ライフサイエンスコーパス: flutamide

1 n reversed the anti-proliferative effects of flutamide.

2 these mutant ARs were strongly stimulated by flutamide.

3 he greater rates of diarrhea and anemia with flutamide.

4 ascular or thromboembolic complications than flutamide.

5 Forty-eight patients received DES and 44 flutamide.

6 e AhR-dependent growth inhibitory effects of flutamide.

7 on therapy (ADT) comprised of leuprolide and flutamide.

8 ve mutant pAd-S(T34A), and then treated with Flutamide.

9 ctional effect of Survivin on sensitivity to Flutamide.

10 f casodex but remarkably superior to that of flutamide.

11 e abrogated by ovariectomy or treatment with flutamide.

12 the presence or absence of the AR antagonist flutamide.

13 ter 3 months of treatment with goserelin and flutamide.

14 ut not in the presence of the anti-androgen, flutamide.

15 evented by the androgen receptor antagonist, flutamide.

16 placebo, toremifene was more effective than flutamide.

17 ere pre-treated with the androgen antagonist flutamide (15 mg/kg sc) or ethanol (0.25 ml) and infused

18 atment with compounds associated with iDILI; flutamide, 2-hydroxyflutamide, and tolcapone, and their

19 ed increased susceptibility to inhibition by flutamide, 2-hydroxyflutamide, and tolcapone, via effect

20 Flutamide (25 mg/kg body weight, sc) was administered at

21 Additionally, all patients received flutamide 250 mg orally three times daily, initiated on

22 sisted of goserelin 3.6 mg every 4 weeks and flutamide 250 mg tid for 2 months before and concurrent

23 with improvement for mild hirsutism, as has flutamide (250 mg) twice daily and spironolactone for mo

24 7 months, P = .016) and longer survival than flutamide (43.2 v 28.5 months, P = .040).

25 overall response rate was similar (DES, 62%; flutamide, 50%).

26 blasts (hGF), and to evaluate the effects of flutamide (a common anti-androgen) in this system.

27 he cellular accumulation of the antiandrogen flutamide, a drug commonly used in the treatment of pros

28 sing 2-deoxy-D-glucose/sodium azide restored flutamide accumulation to that of parental cells while i

29 Moreover, the salutary effects of flutamide administration appear to be mediated at least

30 Although studies have demonstrated that flutamide administration following T-H improves hepatic

31 ory mediators and hepatic injury produced by flutamide administration following T-H is likely due to

32 182,780 prevented those salutary effects of flutamide administration on pro-inflammatory responses a

33 uced by T-H were significantly attenuated by flutamide administration.

34 Flutamide alone did not induce Fos (VF vs. VE, p>0.05).

35 terone directly effects the skin, as topical flutamide also accelerated barrier recovery in normal ma

36 d ovarian cancer cell lines (SKOV3 and Hey), flutamide also increased miR-449a and miR-449b-5p levels

37 Flutamide altered initial response, increasing latency t

38 study was undertaken to test the efficacy of flutamide (an antiandrogen) in the transgenic adenocarci

39 , TRAMP mice were then treated with placebo, flutamide (an antiandrogen; 33 mg/kg/day), or toremifene

40 Similarly, wild-type male mice treated with flutamide, an androgen antagonist, exhibit reduced renal

41 one to "masculinize" them and males received flutamide, an androgen antagonist, to "feminize" them.

42 Conversely, flutamide, an androgen receptor antagonist, did not affe

43 In wild-type mice, co-treatment with flutamide, an androgen receptor antagonist, prevents not

44 ts undergoing androgen ablation therapy with flutamide and compared their phospho-extracellular signa

45 atients with T2b-T4 prostate cancer received flutamide and goserelin acetate for 4 months, with RT be

46 rate, or VX-710, an MRP1 modulator, restored flutamide and hydroxyflutamide accumulation.

47 In summary, these studies indicate that flutamide and hydroxyflutamide but not dihydrotestostero

48 pressing cells in efflux and accumulation of flutamide and hydroxyflutamide, its active metabolite.

