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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 tion that was reversed by the NME inhibitor, imipramine.
13 inistration of the antidepressant medication imipramine.
14  treatment with the tricyclic antidepressant imipramine.
15 SERT can partially respond to fluoxetine and imipramine.
16 treatment with the tricyclic antidepressant, imipramine.
17 r a standard solution containing 1 microg/mL imipramine.
18 s ratio [OR] 0.31, 95% CrI 0.13 to 0.95) and imipramine (0.23, 0.04 to 0.78).
19  treatment with the tricyclic antidepressant imipramine (10 mg/kg per day i.p. for 21 days) markedly
20 animals with L-760,735 (3 mg/kg), but not by imipramine (10 mg/kg).
21 daily doses of both paroxetine (33.9 mg) and imipramine (162.5 mg) were significantly more effective
22 ontinued sertraline (6.0%) than discontinued imipramine (18.4%) because of adverse events.
23 at assessed the effectiveness of concomitant imipramine (180 mg/day) and buspirone (38 mg/day) compar
24     Following an acute-phase open trial with imipramine (2.25 mg/kg per day) involving 110 patients f
25 uoxetine (paroxetine) or failed to increase (imipramine) 3 alpha, 5 alpha-TH PROG brain content.
26 ere either unwilling to start treatment with imipramine (30.6% and 47.4%, respectively) or discontinu
27 ne, 41% for those maintained on a regimen of imipramine, 47% for those switched from imipramine to pl
28 antly more dropouts due to side effects from imipramine (48%) than from both paroxetine (20%) and pla
29 gnificantly higher for patients who received imipramine (82.6%), and nonsignificantly higher for pati
30 nic social defeat stress followed by chronic imipramine (a tricyclic antidepressant) to mice and stud
31                                              Imipramine, a drug in use for the treatment of depressio
32  GP Q95 pseudovirions were more sensitive to imipramine, a GP-destabilizing antiviral.
33 ositions in hSERT to map the binding site of imipramine, a prototypical tricyclic antidepressant, and
34  serotonin reuptake inhibitor (SSRI), and to imipramine, a tricyclic antidepressant, in chronic depre
35                                              Imipramine activates methimazole metabolism catalyzed by
36                                              Imipramine administration induces phosphorylation of MeC
37 the MeCP2 KI mice did not respond to chronic imipramine administration.
38 uble-blind treatment with sertraline or with imipramine after placebo washout.
39 or the PDSS (P=.04 vs CBT alone and P=.03 vs imipramine alone) and 56.3% for the CGI (P=.03 vs imipra
40 amine alone) and 56.3% for the CGI (P=.03 vs imipramine alone), but not significantly better than CBT
41 plus placebo, 31.9% for CBT alone, 19.7% for imipramine alone, 13% for placebo, and 26.3% for CBT com
42 imipramine plus interpersonal psychotherapy, imipramine alone, interpersonal psychotherapy alone, or
43 city are iproniazid, nefazodone, phenelzine, imipramine, amitriptyline, duloxetine, bupropion, trazod
44 ts effect on HIV-1 release was suppressed by Imipramine (an antidepressant agent known to inhibit mic
45                                 In contrast, imipramine, an antidepressant that can trigger manic epi
46     Furthermore, we found that progesterone, imipramine and 3-beta-[2-(diethylamino)ethoxy]androst-5-
47 rder; CBT in post-traumatic stress disorder; imipramine and alarm behavioral intervention in enuresis
48 al inhibitors of host acid sphingomyelinase, imipramine and amitriptyline, which induce degradation o
49                                    Combining imipramine and CBT appeared to confer limited advantage
50               After 6 months of maintenance, imipramine and CBT were significantly more effective tha
51                                         Both imipramine and CBT were significantly superior to placeb
52 isorder that compared treatment outcomes for imipramine and cognitive behavior therapy.
53  in analytical standard solutions as well as imipramine and desipramine in fortified human plasma sam
54 sitive to the serotonin reuptake block drugs imipramine and fluoxetine, demonstrating that serotonin
55 administration of two major antidepressants, imipramine and fluoxetine, strongly and directly altered
56 ted the Cl(-)-mediated affinity increase for imipramine and fluoxetine.
57 ated to dropout rates; women who were taking imipramine and men who were taking sertraline were more
58                                 Furthermore, imipramine and mianserin, two representative compounds,
59 t has only a minor effect on the response to imipramine and no effect on the response to fluoxetine.
60 d affinity (17- to 56-fold) whilst ibogaine, imipramine and paroxetine all bound with lower affinity
61 tissues, we treated stress-exposed mice with imipramine and repeated our multi-OMIC analyses.
