ライフサイエンスコーパス: azacitidine

1 for azacitidine plus vorinostat ( P = .16 v azacitidine).

2 ubcutaneously once weekly during 4 cycles of azacitidine.

3 ong-term remission even after termination of azacitidine.

4 of iadademstat was 90 mug/m(2) per day with azacitidine.

5 differentiating OS outcomes with venetoclax-azacitidine.

6 r acute myeloid leukaemia when combined with azacitidine.

7 outcomes in patients treated with venetoclax-azacitidine.

8 veloping refractory disease under venetoclax-azacitidine.

9 mg (n=3) or 200 mg (n=3) in combination with azacitidine.

10 acute myeloid leukaemia and synergistic with azacitidine.

11 when either was combined with venetoclax and azacitidine.

12 ially be reversed by the HMAs decitabine and azacitidine.

13 syndromes is hypomethylating agents such as azacitidine.

14 rapies such as donor lymphocyte infusion and azacitidine.

15 solidation treatment followed by 4 cycles of azacitidine.

16 responders who received >/= 6 cycles of oral azacitidine.

17 n days 1 to 3) with the same two agents plus azacitidine (250 mg/m2/d on days 4 to 50) for the therap

18 MRD response during the first six cycles of azacitidine, 31 (52%) maintained response without hemato

19 7 g once daily intravenously on days 1-4 and azacitidine 36 mg/m(2) once daily intravenously/subcutan

20 y-five patients received at least 1 cycle of azacitidine, 46 at least 4 cycles, and 35 at least 12 cy

21 ths), the ORR was 38% for patients receiving azacitidine, 49% for azacitidine plus lenalidomide ( P =

22 The combination of venetoclax and 5-azacitidine (5-AZA) for older or unfit patients with acu

23 L include using the hypomethylating agent, 5-azacitidine (5-Aza) or MEK inhibitors trametinib and PD0

24 ed a phase 1/2 study of the combination of 5-azacitidine (5-AZA), valproic acid (VPA), and ATRA in pa

25 proved median overall survival compared with azacitidine (5.5 vs 8.8 months, respectively, P = .03).

26 ts were assigned to maintenance therapy with azacitidine 50 mg/m(2) intravenously or subcutaneously f

27 her for azacitidine plus lenalidomide versus azacitidine (68% v 28%, P = .02) but similar for all arm

28 recommended phase 2 dose was established as azacitidine 75 mg/m(2) for 5 days plus venetoclax 400 mg

29 a Bayesian adaptive design to receive either azacitidine 75 mg/m(2) intravenously/subcutaneously dail

30 2) on day 1-5 or intravenous or subcutaneous azacitidine 75 mg/m(2) on day 1-7 or day 1-5 and day 8 a

31 The go-forward dose is azacitidine 75 mg/m(2) on days 1 through 5 and lenalidom

32 7, combined with subcutaneous or intravenous azacitidine 75 mg/m(2) on days 1-7 in 28-day cycles.

33 2 also received subcutaneous or intravenous azacitidine 75 mg/m(2) on days 1-7.

34 continuous 28-day cycles, plus subcutaneous azacitidine 75 mg/m(2) per day for 7 days of each cycle.

35 ally, for 5 days on, 2 days off weekly, with azacitidine 75 mg/m(2) subcutaneously, for seven of 28 d

36 Azacitidine 75 mg/m(2) was administered intravenously/su

37 ere treated with intravenous or subcutaneous azacitidine (75 mg/m(2)) for 5 days and oral venetoclax

38 Azacitidine (75 mg/m(2)) was administered subcutaneously

39 20 mg/m(2), days 1-5, intravenously [IV]) or azacitidine (75 mg/m(2), days 1-7, IV or subcutaneously)

40 icacy and safety of combination therapy with azacitidine (75 mg/m(2)/d for 5 days) and lenalidomide (

41 onic myelomonocytic leukemia (CMML) 1:1:1 to azacitidine (75 mg/m(2)/day on days 1 to 7 of a 28-day c

42 on day 2, and 400 mg daily thereafter), and azacitidine (75 mg/m2 days 1-7) in 28-day cycles.

43 days per 28-day cycle), in combination with azacitidine (75 mg/m2 for 7 days per 28-day cycle) for t

44 cted with either intravenous or subcutaneous azacitidine (75 mg/m2/d for 7 days every 28 days).

