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1 ihydrotestosterone, cyproterone acetate, and hydroxyflutamide.
2 such as 100 nM 17beta-estradiol or 1 microM hydroxyflutamide.
3 atment with the specific androgen antagonist hydroxyflutamide.
4 esence of 10 nM 17beta-estradiol or 1 microM hydroxyflutamide.
5 y the anti-androgens cyproterone acetate and hydroxyflutamide.
6 y a competition assay with the anti-androgen hydroxyflutamide.
7 c prostate cancer drugs bicalutamide (1) and hydroxyflutamide (2) in reporter gene assays measuring t
9 A pathway could not be blocked completely by hydroxyflutamide, an antiandrogen used in the treatment
13 red with commonly used antiandrogens such as hydroxyflutamide and bicalutamide, leading to a lower po
14 sn705 is an important determinant in binding hydroxyflutamide and its derivatives by participating in
16 1FxxLF peptide interaction, while flutamide, hydroxyflutamide, and bicalutamide caused only partial d
17 aring bound conformations of R-bicalutamide, hydroxyflutamide, and two previously reported nonsteroid
18 -hybrid assay, we report that antiandrogens, hydroxyflutamide, bicalutamide (casodex), cyproterone ac
20 nically important antiandrogens, casodex and hydroxyflutamide, both D36 and D80 block androgen action
21 nonsteroidal AR antagonists bicalutamide and hydroxyflutamide but act as agonists for the androgen re
22 y, these studies indicate that flutamide and hydroxyflutamide but not dihydrotestosterone are transpo
24 m for the enantioselective binding of chiral hydroxyflutamide derivatives and expand upon the previou
25 activity and that two potent antiandrogens, hydroxyflutamide (Eulexin) and bicalutamide (Casodex), f
27 uired because the AR antagonists casodex and hydroxyflutamide failed to translocate beta-catenin.
28 sterone, 10 nM 17beta-estradiol, or 1 microM hydroxyflutamide for the LNCaP mutant AR (mtAR T877A), f
29 tingly, these compounds, in combination with hydroxyflutamide, further suppressed the Adiol-induced A
32 Because ARA70 can promote the antiandrogen hydroxyflutamide (HF)-enhanced AR transactivation, the i
33 e or 10(-9) M testosterone, but not 10(-6) M hydroxyflutamide in human prostate cancer DU145 cells.
34 backbone oxygen of Leu-873 and the ketone of hydroxyflutamide is present when bound to the T877A AR v
36 o testosterone, the binding modes of several hydroxyflutamide-like nonsteroidal ligands for the andro
37 y observed and activated by bicalutamide and hydroxyflutamide, respectively, in prostate cancer patie
39 ctive conditions in the hsp82 mutant strain, hydroxyflutamide was shown to be a potent competitive in
40 tiandrogenic activities and were superior to hydroxyflutamide, which is the currently available antia
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