ライフサイエンスコーパス: fluvoxamine

1 d to between one and two brain half-lives of fluvoxamine.

2 re citalopram, escitalopram, paroxetine, and fluvoxamine.

3 a prospective, open-label treatment trial of fluvoxamine.

4 (1.37, 1.32, 1.28, and 1.25, respectively), fluvoxamine (1.41, 1.35, 1.30, and 1.27, respectively),

5 NT (0.05) > nor-CIT (0.12) >> EIENT (1.15) > fluvoxamine (1.46).

6 patients), cognitive behavioural therapy and fluvoxamine (-7.50 [-13.89 to -1.17]; one trial and six

7 h the selective serotonin reuptake inhibitor fluvoxamine; 91.3% of the patients had the generalized s

8 specific re-uptake inhibitor (fluoxetine or fluvoxamine), a norepinephrine-specific re-uptake inhibi

9 atment with either dehydroepiandrosterone or fluvoxamine, a high-affinity sigma1-receptor agonist, im

10 In the presence of fluvoxamine, a selective serotonin reuptake inhibitor (S

11 Fluvoxamine also resulted in significantly greater decre

12 Effects of the SSRI fluvoxamine and 5-HT(1A)R agonist 8-OH-DPAT were also po

13 the antidepressant-like effects of the SSRI fluvoxamine and 5-HT1A-selective agonist 8-hydroxy-2-dip

14 age effects on whole-brain concentrations of fluvoxamine and fluoxetine in children taking SSRIs.

15 Cytochrome P450 1A2 is inhibited by fluvoxamine and is implicated in drug interactions with

16 Controlled studies of fluvoxamine and other potent and selective serotonin upt

17 d exposed females to the SSRI fluoxetine and fluvoxamine and the 5-HT serotonin receptor antagonist c

18 inhibitors (SSRIs) (paroxetine, fluoxetine, fluvoxamine, and sertraline) and clomipramine, four stud

19 set and the rationale for drug holidays with fluvoxamine appear to be well explained by the brain eli

20 Fluoxetine, sertraline, and fluvoxamine are believed to inhibit cytochrome P450 2C b

21 These data suggest that fluvoxamine attains brain steady-state levels substantia

22 The mean ratio of fluvoxamine brain elimination half-life to plasma half-l

23 F MRS) and to assess the relationships among fluvoxamine brain levels, fluvoxamine plasma levels, and

24 Brain fluvoxamine concentration in the children was lower, con

25 Spectroscopic quantification of whole brain fluvoxamine concentrations and chromatographic determina

26 ing, as determined by stabilization of brain fluvoxamine concentrations.

27 The NH(2)-containing arm of the Y-shaped fluvoxamine coordinates the CYP46A1 heme iron, whereas t

28 Fluvoxamine decreased the clearance of serotonin in rats

29 symptoms were refractory to SSRI treatment (fluvoxamine, fluoxetine, or sertraline) alone.

30 this study was to determine the efficacy of fluvoxamine for the treatment of social phobia (social a

31 (19F MRS) to characterize the elimination of fluvoxamine from the human brain after abrupt drug disco

32 antly higher proportion of responders in the fluvoxamine group (42.9%, N = 18) than in the placebo gr

33 o significant difference between placebo and fluvoxamine groups in the rate of decrease in Hamilton d

34 ency: sertraline > fluoxetine > paroxetine > fluvoxamine > citalopram.

35 -10 weeks after treatment with fluoxetine or fluvoxamine in 15 patients with unipolar major depressio

36 The elimination half-lives of fluvoxamine in brain and plasma were determined to asses

37 Elimination of fluvoxamine in the brain and plasma was optimally descri

38 immobility and increased swimming caused by fluvoxamine in the forced swimming test was blocked in r

39 y was to investigate the pharmacokinetics of fluvoxamine in the human brain by using fluorine-19 magn

40 of this study was to assess the efficacy of fluvoxamine in the treatment of binge-eating disorder.

41 f the selective serotonin reuptake inhibitor fluvoxamine in the treatment of pathological gambling.

42 These findings indicate that fluvoxamine is efficacious in the pharmacologic manageme

43 Fluvoxamine is more effective than placebo in the short-

44 ment response in relation to brain or plasma fluvoxamine level was not feasible because of the marked

45 and chromatographic determination of plasma fluvoxamine levels were performed serially for up to 10

46 Brain fluvoxamine levels were substantially higher than plasma

47 hibited several-fold higher plasma and brain fluvoxamine levels.