45 egimen consisting of hydroxyurea followed by azacitidine, 75 mg/m(2) for 7 days, and gemtuzumab ozoga

46 Of 277 patients from 90 centers, 92 received azacitidine, 93 received azacitidine plus lenalidomide,

47 cebo-controlled trial evaluated CC-486 (oral azacitidine), a hypomethylating agent, in patients with

48 Primary T cells treated with 5-azacitidine, a DNA methyltransferase inhibitor, showed i

49 e, and prednisone (R-CHOP) plus subcutaneous azacitidine, a hypomethylating agent.

50 ce weekly, 28-day cycle) in combination with azacitidine, administered as per label.

51 tivity of enasidenib plus azacitidine versus azacitidine alone in patients with newly diagnosed, muta

52 verall, 279 patients treated with venetoclax-azacitidine and 113 patients treated with placebo-azacit

53 proved in myelodysplastic syndromes (MDS): 5-azacitidine and 5-aza-2'-deoxycitidine (decitabine).

54 rse-risk AML (60.2% and 72.8% for venetoclax-azacitidine and 65.5% and 75.2% for placebo-azacitidine,

55 16, 113 patients were treated: 40 (35%) with azacitidine and 73 (65%) with decitabine.

56 r imatinib, MEK inhibitor U0126, cytarabine, azacitidine and arsenic trioxide.

57 Hypomethylating agents (HMA) azacitidine and decitabine are standard of care for myel

58 The DNA methyltransferase inhibitors azacitidine and decitabine for individuals with myelodys

59 re than a decade, the hypomethylating agents azacitidine and decitabine have been the standard of car

60 The hypomethylating drugs azacitidine and decitabine have shown efficacy in myelod

61 5-Azacitidine and decitabine were approved in the United S

62 her-risk MDS include hypomethylating agents (azacitidine and decitabine), intensive chemotherapy (ICT

63 therapies include the hypomethylating agents azacitidine and decitabine, which should be administered

64 lating agents in hematology, with a focus on azacitidine and decitabine.

65 and gastrointestinal (5 [12%] vs 1 [2%] for azacitidine and ICT, respectively).

66 d active sequential treatment combination of azacitidine and lenalidomide for patient with myelodyspl

67 We aimed to assess azacitidine and lenalidomide in patients with high-risk

68 Patients who are R/R after azacitidine and venetoclax (AZA/VEN) have a dismal outco

69 ted dose and recommended phase 2 dose of the azacitidine and venetoclax combination using a 3 + 3 stu

70 phase 1b/2 study of pivekimab sunirine plus azacitidine and venetoclax in patients with CD123-positi

71 Azacitidine and venetoclax is a standard frontline treat

72 of gilteritinib, an oral FLT3 inhibitor, to azacitidine and venetoclax may improve outcomes in patie

73 ritinib 80 mg once daily in combination with azacitidine and venetoclax.

74 f DNMT1 by using DNA hypomethylating agents (azacitidine and zebularine) restored Kupffer cell autoph

75 or azacitidine plus lenalidomide ( P = .14 v azacitidine), and 27% for azacitidine plus vorinostat (

76 Lenalidomide, azacitidine, and decitabine are all FDA-approved agents

77 Lenalidomide, azacitidine, and decitabine, each recently approved by t

78 a manageable safety profile, consistent with azacitidine, and shows promising clinical activity in pa

79 In one patient, treatment with azacitidine appeared to mitigate this NKL skewing, promo

80 Lenalidomide and azacitidine are active in patients with lower- and highe

81 he DNA methylation inhibitors decitabine and azacitidine are efficacious for hematological neoplasms

82 However, responses to azacitidine are generally temporary, and outcomes after

83 rapies beyond hypomethylating agents such as azacitidine are needed in high-risk myelodysplastic synd

84 nsive chemotherapy, we assessed the value of azacitidine as postremission therapy with respect to dis

85 e-arm expansion to evaluate cusatuzumab plus azacitidine at the cusatuzumab dose level selected in pa

86 Overall, venetoclax plus azacitidine at the RP2D was well tolerated and had favor

87 We previously reported that azacitidine (Aza C) was active in patients with high-ris

88 phase 2 trial comparing injectable and oral azacitidine (AZA) administered over one or three weeks p

