ライフサイエンスコーパス: exemestane

1 romatase inhibitors (anastrozole, letrozole, exemestane).

2 (100 mg palbociclib, 5 mg everolimus, 25 mg exemestane).

3 s no better than either fulvestrant alone or exemestane.

4 nt plus placebo, and 29 in those assigned to exemestane.

5 nd 3.4 months (3.0-4.6) in those assigned to exemestane.

6 231 to fulvestrant plus placebo, and 249 to exemestane.

7 values better than 1 nM, exceeding that for exemestane.

8 Only seven women were treated with exemestane.

9 e therapy after 2 to 3 years of tamoxifen to exemestane.

10 ch tumors may derive additional benefit from exemestane.

11 7 phase III trial comparing anastrozole with exemestane.

12 44% in the placebo group elected to receive exemestane.

13 mpared with a 7% increase from baseline with exemestane.

14 associated with either adjuvant tamoxifen or exemestane.

15 evaluated 2 alternative dosing schedules of exemestane.

16 (HR) of 0.81 (95% CI, 0.72 to 0.92) favored exemestane.

17 as wild type from addition of everolimus to exemestane.

18 ombination with the aromatase inhibitor (AI) exemestane.

19 lvestrant (0.44; 0.28-0.70), everolimus plus exemestane (0.42; 0.28-0.67), and, in patients with a PI

20 ose assigned to fulvestrant plus placebo and exemestane (0.95, 0.79-1.14; log-rank p=0.56).

21 e, 222 were reported as intercurrent deaths (exemestane, 107; tamoxifen, 115).

22 of -2.0 or more were accrued (147 allocated exemestane, 153 anastrozole); and 197 patients with base

23 ere detected after 8 hours of treatment with exemestane (200 nmol/L).

24 Participants were randomly assigned to exemestane 25 mg by mouth once daily and entinostat (EE)

25 romatase inhibitor were randomly assigned to exemestane 25 mg daily plus entinostat 5 mg once per wee

26 e 1, patients received everolimus 10 mg plus exemestane 25 mg daily, with 10 mL of alcohol-free dexam

27 sive breast cancer were randomly assigned to exemestane 25 mg versus anastrozole 1 mg, daily.

28 e oral tamoxifen 20 mg/day or switch to oral exemestane 25 mg/day to complete a total of 5 years of a

29 g on days 15, 29, and every 28 days) or oral exemestane (25 mg once daily) on a 28-day cycle.

30 : Patients were randomized to treatment with exemestane (25 mg oral daily) together with everolimus (

31 , raloxifene (60 mg per day for 5 years) and exemestane (25 mg per day for 5 years) should also be di

32 60 postmenopausal women randomly assigned to exemestane (25 mg per day) compared with placebo in the

33 s anastrozole-matched placebo; or daily oral exemestane (25 mg).

34 moxifen were randomly assigned to 5 years of exemestane (25 mg/d orally) or 5 years of placebo.

35 cludes anastrozole (1 mg/day) in addition to exemestane (25 mg/day), raloxifene (60 mg/day), or tamox

36 In this randomized clinical trial, exemestane, 25 mg, given 3 times weekly in compliant pat

37 Exemestane, 25 mg, once daily, 3 times weekly, or once w

38 In all, 930 BCFS events have been reported (exemestane, 423; tamoxifen, 507), giving an unadjusted h

39 disease-free survival had been reported (354 exemestane, 455 tamoxifen); unadjusted hazard ratio 0.76

40 Exemestane (6-methyleneandrosta-1,4-diene-3,17-dione) is

41 Aromatase inhibitors (AIs) such as exemestane, 6-methylideneandrosta-1,4-diene-3,17-dione,

42 ith baseline T-scores of less than -2.0 (101 exemestane, 96 anastrozole).

43 er two monthly treatments with goserelin and exemestane, a sensitive assay for serum estradiol was ch

44 Exemestane, a steroidal aromatase inhibitor, reduced inv

45 We postulated that exemestane-a mildly androgenic steroid-might have a less

46 76 (95% CI 0.66-0.88, p=0.0001) in favour of exemestane, absolute benefit 3.3% (95% CI 1.6-4.9) by en

47 exemestane and 2.8 months with placebo plus exemestane, according to assessments by local investigat

48 ficacy of this panel in the Tamoxifen versus Exemestane Adjuvant Multicenter (TEAM) trial.

