ライフサイエンスコーパス: imipramine

1 nt prescription (desipramine, fluoxetine, or imipramine).

2 rtraline was generally better tolerated than imipramine.

3 nidirectional and inhibited by amiloride and imipramine.

4 lthough fluoxetine was better tolerated than imipramine.

5 for placebo, and 26.3% for CBT combined with imipramine.

6 showing that EGL-2 currents are inhibited by imipramine.

7 asures of mood, there was a robust effect of imipramine.

8 often than patients switched to placebo from imipramine.

9 r metabolic alteration of the antidepressant imipramine.

10 e the increased sensitivity of human SERT to imipramine.

11 n that was more marked in those treated with imipramine.

12 treatment with the tricyclic antidepressant imipramine.

13 SERT can partially respond to fluoxetine and imipramine.

14 treatment with the tricyclic antidepressant, imipramine.

15 r a standard solution containing 1 microg/mL imipramine.

16 s ratio [OR] 0.31, 95% CrI 0.13 to 0.95) and imipramine (0.23, 0.04 to 0.78).

17 treatment with the tricyclic antidepressant imipramine (10 mg/kg per day i.p. for 21 days) markedly

18 animals with L-760,735 (3 mg/kg), but not by imipramine (10 mg/kg).

19 daily doses of both paroxetine (33.9 mg) and imipramine (162.5 mg) were significantly more effective

20 ontinued sertraline (6.0%) than discontinued imipramine (18.4%) because of adverse events.

21 at assessed the effectiveness of concomitant imipramine (180 mg/day) and buspirone (38 mg/day) compar

22 Following an acute-phase open trial with imipramine (2.25 mg/kg per day) involving 110 patients f

23 uoxetine (paroxetine) or failed to increase (imipramine) 3 alpha, 5 alpha-TH PROG brain content.

24 ere either unwilling to start treatment with imipramine (30.6% and 47.4%, respectively) or discontinu

25 ne, 41% for those maintained on a regimen of imipramine, 47% for those switched from imipramine to pl

26 antly more dropouts due to side effects from imipramine (48%) than from both paroxetine (20%) and pla

27 gnificantly higher for patients who received imipramine (82.6%), and nonsignificantly higher for pati

28 nic social defeat stress followed by chronic imipramine (a tricyclic antidepressant) to mice and stud

29 Imipramine, a drug in use for the treatment of depressio

30 ositions in hSERT to map the binding site of imipramine, a prototypical tricyclic antidepressant, and

31 serotonin reuptake inhibitor (SSRI), and to imipramine, a tricyclic antidepressant, in chronic depre

32 Imipramine activates methimazole metabolism catalyzed by

33 Imipramine administration induces phosphorylation of MeC

34 the MeCP2 KI mice did not respond to chronic imipramine administration.

35 uble-blind treatment with sertraline or with imipramine after placebo washout.

36 or the PDSS (P=.04 vs CBT alone and P=.03 vs imipramine alone) and 56.3% for the CGI (P=.03 vs imipra

37 amine alone) and 56.3% for the CGI (P=.03 vs imipramine alone), but not significantly better than CBT

38 plus placebo, 31.9% for CBT alone, 19.7% for imipramine alone, 13% for placebo, and 26.3% for CBT com

39 imipramine plus interpersonal psychotherapy, imipramine alone, interpersonal psychotherapy alone, or

40 city are iproniazid, nefazodone, phenelzine, imipramine, amitriptyline, duloxetine, bupropion, trazod

41 ts effect on HIV-1 release was suppressed by Imipramine (an antidepressant agent known to inhibit mic

42 In contrast, imipramine, an antidepressant that can trigger manic epi

43 Furthermore, we found that progesterone, imipramine and 3-beta-[2-(diethylamino)ethoxy]androst-5-

44 Combining imipramine and CBT appeared to confer limited advantage

45 After 6 months of maintenance, imipramine and CBT were significantly more effective tha

46 Both imipramine and CBT were significantly superior to placeb

47 isorder that compared treatment outcomes for imipramine and cognitive behavior therapy.