89 responses (20% complete remission [CR]) with azacitidine (AZA) alone, short response duration, and a

90 sent study, we report a comparative study of azacitidine (AZA) and decitabine (DAC) in combination wi

91 Although azacitidine (AZA) improves survival in patients with hig

92 Azacitidine (AZA) is a DNA methyltransferase inhibitor w

93 The nucleotide analogue azacitidine (AZA) is currently the best treatment option

94 Azacitidine (AZA) is effective treatment for myelodyspla

95 Azacitidine (AZA) is the current standard of care for hi

96 MDS patients collected before treatment with azacitidine (AZA) or decitabine (DEC).

97 with hypomethylating agent (HMA) therapy and azacitidine (AZA) plus ivosidenib (IVO) specifically for

98 Both lenalidomide (LEN) and azacitidine (AZA) possess significant antitumor activity

99 In vivo, miRisten potentiated the VEN/azacitidine (AZA) regimen, an FDA-approved therapy for o

100 Azacitidine (AZA) up-regulates the expression of tumor A

101 Azacitidine (AZA), a hypomethylating agent used in MDS,

102 Azacitidine (AZA), a mainstay therapeutic agent for stem

103 eated with the methyltransferase inhibitor 5-azacitidine (aza-CR) followed by the histone deacetylase

104 Azacitidine (AzaC) mitigates graft-versus-host disease (

105 hypomethylating agents, decitabine (Dec) and azacitidine (AzaC), induce FOXP3 expression in CD4(+)CD2

106 Combination treatment strategies using an azacitidine backbone are demonstrating promising early r

107 clinical trials of novel targeted therapies, azacitidine-based combination therapeutic strategies, an

108 n Patients with higher-risk MDS treated with azacitidine-based combinations had similar ORR to azacit

109 Whether azacitidine-based combinations with lenalidomide or vori

110 treatment with the DNA-demethylating agent, azacitidine, causes increased mRNA levels in embryonic c

111 This phase 2 study evaluated oral azacitidine (CC-486) plus cyclophosphamide, doxorubicin,

112 y 2023, 107 patients received venetoclax and azacitidine combination at the RP2D.

113 5% CI 61-84) patients in the enasidenib plus azacitidine combination group and 12 (36%; 20-55) patien

114 yeloid leukemia patients to a venetoclax and azacitidine combination in a new clinical trial.

115 cy of the clinically approved venetoclax and azacitidine combination in vitro, in primary cells, and

116 The lenalidomide/azacitidine combination is well-tolerated and highly act

117 nal responses to ivosidenib + venetoclax +/- azacitidine combination therapy across hematopoiesis in

118 ch predicted clinical outcomes of venetoclax-azacitidine combination therapy in patients with AML.

119 ro response to the currently used venetoclax-azacitidine combination.

120 y, tolerability, and preliminary activity of azacitidine combined with venetoclax for treatment-naive

121 the favourable safety profile suggests that azacitidine could add to the treatment options in these

122 US regulatory approval of azacitidine, decitabine, and lenalidomide between 2004 a

123 her-risk MDS, hypomethylating agents such as azacitidine, decitabine, or decitabine/cedazuridine are

124 with a hypomethylating agent (HMA) including azacitidine, decitabine, or oral decitabine/cedazuridine

125 Oral and SC azacitidine decreased DNA methylation in blood, with max

126 Furthermore, treatment of Cdx2 AML with azacitidine decreases leukemic burden.

127 Furthermore, azacitidine did not increase the rate of infection or bl

128 The median treatment-free duration following azacitidine discontinuation was 20.8 months; the longest

129 Lenalidomide and azacitidine each have activity in myelodysplastic syndro

130 ss all ELN risk groups compared with placebo-azacitidine, ELN classification systems poorly discrimin

131 Azacitidine exposure caused major changes in CTCF occupa

132 Azacitidine exposure increased with escalating oral dose

133 ext of gene expression, DNA methylation, and azacitidine exposure.

134 l report a phase 2 study of lenalidomide and azacitidine for higher risk myelodysplastic syndromes (M

135 vestigate the combination of iadademstat and azacitidine for the treatment of adult patients with new

136 positive (MRDpos) during screening received azacitidine for up to 2 years to prevent relapse.

