ライフサイエンスコーパス: bicalutamide

1 inhibit radioligand binding in comparison to bicalutamide).

2 s (cyproterone acetate, hydroxyflutamide and bicalutamide).

3 ted by treatment with the polyamide and with bicalutamide.

4 as completely resistant to the antiandrogen, bicalutamide.

5 ssed AR and were resistant to treatment with bicalutamide.

6 effect that was blocked by the antiandrogen bicalutamide.

7 R was inhibited by a specific AR antagonist, bicalutamide.

8 estosterone and inhibitory concentrations of bicalutamide.

9 d estradiol and diminished the antagonism of bicalutamide.

10 and 86% (95% CI, 60%-96%) among those taking bicalutamide.

11 and sensitized androgen-independent cells to bicalutamide.

12 insensitive to androgen receptor blockade by bicalutamide.

13 y the agonist as well as another antagonist, bicalutamide.

14 Mnk1/2, also sensitized CRPC cells to RAD001+bicalutamide.

15 adiotherapy (sRT) with or without 2 years of bicalutamide.

16 ates were 84% with enzalutamide and 34% with bicalutamide.

17 alutamide, and 35 were randomized to receive bicalutamide.

18 ths with enzalutamide versus 5.7 months with bicalutamide.

19 mly assigned, 184 to enzalutamide and 191 to bicalutamide.

20 er cytoplasmic retention of ARpolyQ bound to Bicalutamide.

21 nizing hormone-releasing hormone agonist and bicalutamide.

22 term treatment of parental LNCaP cells with bicalutamide.

23 rebuild the sensitivity of LNCaP-B cells to bicalutamide.

24 subjected to androgen ablation therapy with bicalutamide.

25 that renders AR responsive to the antagonist bicalutamide.

26 and enhancer sites to a greater extent than bicalutamide.

27 umors initially refractory to treatment with bicalutamide.

28 lso examined in response to the antiandrogen bicalutamide.

29 ger exhibited gene repression in response to bicalutamide.

30 similar to castration compared with that of bicalutamide.

31 mediated apoptosis induced by rapamycin and bicalutamide.

32 e androgen receptor (AR) compared to that of bicalutamide.

33 ly used antiandrogenic prostate cancer drugs bicalutamide (1) and hydroxyflutamide (2) in reporter ge

34 ation therapy with 2 years of placebo versus bicalutamide 150 mg daily.

35 monstrated selective toxicity of combination bicalutamide-(18)F-FDG in AR-positive 22RV1 and MDA-MB-2

36 d several analogs of the potent antiandrogen bicalutamide: [18F]bicalutamide, 4-[76Br]bromobicalutami

37 rogressive prostate cancer were treated with bicalutamide 200 mg daily.

38 90% versus <50%), even at exposure levels of bicalutamide 3-fold greater than what can be attained in

39 f the potent antiandrogen bicalutamide: [18F]bicalutamide, 4-[76Br]bromobicalutamide, and [76Br]bromo

40 g orally twice daily (experimental group) or bicalutamide 50 mg orally daily (control group).

41 to enzalutamide 160 mg per day (n = 198) or bicalutamide 50 mg per day (n = 198).

42 system to receive enzalutamide 160 mg/day or bicalutamide 50 mg/day, both taken orally, in addition t

43 receive oral enzalutamide (160 mg daily) or bicalutamide (50 mg daily) in addition to ADT.

44 l twice daily; experimental arm) or ADT with bicalutamide (50 mg oral once daily; control arm).

45 wice daily (experimental group), or ADT with bicalutamide, 50 mg orally daily (control group), until

46 Bicalutamide, a nonsteroidal antiandrogen, is widely use

47 ranscription and is critical for antagonist (bicalutamide) action.

48 The sensitivity to bicalutamide after progression on flutamide deserves fur

49 To determine whether bicalutamide agonist activity was being suppressed by NC

50 NCaP cells but did not reveal any detectable bicalutamide agonist activity.

51 LAR cell lines were uniquely sensitive to bicalutamide (an AR antagonist).

52 Results: Bicalutamide, an antiandrogen drug, was found to share s

53 tions responded to subsequent treatment with bicalutamide, an AR antagonist that blocks the mutant AR

54 at allows sterically hindered C2-substituted bicalutamide analogues to be obtained.

55 ation of tumor growth through combination of bicalutamide and (18)F-FDG in the AR-positive model in c

56 teinizing hormone-releasing hormone agonist, bicalutamide and bevacizumab or ADT alone, for 6 months.