48 in analytical standard solutions as well as imipramine and desipramine in fortified human plasma sam

49 sitive to the serotonin reuptake block drugs imipramine and fluoxetine, demonstrating that serotonin

50 administration of two major antidepressants, imipramine and fluoxetine, strongly and directly altered

51 ted the Cl(-)-mediated affinity increase for imipramine and fluoxetine.

52 ated to dropout rates; women who were taking imipramine and men who were taking sertraline were more

53 t has only a minor effect on the response to imipramine and no effect on the response to fluoxetine.

54 d affinity (17- to 56-fold) whilst ibogaine, imipramine and paroxetine all bound with lower affinity

55 d significantly better to sertraline than to imipramine and that postmenopausal women had similar rat

56 lapse specifically due to discontinuation of imipramine and to test the hypothesis that maintenance t

57 Two pharmaceutical compounds (cimetidine and imipramine) and one new protease inhibitor compound were

58 ponse rates were 59% for sertraline, 64% for imipramine, and 44% for placebo (P = .02 for sertraline

59 al monoamine-based tricyclic antidepressant, imipramine, and a rapidly acting, non-monoamine-based an

60 Importantly, desipramine, imipramine, and a third ASMase inhibitor, SR33557, but n

61 ctive loss of antagonist potencies (cocaine, imipramine, and citalopram but not paroxetine or mazindo

62 etine (Prozac), the tricyclic antidepressant imipramine, and dopamine.

63 idepressant effects of A1R upregulation, SD, imipramine, and ketamine treatment.

64 w a favorable response to sertraline than to imipramine, and men were significantly more likely to sh

65 o class 2 amphiphiles (e.g. trifluoperazine, imipramine, and U18666A); these agents may therefore act

66 On using desipramine and imipramine as "arbitrarily selected standards" or "refer

67 en peak height ratio and concentration using imipramine as a pharmaceutical test compound.

68 responsive to the tri-cyclic antidepressant imipramine as evidenced by their attenuated depressive b

69 adigm, we show that action of fluoxetine and imipramine at the 5HT reuptake transporter (SERT) and at

70 facilitated significantly by co-prescribing imipramine before and during the benzodiazepine taper.

71 affective disorder, with both sertraline and imipramine being more effective than placebo.

72 Similarly, the antidepressant drug imipramine blocked the initial stress-induced microglial

73 Imipramine blue (IB) is a newly identified anti-invasive

74 ere, we have tested a potent new drug called imipramine blue (IB), which is a chimeric molecule with

75 pine taper and a 5-week posttaper phase with imipramine, buspirone, and placebo treatment being conti

76 olam, patients were treated for 4 weeks with imipramine, buspirone, or placebo under double-blind con

77 n of 100 microM inhibited N-demethylation of imipramine by 75% and 30%, respectively, with a lower ef

78 amphiphiles (e.g. U18666A, progesterone, and imipramine) caused lysosomal cholesterol to increase to

79 Several of these drugs, including imipramine, citalopram, sertraline, and fluoxetine (Proz

80 Quinidine inhibited the hydroxylation of imipramine competitively by 60% and 98% at concentration

81 effect shows a similar, direct dependency on imipramine concentration.

82 er the switch to placebo from phenelzine and imipramine could be due to the two drugs' different mech

83 Using imipramine-d3 as an internal standard, the RSD of peak h

84 swim was reduced by acute administration of imipramine, demonstrating that loss of pMeCP2 does not i

85 n addition, analyses of fortified samples of imipramine desipramine were measured relative to their c

86 is responsible for increased sensitivity to imipramine, desipramine, and nortriptyline.

87 Patients maintained with imipramine did not have lower relapse rates than those s

88 Imipramine-displaceable 5-[3H]HT binding to intact L-S1

89 re (4 C), enabled quantitative assessment of imipramine-displaceable 5-[3H]HT binding to the 5-HT tra

90 ly, inhibition of acid sphingomyelinase with imipramine disrupts ACEC formation, association of cilio

91 The imipramine effect remained highly significant even after

92 Imipramine effects were limited to feedback-related regi

93 All medication doses were transformed into imipramine-equivalent doses.

94 nefit appears to plateau at around 250 mg of imipramine equivalents (50 mg of fluoxetine).