137 nd efficacy of venetoclax with decitabine or azacitidine from a large, multicenter, phase 1b dose-esc

138 ndomly assigned 1:1 to treatment with either azacitidine given at a dose of 300 mg once a day (200 mg

139 ere were two treatment-related deaths in the azacitidine group (one endocarditis and one candidiasis)

140 he 12-month DFS was estimated at 64% for the azacitidine group and 42% for the control group.

141 ween Nov 9, 2018, to Feb 22, 2021; 42 in the azacitidine group and 44 in the ICT group.

142 ival was 5.6 months (95% CI 2.7 -8.1) in the azacitidine group versus 2.8 months (1.9-4.8) in the ICT

143 e reported in 32 (76%) of 42 patients in the azacitidine group versus 42 (98%) of 43 patients in the

144 Eprenetapopt and venetoclax with azacitidine had an acceptable safety profile and encoura

145 The combination of iadademstat and azacitidine has a manageable safety profile and shows pr

146 Bexmarilimab in combination with azacitidine has a manageable safety profile, consistent

147 minary reports suggest that treatment with 5-azacitidine has clinical activity in patients with relap

148 Decitabine (DAC) and 5-azacitidine have recently been approved for the treatmen

149 potent, more specific drugs that behave like azacitidine imperative.

150 Although outcomes with venetoclax-azacitidine improved across all ELN risk groups compared

151 That azacitidine improves survival in patients with high-risk

152 to predict treatment responses to venetoclax-azacitidine in a prospective, multicenter, phase 2 trial

153 1 trial and strong preclinical synergy with azacitidine in acute myeloid leukaemia cell lines.

154 anting further evaluation of magrolimab with azacitidine in AML.

155 rom the recently reported negative trials of azacitidine in combination with eprenetapopt (APR-246),

156 clinical trial data studying entinostat and azacitidine in metastatic breast cancer revealed that in

157 to a phase 1 study combining tagraxofusp and azacitidine in myeloid malignancies.

158 the BCL-2 inhibitor venetoclax combined with azacitidine in older patients, and clinical trials are a

159 ted dose of lenalidomide in combination with azacitidine in patients with acute myeloid leukaemia and

160 re trials of cusatuzumab in combination with azacitidine in patients with previously untreated acute

161 eprenetapopt and venetoclax with or without azacitidine in patients with TP53-mutated acute myeloid

162 efficacy of low-dose decitabine vs low-dose azacitidine in this group of patients.

163 nical trials that combined eprenetapopt with azacitidine in TP53-mutated MDS/AML, we observed complet

164 denib, as monotherapy or in combination with azacitidine, in patients with acute myeloid leukaemia or

165 ted known safety profiles for venetoclax and azacitidine, including constipation (53.3%), nausea (49.

166 epigenetic modifier drugs, panobinostat and azacitidine, increased CD33 expression in some cell line

167 interval 54-71%, P<0.0001) six months after azacitidine initiation with no new safety signals.

168 ematological relapse for >=2 years following azacitidine initiation.

169 ce superior overall response rates (ORRs) to azacitidine is not known.

170 II trial of iadademstat in combination with azacitidine is ongoing (EudraCT No.: 2018-000482-36).

171 Purpose Azacitidine is standard, first-line therapy in higher-ri

172 Although azacitidine is the mainstay of treatment in MDS, only ha

173 mbination of cusatuzumab with venetoclax and azacitidine is underway (NCT04150887).

174 The combination of lenalidomide and azacitidine is well tolerated with encouraging clinical

175 Combination treatment with eprenetapopt and azacitidine is well-tolerated yielding high rates of cli

176 cy in comparison to intermittent higher-dose azacitidine, linked to more specific epigenetic modulati

177 ) assigned to either observation (N = 60) or azacitidine maintenance (N = 56; 50 mg/m(2), subcutaneou

178 We conclude that azacitidine maintenance after CR/CRi after intensive che

179 n the observation group (n = 32) than in the azacitidine maintenance group (n = 9).

180 showed an overall survival benefit with oral azacitidine maintenance.

181 es in older patients treated with venetoclax-azacitidine may be suboptimal.