49 The Tamoxifen and Exemestane Adjuvant Multinational (TEAM) trial included

50 r 5 years of median follow-up, the Tamoxifen Exemestane Adjuvant Multinational (TEAM) trial reported

51 participating in the international Tamoxifen Exemestane Adjuvant Multinational (TEAM) trial.

52 766 patients enrolled in the TEAM (Tamoxifen Exemestane Adjuvant Multinational) randomized clinical t

53 ree survival noted in patients who switch to exemestane after 2-3 years on tamoxifen persist after tr

54 romatase inhibitors may allow treatment with exemestane after a nonsteroidal aromatase inhibitor and

55 findings of the TEAM trial confirm that both exemestane alone and sequential treatment with tamoxifen

56 th the aromatase inhibitor exemestane versus exemestane alone.

57 Exemestane also inhibits the inflammatory increases in i

58 rcinoma in situ) breast cancers was 0.35% on exemestane and 0.77% on placebo (hazard ratio, 0.47; 95%

59 survival was 6.9 months with everolimus plus exemestane and 2.8 months with placebo plus exemestane,

60 ed; 72% in the exemestane group continued on exemestane and 44% in the placebo group elected to recei

61 llow-up of 4.1 years, 4-year EFS was 91% for exemestane and 91.2% for anastrozole (stratified hazard

62 [n = 17 806]), and the aromatase inhibitors exemestane and anastrozole (RR, 0.45 [95% CI, 0.26-0.70]

63 ars did not differ significantly between the exemestane and anastrozole treatment groups (2.11%, 95%

64 parallel set of spectroscopic studies using exemestane and anastrozole.

65 received at least one dose of everolimus and exemestane and at least one confirmed dose of dexamethas

66 matitis in patients receiving everolimus and exemestane and could be a new standard of oral care for

67 The combination of exemestane and entinostat did not improve survival in AI

68 breast cancers were detected in those given exemestane and in 32 of those given placebo, with a 65%

69 ibitor constant for the aromatase inhibitors exemestane and letrozole.

70 differ significantly between patients taking exemestane and patients taking anastrozole (-0.92%, 95%

71 and total hip between patients treated with exemestane and patients treated with anastrozole.

72 core predicts DRFS for patients treated with exemestane and patients treated with tamoxifen followed

73 we compared everolimus and exemestane versus exemestane and placebo (randomly assigned in a 2:1 ratio

74 Remarkably, combinations of exemestane and sulforaphane act highly synergistically,

75 onths, 162 (7%) and 115 (5%) patients in the exemestane and tamoxifen groups, respectively, had fract

76 exemestane; the absolute difference (between exemestane and tamoxifen) at 10 years in the population

77 responded to an absolute difference (between exemestane and tamoxifen) at 10 years of 4.0% (95% CI, 1

78 xifen, raloxifene, arzoxifene, lasofoxifene, exemestane, and anastrozole.

79 uential treatment with tamoxifen followed by exemestane are reasonable options as adjuvant endocrine

80 itors, including letrozole, anastrozole, and exemestane, are being incorporated into trials evaluatin

81 Overall, slightly more women in the exemestane arm (32%) than in the placebo arm (28%) disco

82 l (letrozole and anastrozole) and steroidal (exemestane) aromatase inhibitors may allow treatment wit

83 o evaluate the steroidal aromatase inhibitor exemestane as extended adjuvant therapy in this setting.

84 With 30 months of median follow-up, original exemestane assignment resulted in a borderline statistic

85 substantial proportion of patients, original exemestane assignment resulted in non-statistically sign

86 of AI treatment (anastrozole, letrozole, or exemestane), between August 1999 and June 2010 were retr

87 Within 6 months of switching to exemestane, BMD was lowered by 0.051 g/cm(3) (2.7%; 95%

88 s were aware of assignment to fulvestrant or exemestane, but not of assignment to anastrozole or plac

89 Despite premature closure and crossover to exemestane by a substantial proportion of patients, orig

90 The protective effect of switching to exemestane compared with continuing on tamoxifen on risk

91 s channel unoccupied in the enzyme-substrate/exemestane complexes.

92 Tucidinostat plus exemestane could represent a new treatment option for th

93 ents in both groups also received 25 mg oral exemestane daily.