48 = 1.00 (95% confidence interval, 0.63-1.57); fluvoxamine maleate, hazard ratio = 0.98 (95% confidence

49 ent and selective serotonin uptake inhibitor fluvoxamine maleate.

50 ngs from this preliminary study suggest that fluvoxamine may be effective in reducing the urge to gam

51 nical response and a blood sample for plasma fluvoxamine measurement were obtained at each 19F MRS se

52 opram, duloxetine, escitalopram, fluoxetine, fluvoxamine, milnacipran, mirtazapine, paroxetine, rebox

53 der were randomly assigned to receive either fluvoxamine (N=42) or placebo (N=43) in a 9-week, parall

54 ve increased when they are administered with fluvoxamine, nefazodone, fluoxetine, and sertraline.

55 These findings suggest that fluvoxamine or fluoxetine prescriptions adjusted for dos

56 old and stabilized with a consistent dose of fluvoxamine or fluoxetine, were recruited for the study;

57 mal tubular epithelial cells, stimulation by fluvoxamine or oxidative stress caused the sigma1-recept

58 probes) exposed to two SSRIs (fluoxetine and fluvoxamine) or to 4-nonylphenol.

59 fewer discontinuations than did duloxetine, fluvoxamine, paroxetine, reboxetine, and venlafaxine.

60 elationships among fluvoxamine brain levels, fluvoxamine plasma levels, and clinical efficacy.

61 i analysis showed that a single injection of fluvoxamine produced a significant increase in dendritic

62 f the serotonin selective reuptake inhibitor fluvoxamine revealed that endogenous 5-HT is sufficient

63 e effect of estradiol and/or progesterone on fluvoxamine's AD-like effects was investigated.

64 coupled receptor 30, whereas its blockade of fluvoxamine's effects was ER alpha-mediated.

65 Fluvoxamine stimulation in these cells also activated ni

66 Brain fluvoxamine T1 values from 140 to 230 msec were observed

67 tly greater proportion of patients receiving fluvoxamine than those receiving placebo discontinued tr

68 e mice D-22 enhances the effects of the SSRI fluvoxamine to inhibit 5-HT clearance and to produce ant

69 were used to assess the ability of the SSRI fluvoxamine to modulate the clearance of locally applied

70 -HT) clearance, as well as on the ability of fluvoxamine to slow 5-HT clearance, were investigated.

71 nce and both hormones blocked the ability of fluvoxamine to slow 5-HT clearance.

72 the selective serotonin reuptake inhibitor, fluvoxamine, to inhibit serotonin transporter function i

73 Eight (53%) of 15 patients in the fluvoxamine-treated group were categorized as responders

74 However, in the same patients, fluoxetine or fluvoxamine treatment normalized the CSF ALLO content.

75 Fluvoxamine treatment resulted in gambling abstinence in

76 vealed prompt peritubular vasodilation after fluvoxamine treatment, which was blocked by the sigma1-r

77 the increase in CSF ALLO after fluoxetine or fluvoxamine treatment.

78 Seven of the 10 patients who completed the fluvoxamine trial were judged treatment responders at th

79 se patients completed an 8-week single-blind fluvoxamine trial.

80 ic rat kidney, sigma1-receptor activation by fluvoxamine triggered the Akt-nitric oxide synthase sign

81 c and antidysphoric actions of fluoxetine or fluvoxamine via its positive allosteric modulation of GA

82 The mean daily dose of fluvoxamine was 202 mg (SD = 86).

83 Compared with placebo, fluvoxamine was associated with a significantly greater

84 In this placebo-controlled trial, fluvoxamine was found to be effective according to most

85 The elimination half-life of fluvoxamine was found to be substantially longer for the

86 Fluvoxamine was superior to placebo in reducing repetiti

87 Similarly, fluvoxamine was superior to placebo on all social phobia

88 Overall, fluvoxamine was well tolerated and safe.

89 mild sedation and nausea in a few patients, fluvoxamine was well tolerated.

90 ight binders, the widely used antidepressant fluvoxamine, was cocrystallized with CYP46A1.

91 subjects completing clinical treatment with fluvoxamine were enrolled in the study.

92 chieved steady-state brain concentrations of fluvoxamine within 30 days after consistent daily dosing