low- or intermediate-1-risk

171 CDA substrate, boosted the plasma levels of decitabine in rhesus monkeys.

172 All patients received oral cedazuridine/decitabine in subsequent cycles.

173 ug was less than 90% of that for intravenous decitabine in the cohort and if no dose-limiting toxicit

174 were used to study the effects of HDACIs and decitabine in this system.

175 ic LC-MS/MS method to simultaneously measure decitabine incorporation and DNA hypomethylation.

176 Decitabine induced DNA hypomethylation at all dose level

177 Neither 5-azacytidine nor decitabine induced substantial apoptosis or growth arres

178 ctivator, rifampicin, significantly reversed decitabine-induced ABCC3 and SLCO2A1 expression.

179 This method was applied to characterize decitabine-induced promoter DNA methylation changes of t

180 encing approach was developed to interrogate decitabine-induced transcriptome changes in AML cell lin

181 ransferase inhibitor 5-aza-2'-deoxycytidine (decitabine) induces DNA demethylation and re-expression

182 lude hypomethylating agents (azacitidine and decitabine), intensive chemotherapy (ICT), and allogenei

183 d dosage and time-dependent incorporation of decitabine into myeloid leukemia cell DNA that correlate

184 Patients were assigned to receive 20 mg/m(2) decitabine intravenously for 5 or 10 consecutive days as

185 Decitabine is a promising drug for cancer cells dependen

186 the initial RR-mediated 5-azaC conversion to decitabine is terminated through its own inhibition.

187 eutic activity of the deoxycytidine analogue decitabine is thought to reflect its ability to reactiva

188 Demethylation induced by decitabine is traditionally thought to be active in tumo

189 ation of the DNA methyltransferase inhibitor decitabine led to reexpression of genes shown to be pref

190 t, supporting a functional role for p53R2 in decitabine-mediated cellular responses.

191 Decitabine-mediated hypomethylation of HCT116 displays h

192 the DNA methyltransferase inhibitor (DNMTi) decitabine, MLL-r (but not MLL wild-type cell lines) sho

193 However, in this study of 10-day courses of decitabine, neither of these risk factors was associated

194 tient received a cohort-defined dose of oral decitabine on day -3, a 1-h intravenous infusion of deci

195 of 2 demethylating agents, 5-azacytidine and decitabine on growth and survival of neoplastic MCs and

196 identify a previously unrecognized action of decitabine on the activation of metastasis-suppressive m

197 eport safety and efficacy of venetoclax with decitabine or azacitidine from a large, multicenter, pha

198 istant NPM-ALK(+) KARPAS-299-CR06 cells with decitabine or ectopic miR-150 expression reduced viabili

199 randomized 1:1 to receive oral cedazuridine/decitabine or IV decitabine in cycle 1, followed by cros

200 5-fluorouracil alone or in combination with decitabine or tacedinaline caused radiosensitization of

201 5-fluorouracil alone or in combination with decitabine or tacedinaline reduced tumor cell viability

202 5-fluorouracil alone or in combination with decitabine or tacedinaline, respectively.

203 cil plus the DNA methyltransferase inhibitor decitabine or the histone deacetylase inhibitor tacedina

204 lls are sensitive to 5-aza-2'-deoxycytidine (decitabine) or midostaurin (PKC412), because decitabine

205 Decitabine, or 5-aza-2'-deoxycytidine (5-aza-CdR), is a

206 AML cells acquire resistance to decitabine partly by SAMHD1 up-regulation.

207 ibility and preliminary clinical activity of decitabine plus bortezomib in AML and identifies FLT3 as

208 Further study of decitabine plus cedazuridine as an alternative to parent

209 Oral decitabine plus cedazuridine emulated the pharmacokineti

210 ) on day 1, and cohort-defined doses of oral decitabine plus cedazuridine on days 2-5.