94 d, placebo-controlled, double-blind trial of exemestane designed to detect a 65% relative reduction i

95 We have found that exemestane, different from letrozole and anastrozole, ca

96 Exemestane (EXE) is an aromatase inhibitor used to treat

97 ral tamoxifen (20 mg once a day) followed by exemestane for a total duration of 5 years.

98 ired for MCF-7Ca cells, whereas anastrozole, exemestane, formestane, and tamoxifen were ineffective a

99 6i, participants switched ET (fulvestrant or exemestane) from ET used pre-random assignment and rando

100 Exemestane given for prevention has limited negative imp

101 f random assignment of treatment (19% of the exemestane group and 13% of the placebo group).

102 ed with 508 (22.1%) of 2,294 patients in the exemestane group and 603 (26.2%) of 2,305 patients in th

103 l at 10 years was 67% (95% CI 65-69) for the exemestane group and 67% (65-69) for the sequential grou

104 Adverse events occurred in 88% of the exemestane group and 85% of the placebo group (P=0.003),

105 follow-up, 921 (30%) of 3075 patients in the exemestane group and 929 (31%) of 3045 patients in the s

106 222 deaths occurred in the exemestane group compared with 261 deaths in the tamoxif

107 ients had been randomly assigned; 72% in the exemestane group continued on exemestane and 44% in the

108 ts were more common in the tucidinostat plus exemestane group than in the placebo plus exemestane gro

109 val was demonstrated, with 352 deaths in the exemestane group versus 405 deaths in the tamoxifen grou

110 s were stomatitis (8% in the everolimus-plus-exemestane group vs. 1% in the placebo-plus-exemestane g

111 -exemestane group vs. 1% in the placebo-plus-exemestane group), anemia (6% vs. <1%), dyspnea (4% vs.

112 us exemestane group than in the placebo plus exemestane group.

113 Exemestane had small negative effects on women's self-re

114 with baseline T-score of -2.0 or more taking exemestane had two fragility fractures and two other fra

115 Thus, exemestane has a wide range of previously unrecognized p

116 hibitors such as letrozole, anastrozole, and exemestane have proven to be effective endocrine regimen

117 Assignment to exemestane, having a smoking history, and current employ

118 tly shorter in patients randomly assigned to exemestane (hazard ratio [HR], 1.5; 95% CI, 1.1 to 2.1;

119 hat the on-treatment benefit of switching to exemestane (HR, 0.60; 95% CI, 0.48 to 0.75; P < .001) wa

120 95% CI, 1.11-1.89; P = .006; everolimus plus exemestane: HR, 1.38; 95% CI, 1.06-1.78; P = .02; ET onl

121 Tucidinostat plus exemestane improved progression-free survival compared w

122 The Society includes the aromatase inhibitor exemestane in addition to tamoxifen and raloxifene as a

123 at to the steroidal aromatase inhibitor (AI) exemestane in advanced hormone receptor (HR)-positive, h

124 east cancer patients treated with everolimus-exemestane in first and subsequent lines.

125 ree survival (PFS) when adding everolimus to exemestane in patients with advanced breast cancer exper

126 ion-free survival compared with placebo plus exemestane in patients with advanced, hormone receptor-p

127 a sequential scheme of tamoxifen followed by exemestane in postmenopausal patients with early-stage,

128 (95% CI, 0.71 to 0.92; P = .001) in favor of exemestane in the ER-positive/ER unknown group.

129 versus standard of care (SOC: fulvestrant or exemestane) in patients with ESR1 mutations (ESR1m) and

130 mplying estrogen receptor (ER) dependence of exemestane-induced AREG expression.

131 Furthermore, exemestane-induced aromatase degradation can be complete

132 hanism that underlies exemestane resistance: exemestane induces AREG in an ER-dependent manner.

133 Exemestane induces aromatase degradation in a dose-respo

134 Because exemestane interacts with Asp(309) based on its co-cryst

135 patients treated with tamoxifen followed by exemestane irrespective of nodal status and chemotherapy

136 Exemestane is an active and well-tolerated third-line ho

137 A striking feature of the structure of exemestane is an extended system of conjugated Michael r

138 Entinostat added to exemestane is generally well tolerated and demonstrated

139 reast cancer prevention medication, although exemestane is not FDA approved for this indication.

