ライフサイエンスコーパス: fluvoxamine

1 , and (3) other SSRIs (ie, not fluoxetine or fluvoxamine).

2 mectin, and 1.17 (95% CI, 0.57 to 2.40) with fluvoxamine.

3 d 0.94 (95% CI, 0.66 to 1.36; P = 0.75) with fluvoxamine.

4 mectin, and 1.11 (95% CI, 0.33 to 3.76) with fluvoxamine.

5 re citalopram, escitalopram, paroxetine, and fluvoxamine.

6 nced reduction signal towards the sensing of fluvoxamine.

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

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

9 (1.37, 1.32, 1.28, and 1.25, respectively), fluvoxamine (1.41, 1.35, 1.30, and 1.27, respectively),

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

11 Treatment with fluvoxamine (100 mg twice daily for 10 days) among high-

12 ients were randomly assigned (1:1) to either fluvoxamine (100 mg twice daily for 10 days) or placebo

13 Patients were randomly assigned to either fluvoxamine (100 mg twice daily for 10 days) plus inhale

14 5 [18.1] years), 481 receiving fluoxetine or fluvoxamine (285 women [59.3%]; mean [SD] age, 58.7 [18.

15 -0.97]; adjusted P = .03); and fluoxetine or fluvoxamine (48 of 481 [10.0%] vs 956 of 7215 [13.3%]; R

16 Participants were randomized to receive fluvoxamine, 50 mg twice daily on day 1 followed by 100

17 was a trend toward greater side effects with fluvoxamine (7.45% versus 3.15%; SMD = 0.21; chi(2) = 3.

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

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

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

21 RvD6si synthesis was inhibited by fluvoxamine, a cytochrome P450 inhibitor, but not by 15-

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

23 Prior research suggests that fluvoxamine, a selective serotonin reuptake inhibitor (S

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

25 ious trials have demonstrated the effects of fluvoxamine alone and inhaled budesonide alone for preve

26 Fluvoxamine also resulted in significantly greater decre

27 to evaluate the efficacy and tolerability of fluvoxamine among inpatients with laboratory-confirmed C

28 Fluvoxamine (an SSRI and sigma-1 receptor agonist) was i

29 ous adverse events in 6 participants (2 with fluvoxamine and 4 with placebo) but no deaths.

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

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

32 Among 589 participants who received fluvoxamine and 586 who received placebo included in the

33 741 patients were allocated to fluvoxamine and 756 to placebo.

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

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

36 nute difference in heart rate change between fluvoxamine and nortriptyline, and over 11 mmHg differen

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

38 mergent adverse events among patients in the fluvoxamine and placebo groups.

39 receiving any SSRI that is not fluoxetine or fluvoxamine and risk of death was not statistically sign

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

41 ecifically (1) fluoxetine, (2) fluoxetine or fluvoxamine, and (3) other SSRIs (ie, not fluoxetine or

42 double-blind trial that assessed metformin, fluvoxamine, and ivermectin; 999 participants self-colle

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

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

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

46 The results of this study identified fluvoxamine as effective in preventing clinical deterior

47 RNA sequencing analysis showed few fluvoxamine-associated differences, consistent with the

48 These findings do not support the use of fluvoxamine at this dose and duration in patients with m

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

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

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

52 symptomatic COVID-19, patients treated with fluvoxamine, compared with placebo, had a lower likeliho

53 Brain fluvoxamine concentration in the children was lower, con

54 Spectroscopic quantification of whole brain fluvoxamine concentrations and chromatographic determina

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

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

57 Meanwhile, fluvoxamine could be recommended as a management option,

58 Fluvoxamine decreased the clearance of serotonin in rats

59 th mild to moderate COVID-19, treatment with fluvoxamine does not reduce duration of COVID-19 symptom

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

61 ce indicates a potential therapeutic role of fluvoxamine for COVID-19.

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

63 current protocol reporting randomisation to fluvoxamine from Jan 20 to Aug 5, 2021, when the trial a

64 (19F MRS) to characterize the elimination of fluvoxamine from the human brain after abrupt drug disco

65 Fluvoxamine gave a well-defined reduction peak at ~ - 67

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

67 There was one death in the fluvoxamine group and 12 in the placebo group for the pe

68 ecovery was 12 days (IQR, 11-14 days) in the fluvoxamine group and 13 days (IQR, 12-13 days) in the p

69 One participant in the fluvoxamine group and 2 participants in the placebo grou

70 There were 17 deaths in the fluvoxamine group and 25 deaths in the placebo group in

71 ccine), 1288 completed the trial (674 in the fluvoxamine group and 614 in the placebo group).