211 mary objectives were to assess the safety of decitabine plus cedazuridine, and to determine the dose

212 cordingly, they show that the combination of decitabine plus immune checkpoint blockade effectively r

213 re gastro-intestinal toxicity with 7 days of decitabine priming.

214 he DNA methyltransferase 1 (DNMT1) inhibitor decitabine produce p53-independent cell-cycle exits by r

215 All explored HDACIs in combination with decitabine produced a synergistic effect in growth inhib

216 Indeed, both decitabine(R) and PKC412(R) displayed the up-regulation

217 Importantly, when engrafted into nude mice, decitabine(R) and PKC412(R) had faster proliferation wit

218 Interestingly, decitabine(R) and PKC412(R) had higher capability of col

219 ivation of KIT or DNMT1 reciprocally blocked decitabine(R) or PKC412(R) cell proliferation.

220 demonstrated that resistance to decitabine (decitabine(R)) or PKC412 (PKC412(R)) eventually results

221 on synergized with decitabine in eliminating decitabine(R).

222 pomethylation was related to the activity of decitabine rather than to a mere decrease in leukemia bu

223 The DNA-demethylating agent decitabine recovers FBXL7 expression and limits epitheli

224 Furthermore, decitabine reduces metastases derived from prostate and

225 Myeloid Leukemia, we demonstrate that while Decitabine reduces the global levels of 5-methylcytosine

226 Decitabine regimens can be redesigned to minimize cytoto

227 Decitabine-related methylation changes were concordant w

228 and a potential target for the treatment of decitabine-resistant leukemia.

229 nt with the DNA methyltransferase inhibitor, decitabine, restored expression of some hypermethylated

230 decitabine) or midostaurin (PKC412), because decitabine restores the expression of methylation-silenc

231 The addition of ATRA to decitabine resulted in a higher remission rate and a cli

232 Combination pretreatment with vorinostat and decitabine resulted in even greater cytotoxicity compare

233 ice with the DNA methyltransferase inhibitor decitabine resulted in failure to form GCs after immune

234 nes with the DNA methyltransferase inhibitor decitabine resulted in reversal of aberrant hypermethyla

235 at demethylation of the survivin promoter by decitabine results in p53-dependent survivin repression

236 ty did not differ by the 5-day or the 10-day decitabine schedule.

237 ncy might be prospectively used to inform on decitabine sensitivity in a selected subset of patients

238 we showed that KRAS genomic status predicted decitabine sensitivity in low-grade and high-grade serou

239 hat otherwise rapidly deaminates/inactivates decitabine, severely limiting its half-life, tissue dist

240 Results of a randomized survival study of decitabine should be available in 2008.

241 In this phase II study, low-dose decitabine showed promising results in patients with low

242 Decitabine significantly reduced global methylation comp

243 Primary end points: mean decitabine systemic exposure (geometric least-squares me

244 superiority of the longer 10-day regimen of decitabine that has shown promising results in patients

245 ed that post-MPN AML cells were sensitive to decitabine, the JAK1/2 inhibitor ruxolitinib, or the hea

246 lly collected from MDS patients treated with decitabine, the method again demonstrated correlation be

247 intended molecular pharmacodynamic effect of decitabine therapy can therefore potentially provide ins

248 ecular determinants of clinical responses to decitabine therapy in patients with acute myeloid leukem

249 enous leukemia (MDS/AML) patients undergoing decitabine therapy.

250 ial (NCT01685515) combined 2 small molecules-decitabine to deplete DNMT1 and tetrahydrouridine (THU)

251 AML or MDS in a single-institution trial of decitabine to identify somatic mutations and their relat

252 Administration of oral THU-decitabine to patients with SCD was safe in this study a

253 ition with 5-Aza-2'-deoxycytidine (5-Aza-dC, decitabine) to demonstrate that DNA methylation predomin

254 inical responses were similar to intravenous decitabine treatment for 5 days.

255 cancer stem cell population was inhibited by decitabine treatment in mice.