140 The steroidal inhibitor exemestane is partially non-cross-resistant with nonster

141 One of these candidates, exemestane, is already FDA-approved and may thus be a pr

142 rant plus placebo; eight in that assigned to exemestane), lethargy (three; 11; 11), and nausea or vom

143 nced breast cancer have examined the role of exemestane, letrozole, anastrozole, and fulvestrant in p

144 (block sizes 4-8) to either 5 years of oral exemestane monotherapy (25 mg once a day) or a sequentia

145 difference in disease-free survival between exemestane monotherapy and a sequential scheme of tamoxi

146 er taking fulvestrant (n = 45) compared with exemestane (n = 18; hazard ratio [HR], 0.52; 95% CI, 0.3

147 moxifen, were randomly assigned to switch to exemestane (n=2352) or to continue tamoxifen (n=2372) fo

148 One hundred sixteen patients (exemestane, n = 86; tamoxifen, n = 30; median age, 44 ye

149 The switch from tamoxifen to exemestane neither increased nor decreased endocrine sym

150 significantly improved for patients assigned exemestane + OFS over tamoxifen + OFS.

151 After a median follow-up of 9 years, exemestane + OFS significantly improved disease-free sur

152 improvement in 12-year overall survival with exemestane + OFS was 2.0% (HR, 0.85; 95% CI, 0.70 to 1.0

153 ions of the risk of recurrence with adjuvant exemestane + OFS, compared with tamoxifen + OFS, provide

154 We also examined the effect of exemestane on aromatase mRNA level using real-time rever

155 The effect of exemestane on serum levels of estrogens and other steroi

156 serum estradiol was -89%, -85%, and -60% for exemestane once daily (n = 55), 3 times weekly (n = 56),

157 d baseline T-scores of less than -2.0 taking exemestane, one had a fragility fracture and four had ot

158 ne of two adjuvant oral aromatase inhibitors-exemestane or anastrozole.

159 ts were randomised 1 : 1 to palbociclib plus exemestane or capecitabine.

160 andomly assigned to switch from tamoxifen to exemestane or continue with tamoxifen until 5 years of t

161 Regardless of receiving exemestane or not, experiencing a worsening in any MENQO

162 re was 2.3% were randomly assigned to either exemestane or placebo.

163 compared tamoxifen-alone vs OFS with either exemestane or tamoxifen, indicating premenopausal patien

164 to neoadjuvant AI therapy with anastrozole, exemestane, or letrozole.

165 Clinicians should not prescribe anastrozole, exemestane, or raloxifene for breast cancer risk reducti

166 reast cancer randomly assigned to 5 years of exemestane + ovarian function suppression (OFS) versus t

167 freedom from breast cancer was 85.7% in the exemestane-ovarian suppression group (hazard ratio for r

168 re reported for 30.6% of the patients in the exemestane-ovarian suppression group and 29.4% of those

169 se-free survival at 5 years was 91.1% in the exemestane-ovarian suppression group and 87.3% in the ta

170 he two groups (hazard ratio for death in the exemestane-ovarian suppression group, 1.14; 95% CI, 0.86

171 om breast cancer at 5 years was 92.8% in the exemestane-ovarian suppression group, as compared with 8

172 sults indicate that the clinical benefits of exemestane over tamoxifen are achieved without significa

173 reased at all time points in women receiving exemestane (p<0.001).

174 t grade 3-4 toxicities with palbociclib plus exemestane, palbociclib plus fulvestrant and capecitabin

175 domized, placebo-controlled trial evaluating exemestane, participants completed the Menopause-Specifi

176 samples from the Exemestane Versus Tamoxifen-Exemestane pathology study.

177 Exemestane patients reported more bone/muscle aches (P <

178 se Ib/IIa, open-label trial (NCT02871791) of exemestane plus everolimus and palbociclib for CDK4/6i-r

179 tries with MBC to exemestane plus placebo or exemestane plus everolimus.

180 OFS (95% CI, 64.0% to 84.4%), and 83.2% with exemestane plus OFS (95% CI, 72.7% to 90.0%).

181 H/I)-high tumors did not benefit from either exemestane plus OFS (absolute benefit, -0.4%; HR, 1.03 [

182 -year absolute benefit in BCFI of 11.6% from exemestane plus OFS (hazard ratio [HR], 0.48 [95% CI, 0.