49 Prior exposure to flutamide and response to flutamide withdrawal was also

50 Although both flutamide and toremifene decreased tumor incidence compa

51 anticancer agents such as 5-fluorouracil and flutamide, and is extendable to any drug metabolism stud

52 Clinical studies of nilutamide, flutamide, and ketoconazole have further clarified effic

53 Drug Administration, including leflunomide, flutamide, and nimodipine.

54 ned androgen blockade with the AR antagonist flutamide, and these mutant ARs were strongly stimulated

55 er 9 months of treatment with leuprolide and flutamide, androgen deprivation therapy (ADT) was stoppe

56 e estimated risk of death (hazard ratio) for flutamide as compared with placebo was 0.91 (90 percent

57 teroidal aromatase inhibitor; FemeraTM); (e) Flutamide + ATD (androgen antagonist plus steroidal arom

58 AAD that consisted of leuprolide acetate and flutamide before 3D-CRT.

59 patients received 4 months of goserelin and flutamide before and during RT.

60 d with a variety of antiandrogens, including flutamide, bicalutamide, and megestrol acetate.

61 Two potent anti-androgens, casodex and flutamide, can significantly reduce this activation, con

62 l antiandrogen (bicalutamide, nilutamide, or flutamide; control group) until clinical disease progres

63 dione (ATD) or the androgen receptor blocker flutamide, days 8-14, significantly reduced the expressi

64 Conversely, treatment with Flutamide decreased Survivin expression in LNCaP cells.

65 itivity to bicalutamide after progression on flutamide deserves further study.

66 by castration or by treatment with systemic flutamide) displayed significantly faster barrier recove

67 ve late-stage drug fragment couplings (e.g., flutamide-duloxetine).

68 The absence of flutamide effects on T-induced Fos in the steroid-sensit

69 f pregnant rats with the androgen antagonist flutamide eliminates the gender difference in barrier fo

70 tration of the androgen receptor antagonist, flutamide, equalizes developmental rates in male and fem

71 ncentration of 13.7 mug/L, equal to 71.4 mug flutamide equivalents per liter (FEq/L) in the nonconcen

72 n = 10/group): androgen receptor antagonist (flutamide); estrogen receptor antagonist (fulvestrant);

73 ands with anti-cancer effects and discovered flutamide (Eulexin) as a putative AhR ligand.

74 Dihydrotestosterone (DHT), an agonist, and flutamide (FLT), an antagonist, were administered to Han

75 imultaneous determination of anticancer drug Flutamide (FLU) and antibiotic drug Nitrofurantoin (NF)

76 ed on the crystal structure determination of flutamide, flufenamic acid, and cocaine, where we reduce

77 trated on the crystal structures of cocaine, flutamide, flufenamic acid, the K salt of penicillin G,

78 e flutamide group (6.6 mg/kg); (b) high-dose flutamide group (33 mg/kg); and (c) control placebo grou

79 slow-release flutamide pellets: (a) low-dose flutamide group (6.6 mg/kg); (b) high-dose flutamide gro

80 the trial, 700 were randomly assigned to the flutamide group and 687 to the placebo group.

81 The low-dose flutamide group did not differ significantly from the pl

82 als had tumors was 33 weeks in the high-dose flutamide group, 24.5 weeks in the low-dose flutamide gr

83 flutamide group, 24.5 weeks in the low-dose flutamide group, and 24.5 weeks in the placebo group.

84 In the high-dose flutamide group, however, tumors did not appear until 24

85 difference between the placebo and high-dose flutamide groups was statistically significant (log rank

86 Flutamide had more moderate effects on microglia morphol

87 the effect of DHT, whereas the AR antagonist flutamide had no effect.

88 the competitive androgen receptor antagonist flutamide had significantly less severe hepatitis as det

89 Flutamide had the ability to suppress T antigen-driven c

90 The antiandrogen flutamide, however, had no discernible impact on cortica

91 iated AR-D11FxxLF peptide interaction, while flutamide, hydroxyflutamide, and bicalutamide caused onl

92 rowth factor-beta1 (TGF-beta1) is induced by flutamide in an AhR-dependent manner.

93 However, the effectiveness of flutamide in conjunction with other agents compared with

94 ted the AhR-dependent mechanism of action of flutamide in human hepatocellular carcinoma cells and id

95 e syringeal measures, but the only effect of flutamide in males was to decrease syrinx weight.

96 in via IGF-1 signaling confers resistance to Flutamide in prostate cancer cells.