72 ioration occurred in 0 of 80 patients in the fluvoxamine group and in 6 of 72 patients in the placebo

73 ncy department/urgent care visit): 14 in the fluvoxamine group compared with 21 in the placebo group

74 y hospital due to COVID-19 was lower for the fluvoxamine group compared with placebo (79 [11%] of 741

75 The fluvoxamine group had 1 serious adverse event and 11 oth

76 osite outcome, 26 participants (3.9%) in the fluvoxamine group were hospitalized, had an urgent care

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

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

79 -10 weeks after treatment with fluoxetine or fluvoxamine in 15 patients with unipolar major depressio

80 e included 316 patients, of whom 94 received fluvoxamine in addition to standard care [median age, 60

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

82 r for the accurate and fast determination of fluvoxamine in depression medications as well as biologi

83 The effect of higher-dose fluvoxamine in reducing symptom duration among outpatien

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

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

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

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

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

89 nted for the determination of antidepressant fluvoxamine in urine and blood plasma samples of obsessi

90 epurposed drugs - metformin, ivermectin, and fluvoxamine - in preventing serious SARS-CoV-2 infection

91 Fluvoxamine-induced increase in membrane trafficking boo

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

93 Fluvoxamine is more effective than placebo in the short-

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

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

96 Brain fluvoxamine levels were substantially higher than plasma

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

98 axine, duloxetine, escitalopram, fluoxetine, fluvoxamine, levomilnacipran, milnacipran, mirtazapine,

99 = 1.00 (95% confidence interval, 0.63-1.57); fluvoxamine maleate, hazard ratio = 0.98 (95% confidence

100 ine hydrochloride, fluoxetine hydrochloride, fluvoxamine maleate, paroxetine hydrochloride, and venla

101 s)-specifically fluoxetine hydrochloride and fluvoxamine maleate-with decreased mortality among patie

102 ent and selective serotonin uptake inhibitor fluvoxamine maleate.

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

104 Fluvoxamine may prevent clinical deterioration by stimul

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

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

107 ram, desvenlafaxine, duloxetine, fluoxetine, fluvoxamine, mirtazapine, nefazodone, paroxetine, reboxe

108 were randomly assigned to receive 100 mg of fluvoxamine (n = 80) or placebo (n = 72) 3 times daily f

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

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

111 ally, or more specifically of fluoxetine and fluvoxamine, on the severity of COVID-19 outcomes.

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

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

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

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

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

117 h lower QT-prolonging potential (fluoxetine, fluvoxamine, paroxetine, sertraline).

118 SSRI (citalopram, escitalopram, fluoxetine, fluvoxamine, paroxetine, sertraline, or vilazodone) or a

119 herapy testing metformin, ivermectin, and/or fluvoxamine, participants recorded symptoms daily for 14

120 were enrolled at 103 US sites for evaluating fluvoxamine; participants were 30 years or older with co

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

122 Treatment with oral fluvoxamine plus inhaled budesonide among high-risk outp

123 l of 738 participants were allocated to oral fluvoxamine plus inhaled budesonide, and 738 received pl

124 One hundred mg of fluvoxamine prescribed twice daily for 10 days was well

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

126 The fluvoxamine reduction peak current was linear to its con

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

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

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

130 om 3 trials, under a variety of assumptions, fluvoxamine showed a high probability of being associate

131 The FIASMA fluvoxamine showed beneficial effects on COVID-19 in a r

132 Neither ivermectin nor fluvoxamine showed effect over placebo.

133 Fluvoxamine stimulation in these cells also activated ni

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

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

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

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

138 The effectiveness of fluvoxamine to shorten symptom duration or prevent hospi

139 rane trafficking induced by a canonical SSRI fluvoxamine to show that it involves enhancement of clat

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

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

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

143 are group and 255 out of 3600 (7.08%) in the fluvoxamine-treated group experienced clinical deteriora

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

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

146 Fluvoxamine treatment resulted in gambling abstinence in

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

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

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

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

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

152 icipants were randomized to receive 50 mg of fluvoxamine twice daily for 10 days or placebo.

153 o moderate COVID-19, treatment with 50 mg of fluvoxamine twice daily for 10 days, compared with place

154 Fluvoxamine use was significantly associated with reduce

155 COVID-19, we aimed to assess the efficacy of fluvoxamine versus placebo in preventing hospitalisation

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

157 fully remote (contactless) clinical trial of fluvoxamine vs placebo.

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

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

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

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

162 Among the 161 survivors, fluvoxamine was not significantly associated with time t

163 barrier models, while a single injection of fluvoxamine was sufficient to enable brain accumulation

164 Fluvoxamine was superior to placebo in reducing repetiti

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

166 Overall, fluvoxamine was well tolerated and safe.

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

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

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

170 trials with available results that compared fluvoxamine with placebo were included.

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