183 9.0% with tamoxifen plus OFS, and 89.4% with exemestane plus OFS at 12 years.

184 t chemotherapy and were randomly assigned to exemestane plus OFS or tamoxifen plus OFS.

185 unmasked adjuvant treatment with 5 years of exemestane plus OFS or tamoxifen plus OFS.

186 ere is no strong indication to favour either exemestane plus OFS or tamoxifen plus OFS.

187 om distant recurrence, and improvements with exemestane plus OFS ranged from 1% to 4%.

188 Patients on exemestane plus OFS reported more vaginal dryness, great

189 rticularly in the short term, in patients on exemestane plus OFS than patients on tamoxifen plus OFS.

190 mprovement of 10% to 15% in 5-year BCFI with exemestane plus OFS versus tamoxifen alone.

191 ad an average 5.2% absolute improvement with exemestane plus OFS versus tamoxifen and reached 10% acr

192 For TEXT patients, the benefit of exemestane plus OFS versus tamoxifen plus OFS in 5-year

193 apy had an average absolute improvement with exemestane plus OFS versus tamoxifen plus OFS of 5.1%, a

194 8-year freedom from distant recurrence with exemestane plus OFS versus tamoxifen plus OFS or tamoxif

195 mprovement of 5% or more in 5-year BCFI with exemestane plus OFS versus tamoxifen plus OFS or tamoxif

196 n tamoxifen plus OFS versus tamoxifen alone; exemestane plus OFS versus tamoxifen was a secondary obj

197 roup analyses consistently showed benefit of exemestane plus OFS vs tamoxifen plus OFS for BCI (H/I)-

198 clearly predict greater benefit of adjuvant exemestane plus OFS vs tamoxifen plus OFS for women with

199 -year BCFI (HR, 0.61; 95% CI, 0.44-0.85) for exemestane plus OFS vs tamoxifen plus OFS, while those w

200 t cancer randomized to tamoxifen plus OFS or exemestane plus OFS who had BCI assessed were included.

201 s and sweats over 5 years than were those on exemestane plus OFS, although these symptoms improved.

202 1.1% with tamoxifen plus OFS, and 84.4% with exemestane plus OFS.

203 24.5 years of adjuvant tamoxifen plus OFS or exemestane plus OFS.

204 6.1% with tamoxifen plus OFS, and 79.0% with exemestane plus OFS.

205 OFS and 81.6% (95% CI, 69.8% to 89.2%) with exemestane plus OFS.

206 vant tamoxifen alone, tamoxifen plus OFS, or exemestane plus OFS.

207 plus ovarian function suppression (OFS), or exemestane plus OFS.

208 gnificant disease-free survival benefit with exemestane plus ovarian function suppression (OFS) compa

209 positive breast cancer treated with adjuvant exemestane plus ovarian function suppression (OFS) or ta

210 one receptor-positive breast cancer, testing exemestane plus ovarian function suppression (OFS), tamo

211 rly breast cancer to the aromatase inhibitor exemestane plus ovarian suppression or tamoxifen plus ov

212 early breast cancer, adjuvant treatment with exemestane plus ovarian suppression, as compared with ta

213 ifen, tamoxifen plus ovarian suppression, or exemestane plus ovarian suppression.

214 Further improvement was seen with the use of exemestane plus ovarian suppression.

215 y plus entinostat 5 mg once per week (EE) or exemestane plus placebo (EP).

216 from 189 centers in 24 countries with MBC to exemestane plus placebo or exemestane plus everolimus.

217 During the first year, most patients on exemestane plus triptorelin had E2 levels below the defi

218 ression method and were randomly assigned to exemestane plus triptorelin or tamoxifen plus triptoreli

219 Among patients on exemestane plus triptorelin, 25%, 24%, and 17% had an E2

220 With exemestane plus triptorelin, median reductions from base

221 g/mL at any time point during treatment with exemestane plus triptorelin.