256 V3-1 and RIG-I mRNA was also observed during decitabine treatment in vivo in serially sorted peripher

257 s those enriched in demethylated genes after decitabine treatment included pathways involved in cance

258 ated CpG islands of AIM1 in DERL2 cells, and decitabine treatment induced a significant increase in A

259 In cancer cells, decitabine treatment induces p53R2 mRNA expression, prot

260 Decitabine treatment of latency I EBV+ Burkitt lymphoma

261 ived xenografts to demonstrate that low dose decitabine treatment remarkably enhanced the effects of

262 Decitabine treatment restored TET2 methylation and EZH2

263 d monosomal karyotype AML murine xenografts, decitabine treatment resulted in superior survival rates

264 es the extent of cell cycle arrest following decitabine treatment, supporting a functional role for p

265 t cancer-derived cell lines before and after decitabine treatment, we established that reelin express

266 xcess blasts after failure of azacitidine or decitabine treatment.

267 for stratification of older AML patients to decitabine treatment.

268 hylation and synthesis through conversion to decitabine triphosphate and subsequent DNA incorporation

269 Here, we show that the bioactive metabolite decitabine triphosphate, but not azacytidine triphosphat

270 Patients continued to receive decitabine until disease progression or an unacceptable

271 The CR rate plus CRp was 17.8% with decitabine versus 7.8% with TC (odds ratio, 2.5; 95% CI,

272 pite standard-of-care, randomized 3:2 to THU-decitabine versus placebo in 5 cohorts of 5 patients tre

273 patients received a median of four cycles of decitabine versus two cycles of TC.

274 ificant upregulation of CDKN1A and FOXO3A in decitabine- versus control-treated cells.

275 AEs) were not significantly different in THU-decitabine-versus placebo-treated patients.

276 E-1) DNA demethylation for oral cedazuridine/decitabine vs IV decitabine, and clinical response.

277 compared the safety and efficacy of low-dose decitabine vs low-dose azacitidine in this group of pati

278 Decitabine was administered at a dose of 20 mg per squar

279 Decitabine was associated with improved median overall s

280 A phase II clinical trial with single-agent decitabine was conducted in older patients (>or=60 years

281 ethylation in CD34(+) bone marrow cells when decitabine was delivered by a short pulse (Arm A).

282 Thus, a phase 1 trial of bortezomib and decitabine was developed.

283 dose of cedazuridine was escalated first and decitabine was escalated once CDA inhibition by cedazuri

284 In these neurons and in cortical slices, decitabine was found to rescue the effect of BPA on Kcc2

285 In conclusion, this schedule of decitabine was highly active and well tolerated in this

286 e of intensive chemotherapy, azacitidine, or decitabine was more favorable in patients who had previo

287 Similar results were seen when decitabine was used in combination with another ribonucl

288 y endpoint, and established with intravenous decitabine, was reached at a dose deemed to be safe, the

289 Given the DNA hypomethylating effect of decitabine, we examined the relationship of clinical res

290 did not correlate with clinical response to decitabine, we observed a significant correlation betwee

291 To assess the genome-wide activity of decitabine, we profiled pretreatment and post treatment

292 5-Azacitidine and decitabine were approved in the United States based on c

293 Cedazuridine and decitabine were given initially as separate capsules in

294 histone deacetylase inhibitors (HDACIs) and decitabine were investigated in models of diffuse large

295 The most common drug-related AEs with decitabine were thrombocytopenia (27%) and neutropenia (

296 tered by the combination of panobinostat and decitabine were VHL, TCEB1, WT1, and DIRAS3.

297 e the hypomethylating agents azacitidine and decitabine, which should be administered for a minimum o

298 anned survival analysis showed a benefit for decitabine, which was not observed at the time of the pr

299 II trial compared the efficacy and safety of decitabine with treatment choice (TC) in older patients

300 emulated the pharmacokinetics of intravenous decitabine, with a similar safety profile and dose-depen