57 on is not inhibited by nuclear AR antagonist bicalutamide and can be observed in cells that do not ex

58 s reduced by castration or by treatment with bicalutamide and can be quantified through noninvasive b

59 to goserelin combined with dutasteride (ZD), bicalutamide and dutasteride (ZBD), or bicalutamide, dut

60 tolcapone, and their less toxic counterparts bicalutamide and entacapone utilizing ATP assays and ext

61 development of resistance to treatment with bicalutamide and enzalutamide.

62 lly resemble the nonsteroidal AR antagonists bicalutamide and hydroxyflutamide but act as agonists fo

63 and T877A commonly observed and activated by bicalutamide and hydroxyflutamide, respectively, in pros

64 stration of the androgen receptor antagonist bicalutamide and in androgen receptor-negative prostate

65 This mutation confers agonist activity to bicalutamide and is likely involved in bicalutamide with

66 f the currently used anti-androgens, Casodex/bicalutamide and MDV3100/enzalutamide, and the newly dev

67 ese data suggest that the combinatory use of Bicalutamide and trehalose is a novel approach to facili

68 inizing hormone-releasing hormone [LHRH] +/- bicalutamide) and in castrate-resistant men (enzalutamid

69 izing hormone-releasing hormone agonist plus bicalutamide) and peripheral androgen blockade (finaster

70 unds, (R)-16m, when compared to casodex, (R)-bicalutamide, and enzalutamide, displayed very promising

71 riety of antiandrogens, including flutamide, bicalutamide, and megestrol acetate.

72 In contrast to bicalutamide, ARN-509 lacked significant agonist activit

73 uced damage to cells, suggesting the role of bicalutamide as a radiosensitizer to (18)F-FDG-mediated

74 nt W741L AR ligand-binding domain bound to R-bicalutamide at 1.8-A resolution.

75 ve either antiandrogen therapy (24 months of bicalutamide at a dose of 150 mg daily) or daily placebo

76 l, BMS-641988 showed increased efficacy over bicalutamide (average percent tumor growth inhibition >9

77 A comparison of flutamide with bicalutamide awaits maturation of survival data.

78 A series of chiral analogues of bicalutamide bearing electrophilic groups (isothiocyanat

79 s of cholesterol removal from the brain, and bicalutamide (BIC) is a drug of choice for the treatment

80 Bicalutamide (Bic) is frequently used in androgen depriv

81 herefore, cotreatment with an AR antagonist, bicalutamide, blocked the estren-induced increase in PSA

82 Further, the combination of rapamycin and bicalutamide, but not the individual drugs, induced sign

83 ith Akt1 was inhibited by the anti-androgen, bicalutamide, but was not affected by inhibition of phos

84 agonists (including the clinically used drug bicalutamide) can enhance AR recruitment of corepressor

85 econd-line antiandrogen therapies, including bicalutamide (CASODEX((R))) and enzalutamide (XTANDI((R)

86 Using the antiandrogen Bicalutamide (Casodex((R))), which slows down AR activat

87 that produced by the synthetic antiandrogen bicalutamide (Casodex) at the same concentration.

88 microM), in comparison with the antiandrogen bicalutamide (Casodex) in AIPC cells.

89 rting this, treatment with the AR antagonist bicalutamide (Casodex) induced mesenchymal splicing patt

90 The use of the antiandrogen bicalutamide (Casodex) rescued LNCaP cells from 5-alpha-

91 report that antiandrogens, hydroxyflutamide, bicalutamide (casodex), cyproterone acetate, and RU58841

92 ntiandrogens, hydroxyflutamide (Eulexin) and bicalutamide (Casodex), fail to block completely the Adi

93 tion can be blocked by an anti-androgen drug bicalutamide (Casodex), implicating the involvement of a

94 tiandrogens, hydroxyflutamide (Eulexin), and bicalutamide (casodex), that are widely used for the tre

95 d by AR-specific siRNA or androgen inhibitor bicalutamide (Casodex).

96 tion, while flutamide, hydroxyflutamide, and bicalutamide caused only partial disruption of the compl

97 ic hormone-sensitive PCa commencing LHRH +/- bicalutamide (cohort 1) and 7 men with castrate-resistan

98 The anti-androgen bicalutamide completely abolished AR mediated FGF8.luc i

99 Nonetheless, bicalutamide could not stimulate interactions between th

100 ated androgen-independent PCa and found that bicalutamide could stimulate AR nuclear translocation.