62 d significantly better to sertraline than to imipramine and that postmenopausal women had similar rat
63 lapse specifically due to discontinuation of imipramine and to test the hypothesis that maintenance t
64                Our SERT structure with bound imipramine and vilazodone reveals a unique binding pocke
65 Two pharmaceutical compounds (cimetidine and imipramine) and one new protease inhibitor compound were
66 ponse rates were 59% for sertraline, 64% for imipramine, and 44% for placebo (P = .02 for sertraline
67 al monoamine-based tricyclic antidepressant, imipramine, and a rapidly acting, non-monoamine-based an
68                    Importantly, desipramine, imipramine, and a third ASMase inhibitor, SR33557, but n
69 ated for the microextraction of glimepiride, imipramine, and carbamazepine.
70 ctive loss of antagonist potencies (cocaine, imipramine, and citalopram but not paroxetine or mazindo
71 etine (Prozac), the tricyclic antidepressant imipramine, and dopamine.
72 idepressant effects of A1R upregulation, SD, imipramine, and ketamine treatment.
73 w a favorable response to sertraline than to imipramine, and men were significantly more likely to sh
74 o class 2 amphiphiles (e.g. trifluoperazine, imipramine, and U18666A); these agents may therefore act
75                     On using desipramine and imipramine as "arbitrarily selected standards" or "refer
76 en peak height ratio and concentration using imipramine as a pharmaceutical test compound.
77  responsive to the tri-cyclic antidepressant imipramine as evidenced by their attenuated depressive b
78 nin uptake and impedes dissociation of [(3)H]imipramine at low nanomolar concentrations.
79 adigm, we show that action of fluoxetine and imipramine at the 5HT reuptake transporter (SERT) and at
80 d sphingomyelinase (ASMase), desipramine and imipramine, attenuated ATP-induced TF decryption.
81  facilitated significantly by co-prescribing imipramine before and during the benzodiazepine taper.
82 affective disorder, with both sertraline and imipramine being more effective than placebo.
83 ctrostatic profile of the cavity facilitates imipramine binding and in silico mutations of hydrophobi
84 u AF60097 is demonstrated by the potentiated imipramine binding and increased hippocampal serotonin l
85 essential for the EAG1 channel inhibition by imipramine binding to the PAS domain.
86 rease or decrease EAG1 current inhibition by imipramine binding to the PAS domain.
87 ular mechanism of EAG1 current inhibition by imipramine binding to the PAS domain.
88 s to negatively charged glutamates decreased imipramine binding.
89           Similarly, the antidepressant drug imipramine blocked the initial stress-induced microglial
90                                              Imipramine blue (IB) is a newly identified anti-invasive
91 ere, we have tested a potent new drug called imipramine blue (IB), which is a chimeric molecule with
92 pine taper and a 5-week posttaper phase with imipramine, buspirone, and placebo treatment being conti
93 olam, patients were treated for 4 weeks with imipramine, buspirone, or placebo under double-blind con
94                                 Detection of imipramine by 213 nm ps-LDPI-MS shows less fragmentation
95 n of 100 microM inhibited N-demethylation of imipramine by 75% and 30%, respectively, with a lower ef
96 siology we show that a small molecule ligand imipramine can bind to the PAS domain of EAG1 channels a
97 amphiphiles (e.g. U18666A, progesterone, and imipramine) caused lysosomal cholesterol to increase to
98 uticals, including carbamazepine, verapamil, imipramine, ciprofloxacin, tetracycline and rifampicin.
99            Several of these drugs, including imipramine, citalopram, sertraline, and fluoxetine (Proz
100                                              Imipramine class tricyclic antidepressants have low ioni
101     Quinidine inhibited the hydroxylation of imipramine competitively by 60% and 98% at concentration
102 effect shows a similar, direct dependency on imipramine concentration.
103 d by chronic administration of fluoxetine or imipramine; conversely, it was reduced by acute and chro
104 er the switch to placebo from phenelzine and imipramine could be due to the two drugs' different mech
105                                        Using imipramine-d3 as an internal standard, the RSD of peak h
106  swim was reduced by acute administration of imipramine, demonstrating that loss of pMeCP2 does not i
107 n addition, analyses of fortified samples of imipramine desipramine were measured relative to their c
108                       Ionization energies of imipramine, desipramine, amitriptyline, and clomipramine
109 detection of four tricyclic antidepressants: imipramine, desipramine, amitriptyline, and clomipramine
110  is responsible for increased sensitivity to imipramine, desipramine, and nortriptyline.
111                     Patients maintained with imipramine did not have lower relapse rates than those s
112                                              Imipramine-displaceable 5-[3H]HT binding to intact L-S1
113 re (4 C), enabled quantitative assessment of imipramine-displaceable 5-[3H]HT binding to the 5-HT tra
114 ly, inhibition of acid sphingomyelinase with imipramine disrupts ACEC formation, association of cilio
115 ving 2.1 nM allosteric potency in inhibiting imipramine dissociation.