222 cer, adjuvant OFS combined with tamoxifen or exemestane produces large improvements in BCFI compared

223 Our primary aim was to test whether exemestane prolongs disease-free survival (DFS).

224 propose a possible mechanism that underlies exemestane resistance: exemestane induces AREG in an ER-

225 Exemestane-resistant breast cancer cell lines (i.e., Exe

226 Exemestane should be considered another option as up-fro

227 ide guidance for selecting patients for whom exemestane should be preferred over tamoxifen in the set

228 study, the combination of tucidinostat with exemestane showed preliminary signs of encouraging anti-

229 Exemestane significantly reduced invasive breast cancers

230 of parental MCF-7aro cells with 1 micromol/L exemestane strongly induced the expression of AREG.

231 subgroup of women included in the Intergroup Exemestane Study (IES), a large randomised trial that co

232 Intergroup Exemestane Study (IES), an investigator-led study in 4,7

233 Conclusion The Intergroup Exemestane Study and contemporaneous studies have establ

234 Purpose The Intergroup Exemestane Study, an investigator-led study of 4,724 pos

235 rozole (T+LET R), anastrozole (T+ANA R), and exemestane (T+EXE R), as well as long-term estrogen depr

236 ranslational design within the Tamoxifen and Exemestane (TEXT) and SOFT trials.

237 hat led to discontinuation of everolimus and exemestane (the most common were rash, hyperglycaemia, a

238 In the presence of 200 nmol/L exemestane, the t(1/2) of aromatase was reduced to 12.5

239 mprovement in overall survival was seen with exemestane; the absolute difference (between exemestane

240 moxifen were switched after 2.5-3.0 years to exemestane therapy for a total duration of 5.0 years of

241 l care for patients receiving everolimus and exemestane therapy.

242 assigned to continue tamoxifen or switch to exemestane to complete 5 years of adjuvant endocrine the

243 assigned to continue tamoxifen or switch to exemestane to complete a total of 5 years of adjuvant en

244 accrual to B-33, unblinding, and offering of exemestane to patients in the placebo group.

245 nhibitor everolimus may be administered with exemestane to postmenopausal women with MBC whose diseas

246 We show here that exemestane transcriptionally activates NAD(P)H:quinone o

247 We hypothesized that MA.27 anastrozole- or exemestane-treated patients with new or worsening vasomo

248 rols from the BOLERO-2 trial (everolimus and exemestane treatment in patients with hormone receptor-p

249 The impact of exemestane treatment on tumor-related signs and symptoms

250 We have found that exemestane treatment significantly reduces aromatase pro

251 In MA.27, anastrozole or exemestane treatment-emergent symptoms were not associat

252 rian Function Trial (SOFT) and Tamoxifen and Exemestane Trial (TEXT).

253 rian Function Trial (SOFT) and Tamoxifen and Exemestane Trial (TEXT).

254 The Tamoxifen and Exemestane Trial (TEXT)/Suppression of Ovarian Function

255 The TEXT (Tamoxifen and Exemestane Trial) and SOFT (Suppression of Ovarian Funct

256 nostat combined with the aromatase inhibitor exemestane versus exemestane alone.

257 randomized trial, we compared everolimus and exemestane versus exemestane and placebo (randomly assig

258 nt-by-marker effect for PgR was observed for exemestane versus tamoxifen (PgR-rich hazard ratio [HR],

259 Preferential exemestane versus tamoxifen treatment benefit was not pr

260 -fixed paraffin-embedded BC samples from the Exemestane Versus Tamoxifen-Exemestane pathology study.

261 R-positive) early breast cancer treated with exemestane versus tamoxifen.

262 Exemestane was administered at a dose of 25 mg/d orally

263 e therapy after 2 to 3 years of tamoxifen to exemestane was associated with clinically relevant impro

264 At 12 months, exemestane was associated with fewer hot flashes and les

265 During a median follow-up period of 3 years, exemestane was associated with no serious toxic effects

266 s) letrozole, anastrozole, and the steroidal exemestane were approved in the U.S. in the late 1990s f

267 The efficacy and safety of exemestane were clinically and radiographically evaluate

268 d hypercholesterolemia were less frequent on exemestane, whereas mild liver function abnormalities an

269 y a small excess number of women being given exemestane with clinically important worsening of QOL at

270 switch to the steroidal aromatase inhibitor exemestane with continuation of tamoxifen in the adjuvan

271 h or Without Arimidex) trial, which compared exemestane with fulvestrant-containing regimens in patie

272 sma from the SoFEA (Study of Faslodex Versus Exemestane With or Without Arimidex) trial, which compar