95 (sedentary vs. activity wheel)x2 (saline vs. imipramine) factorial design.

96 ouble-blind, randomized controlled trials of imipramine for children and adolescents with acute stres

97 hotherapy, and supportive psychotherapy with imipramine for human immunodeficiency virus (HIV)-positi

98 tidepressant (nortriptyline for the elderly, imipramine for the midlife patients).

99 (60% in the sertraline group and 44% in the imipramine group), neither the intent-to-treat remission

100 acteristic of binding to NETs (desipramine > imipramine > citalopram).

101 either sertraline hydrochloride (n = 117) or imipramine hydrochloride (n = 51), were crossed over or

102 domized, 12-week placebo-controlled trial of imipramine hydrochloride combined with weekly relapse pr

103 logical treatment dosages averaged 100 mg of imipramine hydrochloride equivalent in the chronically i

104 and efficacy of sertraline hydrochloride and imipramine hydrochloride in treating dysthymia.

105 k, double-blind, placebo-controlled trial of imipramine hydrochloride.

106 nd 30%, respectively, with a lower effect on imipramine hydroxylation.

107 Oral treatment of infected BALB/c mice with imipramine in combination with sodium stibogluconate cle

108 or antidepressants in general (0.55) and for imipramine in particular (0.48).

109 The metabolism of imipramine in the brains of rats was analyzed to study t

110 zine in the locus coeruleus and decreased by imipramine in the dorsal raphe.

111 s obtained for standard aqueous solutions of imipramine in the range from 0.025 to 10 microg/mL.

112 lso found for human urine sample spiked with imipramine in the range of 0.025-10 microg/ mL.

113 ce, fluoxetine appeared to be no better than imipramine in the treatment of atypical depression, alth

114 antidepressant effects of the tricyclic drug imipramine in this paradigm.

115 olerability than a tricyclic antidepressant (imipramine) in depressed patients with HIV infection.

116 rotonin re-uptake inhibitors, paroxetine and imipramine, in doses equipotent to those of fluoxetine i

117 Phenelzine increased locus coeruleus TH and imipramine increased dorsal raphe TPH2 gene expression i

118 For a P450-imipramine incubation mixture, the formation of the N-de

119 more expression changes in the hippocampus; imipramine induced more expression changes in the nucleu

120 at p21 restrains neurogenesis in the SGZ and imipramine-induced stimulation of neurogenesis might be

121 ive acid sphingomyelinase (ASMase) inhibitor imipramine inhibited TNF-alpha-induced apoptosis and C16

122 Desipramine and imipramine, inhibitors of acid sphingomyelinase (ASMase)

123 In contrast, imipramine inhibits the metabolism of methimazole cataly

124 tant (K(m)) of the P450 biotransformation of imipramine into desipramine and to determine the IC50 va

125 results suggest that the response of FMO1 to imipramine involves a distribution between two sites tha

126 ndicated that modulation of FMO1 activity by imipramine is controlled to a great extent by two areas

127 se paroxetine was much better tolerated than imipramine, its overall effectiveness may be greater.

128 [corrected] (2) SSRIs bind to the [(3)H]imipramine locus with a [corrected] higher affinity when

129 ther things being equal, a patient receiving imipramine maintenance was 92.5% lower in the hazard rat

130 xiety and that the antidepressant effects of imipramine may be mediated by the alpha(2A)-AR.

131 Imipramine may reduce substance abuse among patients who

132 The switch from sertraline to imipramine (mean dosage, 221 mg/d) and from imipramine t

133 luding acetaminophen, clozapine, diclofenac, imipramine, meclofenamic acid, and ticlopidine.

134 Instead, a imipramine-mediated decreased IL-10 level allows optimal

135 deciphers a detailed molecular mechanism of imipramine-mediated regulation of IL-10/IL-12 reciprocit

136 eductase concentration-dependent increase in imipramine metabolism and suggest that the reductase lev

137 ition for a binding site since alteration of imipramine metabolism has no effect on the parameters of

138 ith the involvement of several P450 forms in imipramine metabolism.