101 we observed that the AR antagonist Casodex (bicalutamide) disrupted telomeric complexes in AR-positi

102 ng to androgen response elements and, unlike bicalutamide, does not exhibit agonist properties in the

103 (ZD), bicalutamide and dutasteride (ZBD), or bicalutamide, dutasteride, and ketoconazole (ZBDK) for 3

104 ate cancer is the nonsteroidal antiandrogen, bicalutamide, either as monotherapy or with adjuvant cas

105 an agonist (RU59063) and three antagonists (bicalutamide, enzalutamide and apalutamide) as well as i

106 AR transactivation that hydroxyflutamide and bicalutamide failed to block.

107 Ketoconazole or antiandrogens (eg, bicalutamide, flutamide, nilutamide) may be offered, acc

108 All current antiandrogens, such as Bicalutamide, Flutamide, Nilutamide, and Enzalutamide, t

109 ADT consisted of goserelin and bicalutamide for 2 years.

110 ripheral androgen blockade (finasteride plus bicalutamide) for 12 to 20 months.

111 A variety of regimens, including megestrol, bicalutamide, glucocorticoids, aminoglutethimide, and ke

112 CI 11.5-19.4]) compared with patients in the bicalutamide group (5.8 months [4.8-8.1]; hazard ratio 0

113 leuprolide group and by 6.4% +/- 1.1% in the bicalutamide group (P =.01).

114 de group and increased by 2.5 +/- 0.5 in the bicalutamide group from baseline to 12 months (P <.001).

115 d vasomotor flushing were less common in the bicalutamide group than in the leuprolide group.

116 ness and enlargement were more common in the bicalutamide group than in the leuprolide group.

117 enzalutamide group vs 38 [20%] of 189 in the bicalutamide group), back pain (35 [19%] vs 34 [18%]), a

118 was recorded in 69.7% of the patients in the bicalutamide group, as compared with 10.9% of those in t

119 by means of central review, was 5.8% in the bicalutamide group, as compared with 13.4% in the placeb

120 prostate cancer at 12 years was 14.5% in the bicalutamide group, as compared with 23.0% in the placeb

121 verall survival at 12 years was 76.3% in the bicalutamide group, as compared with 71.3% in the placeb

122 ompared with none of the three deaths in the bicalutamide group.

123 ide group and 16.7 months (10.2-21.9) in the bicalutamide group.

124 23%) of 189 patients in the enzalutamide and bicalutamide groups, respectively.

125 of progression or death by 76% compared with bicalutamide (hazard ratio [HR], 0.24; 95% CI, 0.18 to 0

126 agenesis, comparing bound conformations of R-bicalutamide, hydroxyflutamide, and two previously repor

127 support the use of enzalutamide rather than bicalutamide in patients with asymptomatic or mildly sym

128 the efficacy and safety of enzalutamide with bicalutamide in patients with metastatic castration-resi

129 te cancer progression or death compared with bicalutamide in patients with nonmetastatic or metastati

130 structure demonstrates that the B ring of R-bicalutamide in the W741L mutant is accommodated at the

131 ncy compared with the standard antiandrogen, bicalutamide, in both binding affinity to the AR and inh

132 ociated with improved outcomes compared with bicalutamide, in terms of the rate and duration of PSA r

133 pre-treatment with AR antagonists including bicalutamide increased eIF4E phosphorylation that induce

134 Thus, the combination of rapamycin and bicalutamide induce apoptosis in prostate cancer cells b

135 tor (ARSI), Enzalutamide (MDV-3100, ENZA) or bicalutamide induced autophagy in androgen-dependent and

136 LNCaP-B cells were resistant to bicalutamide-induced cell growth inhibition, and CSE ove

137 The antiandrogen bicalutamide is widely used in the treatment of advanced

138 Taken together, these results indicate that bicalutamide lacks agonist activity and functions as an

139 d antiandrogens such as hydroxyflutamide and bicalutamide, leading to a lower possibility of inducing

140 both the isolated AR NH(2) terminus and the bicalutamide-liganded AR could interact with the SRC-1 g

141 id receptor coactivator (SRC)-1, whereas the bicalutamide-liganded AR did not undergo a detectable NH

142 Moreover, specific DNA binding by the bicalutamide-liganded AR was demonstrated in vivo using

143 The non-steroidal anti-androgen bicalutamide may offer an equivalent progression-free su

144 affinities for all ligands tested except for bicalutamide, mifepristone, DHT, and R1881 in a competit

145 ly in the long-course ADT group), daily oral bicalutamide monotherapy 150 mg, or monthly subcutaneous

