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1 h two different doses of the SRD5A inhibitor dutasteride.
2 e assigned by random number table to receive dutasteride (0.5 mg per day) or placebo orally for 24 mo
3 e in score from baseline: placebo, -3.6%, vs dutasteride, 2.1%; p=0.01), whereas the mental component
4 4 were included in the efficacy analysis (21 dutasteride, 23 placebo).
5 re randomly assigned to treatment groups (25 dutasteride, 25 placebo), and 44 were included in the ef
6 weeks plus placebo (4 groups) or 2.5 mg/d of dutasteride (4 groups).
7 h (a) placebo; (b) testosterone (T); (c) T + Dutasteride (5a reductase inhibitor; AvodartTM); (d) T +
8                                              Dutasteride (5alpha-reductase inhibitor) is approximatel
9 raterone alone, followed by abiraterone plus dutasteride (a 5alpha-reductase inhibitor), 3-keto-5alph
10                                              Dutasteride also induces cyclooxygenase type 2 (COX-2),
11  cancer versus benign prostate tissue making dutasteride an attractive agent to study.
12                                              Dutasteride and finasteride are currently the only prove
13 lude 5alpha-reductase (5AR) inhibitors (i.e. dutasteride and finasteride) to block the conversion of
14 dil and the two 5-alpha reductase inhibitors dutasteride and finasteride.
15    The dose-adjusted differences between the dutasteride and placebo groups for fat-free mass were no
16 chanism of action and adverse event profile (dutasteride); and comparing reports of suicidality befor
17 mide and dutasteride (ZBD), or bicalutamide, dutasteride, and ketoconazole (ZBDK) for 3 months before
18                              Finasteride and dutasteride, as SRD5A2 inhibitors, are widely used antia
19 oid staining was reversed by finasteride and dutasteride, as well as by APV.
20 ontrolled, parallel-group study, we compared dutasteride, at a dose of 0.5 mg daily, with placebo.
21 Study 36-item Short Form version 2, favoured dutasteride (change in score from baseline: placebo, -3.
22 ss, anxiety, food cravings, and bloating) on dutasteride compared with placebo.
23    In addition, flufenamic acid, travoprost, dutasteride, cyflumetofen, flutoanil, and teriflunomide
24                                 Furthermore, dutasteride did not deplete the three 5beta-reduced meta
25  while D4A concentrations rose, showing that dutasteride effectively blocks production of a tumour-pr
26                                              Dutasteride elicited the same phenotype in a second gast
27  differ in men in whom DHT was suppressed by dutasteride from those treated with placebo, indicating
28 eason score of 7 to 10 among 3299 men in the dutasteride group and 233 among 3407 men in the placebo
29 muscle strength as indicated by QMA, and the dutasteride group had an increase in strength of 1.3% (0
30                                          The dutasteride group had fewer patients reporting falls tha
31 ategory of cardiac failure was higher in the dutasteride group than in the placebo group (0.7% [30 me
32 r was detected in 659 of the 3305 men in the dutasteride group, as compared with 858 of the 3424 men
33 umors with a Gleason score of 8 to 10 in the dutasteride group, as compared with only 1 in the placeb
34         The mean fat-free mass gained by the dutasteride groups was 0.6 kg (95% CI, -0.1 to 1.2 kg) w
35                                              Dutasteride had no effect on mood in controls.
36             RECENT FINDINGS: Finasteride and dutasteride have equal efficacy and safety for the treat
37 will use the dual 5alpha-reductase inhibitor dutasteride in a group of men identified at increased ri
38 and safety of the 5alpha-reductase inhibitor dutasteride in patients with SBMA, and to identify outco
39 e to the 5alpha-R inhibitors finasteride and dutasteride inhibited T conversion into DHT.
40 specific 5alpha-reductase inhibitor, whereas dutasteride is an inhibitor of both type 1 and type 2 5a
41                                              Dutasteride is the first drug that can inhibit both isoe
42 trual cycles, either double-blind placebo or dutasteride (low-dose 0.5 mg/day in the first eight PMDD
43  representing a relative risk reduction with dutasteride of 22.8% (95% confidence interval, 15.2 to 2
44 n of European ancestry from the REduction by DUtasteride of Prostate Cancer Events (REDUCE) study.
45  selenium) trial as well as the Reduction by Dutasteride of Prostate Cancer Events (REDUCE) trial (te
46 Cancer Prevention Trial (PCPT), Reduction by Dutasteride of Prostate Cancer Events (REDUCE) trial, an
47     We await the results of the Reduction by Dutasteride of Prostate Cancer Events (REDUCE).
48 rial known as the REDUCE trial (Reduction by Dutasteride of Prostate Cancer Events) in the context of
49 esting the absence of effect of the low-dose dutasteride on 5alpha-reductase.
50 the low-dose group, no significant effect of dutasteride on PMDD symptoms was observed compared with
51 r study did not show a significant effect of dutasteride on the progression of muscle weakness in SBM
52  by the potentiation of apoptosis induced by dutasteride or finasteride upon pharmacological inhibiti
53 kly for up to 3 weeks while taking 0.5 mg of dutasteride per day.
54 ing placebo plus testosterone enthanate with dutasteride plus testosterone enanthate from May 2005 th
55  will review the design and rationale of the dutasteride prostate cancer chemoprevention trial known
56  Over the course of the 4-year study period, dutasteride reduced the risk of incident prostate cancer
57    We conducted a study to determine whether dutasteride reduces the risk of incident prostate cancer
58 eductase inhibitors (5-ARIs) finasteride and dutasteride, refined indications, efficacy, and safety a
59 sion protein E-cadherin by the 5AR inhibitor dutasteride requires both ERbeta and TGFbeta.
60 e enhancement was blocked by finasteride and dutasteride, selective inhibitors of 5alpha-reductase, a
61  treated with the 5alpha-reductase inhibitor dutasteride, the peroxisome proliferator-activated recep
62 ccurred in 11 of 11 patients after 1 week of dutasteride therapy (P < .01).
63 rse events was similar to that in studies of dutasteride therapy for benign prostatic hyperplasia, ex
64                                   Short-term dutasteride therapy reduces Doppler US flow in the prost
65                                              Dutasteride therapy, as compared with placebo, resulted
66 administering the 5alpha-reductase inhibitor dutasteride to block conversion of progesterone to its n
67 levels of DHT were decreased by >90% in both dutasteride-treated patient groups versus the untreated
68                              The higher-dose dutasteride treatment group was found to include signifi
69                                              Dutasteride treatment was associated with highly variabl
70 nsed prescriptions of 5-ARI, finasteride, or dutasteride were considered 5-ARI users (n = 26 190).
71                              Men assigned to dutasteride were similar at baseline to those assigned t
72 ostate Cancer Events (REDUCE) trial (testing dutasteride) were reviewed.
73 s (ie, first end point) was with 0.5 mg/d of dutasteride, which was significantly more efficacious th
74 metabolites were depleted by the addition of dutasteride, while D4A concentrations rose, showing that
75 ined with dutasteride (ZD), bicalutamide and dutasteride (ZBD), or bicalutamide, dutasteride, and ket
76 randomly assigned to goserelin combined with dutasteride (ZD), bicalutamide and dutasteride (ZBD), or