139 amine, duloxetine, escitalopram, fluoxetine, imipramine, mirtazapine, nefazodone, nortriptyline, paro

140 dFMO1 also catalyzed imipramine N-oxidation, with a K(m) of 4.7 microM and a

141 mly assigned to receive paroxetine (N = 25), imipramine (N = 25), or placebo (N = 25) in a 12-week tr

142 y (n = 24) and supportive psychotherapy with imipramine (n = 26) had significantly greater improvemen

143 ssigned to treatment with paroxetine (N=35), imipramine (N=39), or placebo (N=43) for 10 weeks.

144 ) only (n=77); placebo only (n=24); CBT plus imipramine (n=65); or CBT plus placebo (n=63).

145 (either cognitive behavior therapy [N=36] or imipramine [N=22]).

146 When treated with imipramine, neither Per3(-/-) nor WT mice exhibited an a

147 erozygotes were prolonged in forced swim and imipramine normalized this behavior.

148 MeCP2 is required for the effects of chronic imipramine on depressive-like behaviors induced by chron

149 phenelzine and the tricyclic antidepressant imipramine on HPA activity and forebrain GR gene express

150 Uptake was greatly reduced by imipramine or KB-R7943 if these were added when [fMg2+]i

151 sensitive to temperature, is insensitive to imipramine or KB-R7943, but is inactivated by depolariza

152 licated in depression and its treatment with imipramine or ketamine.

153 ocampal neurogenesis, whereas treatment with imipramine or minocycline had minimal or no anti-depress

154 sed patients with HIV infection responded to imipramine or paroxetine at a higher rate than to placeb

155 2 years' duration and who had improved with imipramine or phenelzine were stabilized for 6 months an

156 he inhibition of its binding by desipramine, imipramine, or citalopram.

157 ere randomly assigned to receive fluoxetine, imipramine, or placebo for a 10-week clinical trial.

158 domized prospective fashion with sertraline, imipramine, or placebo.

159 eeks of acute-phase therapy with sertraline, imipramine, or placebo.

160 ed to 12 weeks of treatment with sertraline, imipramine, or placebo.

161 compounds hydroxyzine pamoate (Vistaril) and imipramine pamoate (Tofranil-PM); and the peptide hormon

162 Compared to imipramine, paroxetine resulted in a lower incidence of

163 ol, phenobarbital, pargyline, D-amphetamine, imipramine, piracetam or N-methyl-D-aspartate (NMDA) inc

164 er heart failure, induced with a propranolol-imipramine-plasma expansion treatment.

165 ne of four maintenance treatment conditions: imipramine plus interpersonal psychotherapy, imipramine

166 Among responders, imipramine produced a response of higher quality.

167 e hypothesis that maintenance treatment with imipramine protects patients with panic disorder and ago

168 d mutagenesis as primary determinants of the imipramine response.

169 Moreover, coadministration of rolipram with imipramine resulted in a more rapid induction of CREB th

170 nt with either cognitive behavior therapy or imipramine; results obtained with emotion-focused psycho

171 Chronic imipramine reversed this downregulation and increased hi

172 8-1.03), carbamazepine (RR 0.68, 0.44-1.06), imipramine (RR 0.95, 0.66-1.36), and paliperidone (RR 0.

173 C5 overexpression in the hippocampus blocked imipramine's ability to reverse depression-like behavior

174 Our findings suggest that imipramine's proposed activities on forebrain GR functio

175 ; this replicates acute trials demonstrating imipramine's relative ineffectiveness in patients with a

176 ial defeat stress, chronic administration of imipramine significantly improved social interaction in

177 r all antidepressants, except paroxetine and imipramine, started to rise again.

178 tly greater proportion of patients receiving imipramine than those receiving sertraline or placebo di

179 more likely to show a favorable response to imipramine than to sertraline.

180 more patients dropped out of treatment with imipramine than with fluoxetine.