182 Low-dose decitabine and azacitidine may have broad applicability for cancer mana

183 Overall, 41 patients received SC and oral azacitidine (MDSs, n = 29; CMML, n = 4; AML, n = 8).

184 enty-three patients received ivosidenib plus azacitidine (median age, 76 years; range, 61-88 years).

185 on group and 12 (36%; 20-55) patients in the azacitidine monotherapy group achieved an overall respon

186 tidine-based combinations had similar ORR to azacitidine monotherapy, although patients with CMML ben

187 mproved overall response rates compared with azacitidine monotherapy, suggesting that this regimen ca

188 eated with intensive chemotherapy (n = 9) or azacitidine (n = 11) had an overall response rate of 100

189 as monotherapy (n=32) or in combination with azacitidine (n=46).

190 ts were randomly assigned to enasidenib plus azacitidine (n=68) or azacitidine only (n=33).

191 ss the potential benefit of sabatolimab plus azacitidine on overall survival in this setting.

192 All participants received 75 mg/m(2) azacitidine once a day for days 1-5 for each 28 day cycl

193 ned to enasidenib plus azacitidine (n=68) or azacitidine only (n=33).

194 n the combination group vs five [16%] in the azacitidine-only group), differentiation syndrome (seven

195 ia (25 [37%] of 68 vs six [19%] of 32 in the azacitidine-only group), neutropenia (25 [37%] vs eight

196 mbination group and 14 (44%) patients in the azacitidine-only group; serious treatment-related advers

197 nse system to enasidenib plus azacitidine or azacitidine-only, stratified by acute myeloid leukaemia

198 ctive web response system to enasidenib plus azacitidine or azacitidine-only, stratified by acute mye

199 yndromes with excess blasts after failure of azacitidine or decitabine treatment.

200 -risk MDS to hypomethylating agents, such as azacitidine or decitabine, for patients with higher-risk

201 se events were similar to those reported for azacitidine or eprenetapopt monotherapy, with the most c

202 OR=2.02, 95%CI 1.15-3.56, P=0.02) and use of azacitidine (OR=2.45, 95%CI 1.01-5.90, P=0.05); purine-b

203 val after failure of intensive chemotherapy, azacitidine, or decitabine was more favorable in patient

204 010 with intensive chemotherapy (n = 557) or azacitidine- or decitabine-based therapy (n = 114).

205 In the phase 3 QUAZAR AML-001 trial, oral azacitidine (oral-AZA; formerly CC-486), a hypomethylati

206 tion systems poorly discriminated venetoclax-azacitidine outcomes.

207 The pharmacodynamic effects of DAC and 5-azacitidine outside their known activity as inhibitors o

208 t compared with 16% of patients treated with azacitidine (P = .2).

209 for patients receiving azacitidine, 49% for azacitidine plus lenalidomide ( P = .14 v azacitidine),

210 /m(2)/day on days 1 to 7 of a 28-day cycle); azacitidine plus lenalidomide (10 mg/day on days 1 to 21

211 For patients with CMML, ORR was higher for azacitidine plus lenalidomide versus azacitidine (68% v

212 enters, 92 received azacitidine, 93 received azacitidine plus lenalidomide, and 92 received azacitidi

213 although patients with CMML benefitted from azacitidine plus lenalidomide.

214 evaluate the efficacy and safety of low dose azacitidine plus venetoclax as maintenance therapy in ac

215 Low dose azacitidine plus venetoclax is a feasible maintenance st

216 Azacitidine plus venetoclax is a standard of care for pa

217 domide ( P = .14 v azacitidine), and 27% for azacitidine plus vorinostat ( P = .16 v azacitidine).

218 lenalidomide (10 mg/day on days 1 to 21); or azacitidine plus vorinostat (300 mg twice daily on days

219 acitidine plus lenalidomide, and 92 received azacitidine plus vorinostat.

220 his phase 1 study, we evaluated CC-486 (oral azacitidine) plus 6 cycles of R-CHOP in patients with pr

221 well tolerated in outpatient settings, with azacitidine prolonging survival and decreasing time to a

222 Azacitidine prolongs survival by a median of only 9.5 mo

223 Azacitidine provides important clinical benefits for pat

224 date indicate that cusatuzumab 20 mg/kg plus azacitidine represents the optimal dose for further stud

225 uced viability, and was active in venetoclax-azacitidine-resistant cell lines and primary patient sam

226 ths for patients treated with decitabine and azacitidine, respectively (P = .1).

