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

7 effect that was blocked by the antiandrogen bicalutamide.

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

9 estosterone and inhibitory concentrations of bicalutamide.

10 d estradiol and diminished the antagonism of bicalutamide.

11 ths with enzalutamide versus 5.7 months with bicalutamide.

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

13 er cytoplasmic retention of ARpolyQ bound to Bicalutamide.

14 nizing hormone-releasing hormone agonist and bicalutamide.

15 term treatment of parental LNCaP cells with bicalutamide.

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

17 subjected to androgen ablation therapy with bicalutamide.

18 that renders AR responsive to the antagonist bicalutamide.

19 and enhancer sites to a greater extent than bicalutamide.

20 umors initially refractory to treatment with bicalutamide.

21 lso examined in response to the antiandrogen bicalutamide.

22 ger exhibited gene repression in response to bicalutamide.

23 similar to castration compared with that of bicalutamide.

24 mediated apoptosis induced by rapamycin and bicalutamide.

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

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

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

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

29 90% versus <50%), even at exposure levels of bicalutamide 3-fold greater than what can be attained in

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

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

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

33 Bicalutamide, a nonsteroidal antiandrogen, is widely use

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

35 The sensitivity to bicalutamide after progression on flutamide deserves fur

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

76 Nonetheless, bicalutamide could not stimulate interactions between th

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

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

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

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

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

82 AR transactivation that hydroxyflutamide and bicalutamide failed to block.

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

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

85 ADT consisted of goserelin and bicalutamide for 2 years.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

100 23%) of 189 patients in the enzalutamide and bicalutamide groups, respectively.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

143 24 months of antiandrogen therapy with daily bicalutamide to salvage radiation therapy resulted in si

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

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

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

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

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

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

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

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

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

153 [11%]); those occurring more frequently with bicalutamide were nausea (26 [14%] vs 33 [17%]), constip

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

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

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

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