181 Doses of imipramine that inhibit 5-HT uptake neither reduce aggre

182 80%) prevented by the amine uptake inhibitor imipramine, the MAO inhibitor pargyline and the MEK inhi

183 Similar findings were not demonstrated for imipramine; this replicates acute trials demonstrating i

184 city exists between IL-10 and IL-12 and that imipramine tips the balance toward an increased IL-12/IL

185 with the substance P antagonist L-760,735 or imipramine to block this response were examined in gerbi

186 rain microsomes were capable of metabolizing imipramine to both hydroxylated and N-demethylated produ

187 n of imipramine, 47% for those switched from imipramine to placebo, and 87% for placebo-treated patie

188 lower relapse rates than those switched from imipramine to placebo.

189 imipramine (mean dosage, 221 mg/d) and from imipramine to sertraline (mean dosage, 163 mg/d) resulte

190 t nonresponders benefited from a switch from imipramine to sertraline, or vice versa, despite a high

191 (d) inhibits binding of [(3)H]TCP and [(3)H]imipramine to the desensitized/carbamylcholine-bound Tor

192 in the saline treated animals but not in the imipramine treated animals.

193 ine were more chronically depressed than the imipramine-treated patients.

194 ssed rats, similar to classic antidepressant imipramine treatment (10 mg/kg, i.p.).

195 of prophylactic effectiveness of maintenance imipramine treatment and demonstrate that relapse, altho

196 ypes remains unclear, both are alleviated by imipramine treatment during dim night-time light.

197 Imipramine treatment is effective for primary depression

198 andomized trial that compared sertraline and imipramine treatment of 531 patients with chronic depres

199 Imipramine treatment was safe and associated with improv

200 s in gene expression are reversed by chronic imipramine treatment, and that resilient mice-those resi

201 sponders and nonresponders after ketamine or imipramine treatment.

202 at overlap dramatically with those seen with imipramine treatment.

203 ffects of chronic MAOI (phenelzine) and TCA (imipramine) treatment on neural corticosteroid receptor

204 Imipramine typically increased and phenelzine decreased

205 Patients were randomly assigned to receive imipramine, up to 300 mg/d, only (n=83); cognitive-behav

206 Patients given imipramine, venlafaxine, and duloxetine had more discont

207 suggesting both common and unique effects of imipramine versus ketamine.

208 2 for sertraline vs placebo and P < .001 for imipramine vs placebo).

209 sion (P = .04 and P = .01 for sertraline and imipramine vs placebo, respectively), the Montgomery-Asb

210 Imipramine was an effective antidepressant in patients r

211 This hyperacetylation by chronic imipramine was associated with a selective downregulatio

212 Imipramine was included because its known efficacy for t

213 e monohydroxylated metabolite (m/z 297.2) of imipramine was observed following chip-based monolithic

214 ps, the effectiveness of both fluoxetine and imipramine was significantly better than that of placebo

215 ween the responses of rabbit and pig FMO1 to imipramine was studied by random chimeragenesis and site

216 ects who completed the trial (for them, only imipramine was superior to placebo at week 12).

217 Imipramine was superior to placebo on some self-reported

218 Another antidepressant, imipramine, was without any effect on allopregnanolone o

219 a human urine sample spiked with 1 microg/mL imipramine were loaded onto eight different monolithic c

220 tely treated patients, 57% (24/42) receiving imipramine were rated as responders compared with 7% (3/

221 Sertraline and imipramine were significantly better than placebo in imp

222 However, both paroxetine and imipramine were superior to placebo for patients with lo

223 ysate showed N-demethylation activity toward imipramine, whereas another brain P-450 CYP4F6-expressed

224 ors, as well as the tricyclic antidepressant imipramine, which inhibits MAO activity and reduces oxid

225 such as chlorpromazine, trifluoperazine, and imipramine, which mimic the effect of cholesterol.

226 receptor, confers significant resistance to imipramine while leaving the responses to 5HT or fluoxet

227 ed the efficacy and safety of paroxetine and imipramine with that of placebo in the treatment of bipo

228 fferences in time to response were seen with imipramine, with women responding significantly more slo

229 e therefore hypothesized that phenelzine and imipramine would also affect brainstem GR gene expressio