146 sing hormone analogue injections, daily oral bicalutamide monotherapy 150 mg, or monthly subcutaneous

147 In men with prostate cancer, bicalutamide monotherapy increases bone mineral density,

148 Less is known about the effects of bicalutamide monotherapy on bone mineral density and bod

149 After progression on bicalutamide monotherapy, one third of patients with and

150 r RAD001 with bicalutamide were effective in bicalutamide-naive CRPC patients, but not in bicalutamid

151 er standard oral non-steroidal antiandrogen (bicalutamide, nilutamide, or flutamide; control group) u

152 y GC score, the estimated absolute effect of bicalutamide on 12-year OS was less when comparing patie

153 eceptor (AR) in these cells by AR antagonist bicalutamide or by anti-AR small interfering RNA, inhibi

154 utopsy of patients treated with flutamide or bicalutamide, or by excision of lymph node metastases fr

155 t AR by eplerenone was inhibited by MDV3100, bicalutamide, or greater concentrations of abiraterone.

156 lassic antiandrogens including enzalutamide, bicalutamide, or hydroxyflutamide, could suppress nAR-ne

157 of 26 patients (65%; 95% CI, 46%-81%) taking bicalutamide (P = .008) (difference, 29%; 95% CI, 5%-50%

158 and 42% (95% CI, 19%-68%) among those taking bicalutamide (P = .009); among non-Black patients, the S

159 man-derived tumor xenograft mouse model that bicalutamide pre-treatment is associated with an increas

160 bicalutamide-naive CRPC patients, but not in bicalutamide-pretreated ones.

161 Despite being less active than (R)-bicalutamide, (R)-16m also displayed marked in vivo anti

162 finity than the clinically used antiandrogen bicalutamide, reduce the efficiency of its nuclear trans

163 Ten compounds, mainly from the bicalutamide-related series, showed a binding affinity s

164 pressors, may be a mechanism contributing to bicalutamide resistance.

165 or corepressor) expression as a mechanism of bicalutamide-resistant androgen-independent PCa.

166 vivo xenograft model and blocked renewal of bicalutamide-resistant sphere-forming cells, indicating

167 We previously showed that resistance to bicalutamide results from activation of mechanistic targ

168 zole and fadrozole, antiprostate cancer drug bicalutamide, sedative dexmedetomidine, and two antifung

169 ression of AR activity with the antiandrogen bicalutamide sensitized androgen-dependent, as well as A

170 These results demonstrate that bicalutamide stimulates the assembly of a transcriptiona

171 Additionally, we demonstrated that R-bicalutamide stimulates transcriptional activation in AR

172 d clinical trial comparing enzalutamide with bicalutamide suggest that enzalutamide is associated wit

173 moter in response to the androgen antagonist bicalutamide, suggesting that Ebp1 directly affected the

174 AR antagonists such as bicalutamide that are currently in use for prostate canc

175 Bicalutamide, the most widely used AR antagonist, is a c

176 24 months of antiandrogen therapy with daily bicalutamide to salvage radiation therapy resulted in si

177 tro studies showed that androgen antagonist, bicalutamide, transiently elevated both Tgfbr2(floxE2/fl

178 This study found nuclear AR expression in bicalutamide-treated androgen-independent PCa and found

179 worse adverse events in the enzalutamide or bicalutamide treatment groups, respectively, were hypert

180 The synthesis of [18F]bicalutamide utilized a pseudocarrier approach to effect

181 izing hormone-releasing hormone agonist with bicalutamide versus AD alone.

182 tingly, the combinatory use of trehalose and Bicalutamide was also efficient in the removal of insolu

183 our previous results for the enantiomers of bicalutamide, we found that all (R)-isomers demonstrated

184 mbinations of the mTOR inhibitor RAD001 with bicalutamide were effective in bicalutamide-naive CRPC p

185 more frequently with enzalutamide than with bicalutamide were fatigue (51 [28%] of 183 patients in t

186 [11%]); those occurring more frequently with bicalutamide were nausea (26 [14%] vs 33 [17%]), constip

187 After chemotherapy, goserelin acetate and bicalutamide were prescribed for 15 months.

188 /d) of eIF4E-sensitized CRPC cells to RAD001+bicalutamide, whereas eIF4E overexpression induced resis

189 Knowledge of the binding mechanism for R-bicalutamide will provide molecular rationale for the de

190 d the efficacy of enzalutamide compared with bicalutamide, with planned subset analysis of Black pati

191 ty to bicalutamide and is likely involved in bicalutamide withdrawal syndrome.