97 The role of flutamide in this treatment regimen may need to be reeva

98 nted the potent androgen receptor antagonist flutamide in two key brain regions that control birdsong

99 ppears to enhance the therapeutic effects of Flutamide in vitro and in vivo, revealing a novel strate

100 in patients who had previously progressed on flutamide, independent of the response to flutamide with

101 this hormone-induced switch of expression by flutamide indicated a role of androgen in utilization of

102 eversed by the androgen receptor antagonist, flutamide, indicating that the regulatory effects of T4

103 We found that flutamide inhibited the growth of several cancer cell li

104 Finally, the androgen receptor antagonist flutamide inhibited the increase in neuronal damage and

105 f AR; it was otherwise androgen independent, flutamide insensitive and tolerant to disruption of AR d

106 Flutamide is a novel antiandrogen with fewer side effect

107 Flutamide is an androgen receptor (AR) antagonist approv

108 Therefore, flutamide may be effective in AhR-positive cancers that

109 nisms by which anti-androgen agents, such as flutamide, may prevent ovarian cancer and their efficacy

110 y AR and further suppresses the antiandrogen flutamide-mediated inhibition of AR activity.

111 conazole or antiandrogens (eg, bicalutamide, flutamide, nilutamide) may be offered, accompanied by di

112 current antiandrogens, such as Bicalutamide, Flutamide, Nilutamide, and Enzalutamide, target the buri

113 on these 3 sample cohorts and observed that flutamide normalized miRNA levels in HR tissues, notably

114 was initiated by investigating the impact of flutamide on miRNA expression in women at high risk (HR)

115 uggests a novel dual-inhibitory mechanism of flutamide on the AR pathway (AR expression suppression i

116 ed by rapid autopsy of patients treated with flutamide or bicalutamide, or by excision of lymph node

117 atment with bilateral orchiectomy and either flutamide or placebo.

118 in 33.3% of patients on DES and in 17.6% on flutamide (P = .051).

119 e received s.c. implantation of slow-release flutamide pellets: (a) low-dose flutamide group (6.6 mg/

120 In the current trial, we compared flutamide plus bilateral orchiectomy with placebo plus o

121 and immune functions, the mechanism by which flutamide produces the salutary effects remains unknown.

122 Addition of flutamide significantly reduced secretion of IGFBP1 and

123 d with androgen ablation monotherapy was not flutamide stimulated.

124 Patients with flutamide-stimulated AR mutations responded to subsequen

125 atment with the androgen receptor antagonist flutamide, suggesting that androgens mediated these effe

126 ld, whereas androgen inhibitors (casodex and flutamide) suppressed viral growth up to 3-fold.

127 In addition to flutamide, the biocides fenitrothion, vinclozolin and li

128 LFTs should be monitored during flutamide therapy.

129 The addition of flutamide to bilateral orchiectomy does not result in a

130 trial, we found that adding the antiandrogen flutamide to leuprolide acetate (a synthetic gonadotropi

131 oxifen or with the nonsteroidal antiandrogen flutamide to probe for additional evidence for this sele

132 sion of T antigen in the prostate tissues of flutamide-treated animals (at 10 weeks age) was lower th

133 Tumors from high-dose flutamide-treated animals were more differentiated and r

134 ma (STIC), were collected from untreated and flutamide-treated HR women as well as low-risk (LR) wome

135 ignaling revealed that the urethral plate of flutamide-treated males does not undergo this septation

136 M, which dominated three metastases from one flutamide-treated patient.

137 wing T-H were restored to sham levels in the flutamide-treated T-H animals.

138 Moreover, flutamide treatment blocked T-induced Fos expression onl

139 creased from 26 (baseline) to 94 U/L (during flutamide treatment) (P<.005).

140 creased from 23 (baseline) to 67 U/L (during flutamide treatment) (P<.02); mean alanine aminotransfer

141 changes in the aged hippocampus compared to flutamide treatment, especially in genes related to mito

142 ings that Survivin can mediate resistance to Flutamide treatment, we further investigated whether IGF

143 n response to strong selective pressure from flutamide treatment.

144 The analysis showed that flutamide, troglitazone, diclofenac, isoniazid, and tamo

145 Flutamide, up to concentrations of 2 x 10(-5)M, did not

146 In 30 (46%) of 65 patients, flutamide was discontinued prematurely.

147 Despite this, flutamide was not as active an initial agent as DES.

148 Flutamide was not associated with enhanced benefit in pa

149 ive potency of C47 to the reference compound flutamide was over 5.2, whereas the derivatives were les

150 A comparison of flutamide with bicalutamide awaits maturation of surviva

151 However, cre activity can be induced by flutamide with the CRE-M-AR-LBD(LNCaP) fusion protein.

152 Prior exposure to flutamide and response to flutamide withdrawal was also considered.

153 tients who have failed to respond to CAB and flutamide withdrawal.

154 on flutamide, independent of the response to flutamide withdrawal.