227 -azacitidine and 65.5% and 75.2% for placebo-azacitidine, respectively).

228 03) for patients treated with decitabine and azacitidine, respectively.

229 ent with the DNA methyltransferase inhibitor azacitidine restored DPH1 expression and tagraxofusp sen

230 Addition of magrolimab to venetoclax and azacitidine resulted in more fatal adverse events (19.0%

231 ment of patients with higher risk MDS with 5-azacitidine results in significant improvement in overal

232 Extended scheduling of low-dose azacitidine shows greater efficacy in comparison to inte

233 Furthermore, treatment with 5-azacitidine significantly mimics these effects, suggesti

234 ents alive and relapse-free six months after azacitidine start.

235 al, poorly absorbable hypomethylating agent, azacitidine; the liposomal formulation of cytarabine and

236 sk myelodysplastic syndromes (MDS) receiving azacitidine therapy.

237 ide clinical benefits in MDS patients during azacitidine therapy.

238 ents with relapsed leukemia, the addition of azacitidine to etoposide and amsacrine did not improve r

239 Preclinical work suggested that addition of azacitidine to ivosidenib enhances mIDH1 inhibition-rela

240 he immune synapse: a pharmacologic approach (azacitidine) to increase antigen density of CD70 in myel

241 ecular signatures differentiating venetoclax-azacitidine-treated patients based on overall survival (

242 mplete remissions were seen in 10% to 17% of azacitidine-treated patients; partial remissions were ra

243 DFS was significantly better for the azacitidine treatment group (logrank; P = .04), as well

244 efficacy and safety of MRD-guided preemptive azacitidine treatment to prevent relapse in the phase 2

245 oses of ABBV-075 coupled with bortezomib and azacitidine treatment, despite the lack of in vitro syne

246 ed in patient samples after eprenetapopt and azacitidine treatment, elucidate the mechanism by which

247 MRDpos, of whom 95 (79.8%) were eligible for azacitidine treatment.

248 utated hematopoietic cells were sensitive to azacitidine treatment.

249 Azacitidine upregulates prophagocytic signals on AML cel

250 usly reported clinical trials (n = 309) with azacitidine using the WHO classification system for MDS

251 tment with the combination of venetoclax and azacitidine (ven/aza) inhibits amino acid metabolism, le

252 Despite widespread use of azacitidine-VEN (AZA-VEN), there is increasing appreciat

253 The combination of azacitidine, venetoclax, and gilteritinib resulted in hi

254 with NPM1m or KMT2Ar AML, the combination of azacitidine, venetoclax, and revumenib was able to be sa

255 d the safety and activity of enasidenib plus azacitidine versus azacitidine alone in patients with ne

256 alysis of the international phase 3 study of azacitidine vs conventional care regimens in older (>/=6

257 for the 27 AML patients randomly assigned to azacitidine was 19.3 months compared with 12.9 months fo

258 Oral azacitidine was bioavailable and demonstrated biologic a

259 ound that the combination of tagraxofusp and azacitidine was effective in patient-derived xenografts

260 The maintenance treatment with azacitidine was feasible.

261 Cross-over to SC azacitidine was permitted for nonresponders who received

262 Magrolimab with azacitidine was relatively well tolerated with promising

263 Combination enasidenib plus azacitidine was well tolerated and significantly improve

264 Magrolimab + azacitidine was well tolerated with promising efficacy i

265 Ivosidenib plus azacitidine was well tolerated, with an expected safety

266 ance therapy with eprenetapopt combined with azacitidine was well tolerated.

267 Olutasidenib, with or without azacitidine, was well tolerated and showed meaningful cl

268 tidine and 113 patients treated with placebo-azacitidine were analyzed.

269 tial Cancer and Leukemia Group B trials with azacitidine were recollected and reanalyzed as part of t

270 e 3 or 4 adverse events with enasidenib plus azacitidine were thrombocytopenia (25 [37%] of 68 vs six

271 tosis of tumor cells and is synergistic with azacitidine, which increases expression of eat-me signal

272 We aimed to compare the oral form of azacitidine with investigator's choice standard therapy

273 pos patients can be effectively treated with azacitidine with potential long-term remission even afte

274 Azacitidine with venetoclax is safe and shows encouragin