116                                          The imipramine effect remained highly significant even after
117                                              Imipramine effects were limited to feedback-related regi
118   All medication doses were transformed into imipramine-equivalent doses.
119 nefit appears to plateau at around 250 mg of imipramine equivalents (50 mg of fluoxetine).
120 (sedentary vs. activity wheel)x2 (saline vs. imipramine) factorial design.
121 ouble-blind, randomized controlled trials of imipramine for children and adolescents with acute stres
122 hotherapy, and supportive psychotherapy with imipramine for human immunodeficiency virus (HIV)-positi
123 tidepressant (nortriptyline for the elderly, imipramine for the midlife patients).
124  (60% in the sertraline group and 44% in the imipramine group), neither the intent-to-treat remission
125 acteristic of binding to NETs (desipramine > imipramine > citalopram).
126 either sertraline hydrochloride (n = 117) or imipramine hydrochloride (n = 51), were crossed over or
127 domized, 12-week placebo-controlled trial of imipramine hydrochloride combined with weekly relapse pr
128 logical treatment dosages averaged 100 mg of imipramine hydrochloride equivalent in the chronically i
129 and efficacy of sertraline hydrochloride and imipramine hydrochloride in treating dysthymia.
130 k, double-blind, placebo-controlled trial of imipramine hydrochloride.
131 nd 30%, respectively, with a lower effect on imipramine hydroxylation.
132  Oral treatment of infected BALB/c mice with imipramine in combination with sodium stibogluconate cle
133 or antidepressants in general (0.55) and for imipramine in particular (0.48).
134 sis indicates that the bound S-citalopram or imipramine in S1 is allosterically coupled to the ligand
135                            The metabolism of imipramine in the brains of rats was analyzed to study t
136 zine in the locus coeruleus and decreased by imipramine in the dorsal raphe.
137 s obtained for standard aqueous solutions of imipramine in the range from 0.025 to 10 microg/mL.
138 lso found for human urine sample spiked with imipramine in the range of 0.025-10 microg/ mL.
139 ce, fluoxetine appeared to be no better than imipramine in the treatment of atypical depression, alth
140 antidepressant effects of the tricyclic drug imipramine in this paradigm.
141 olerability than a tricyclic antidepressant (imipramine) in depressed patients with HIV infection.
142 rotonin re-uptake inhibitors, paroxetine and imipramine, in doses equipotent to those of fluoxetine i
143  Phenelzine increased locus coeruleus TH and imipramine increased dorsal raphe TPH2 gene expression i
144                                   For a P450-imipramine incubation mixture, the formation of the N-de
145           Treatment of susceptible mice with imipramine induced a 40.2% recovery of the defeated-susc
146  more expression changes in the hippocampus; imipramine induced more expression changes in the nucleu
147 at p21 restrains neurogenesis in the SGZ and imipramine-induced stimulation of neurogenesis might be
148 ive acid sphingomyelinase (ASMase) inhibitor imipramine inhibited TNF-alpha-induced apoptosis and C16
149                              Desipramine and imipramine, inhibitors of acid sphingomyelinase (ASMase)
150                                 In contrast, imipramine inhibits the metabolism of methimazole cataly
151 tant (K(m)) of the P450 biotransformation of imipramine into desipramine and to determine the IC50 va
152 results suggest that the response of FMO1 to imipramine involves a distribution between two sites tha
153 ndicated that modulation of FMO1 activity by imipramine is controlled to a great extent by two areas
154 se paroxetine was much better tolerated than imipramine, its overall effectiveness may be greater.
155      [corrected] (2) SSRIs bind to the [(3)H]imipramine locus with a [corrected] higher affinity when
156 ther things being equal, a patient receiving imipramine maintenance was 92.5% lower in the hazard rat
157 xiety and that the antidepressant effects of imipramine may be mediated by the alpha(2A)-AR.
158                                              Imipramine may reduce substance abuse among patients who
159                The switch from sertraline to imipramine (mean dosage, 221 mg/d) and from imipramine t
160 luding acetaminophen, clozapine, diclofenac, imipramine, meclofenamic acid, and ticlopidine.
161                                   Instead, a imipramine-mediated decreased IL-10 level allows optimal
162  deciphers a detailed molecular mechanism of imipramine-mediated regulation of IL-10/IL-12 reciprocit
163 eductase concentration-dependent increase in imipramine metabolism and suggest that the reductase lev
164 ition for a binding site since alteration of imipramine metabolism has no effect on the parameters of
165 ith the involvement of several P450 forms in imipramine metabolism.
166 amine, duloxetine, escitalopram, fluoxetine, imipramine, mirtazapine, nefazodone, nortriptyline, paro
167                         dFMO1 also catalyzed imipramine N-oxidation, with a K(m) of 4.7 microM and a
168 mly assigned to receive paroxetine (N = 25), imipramine (N = 25), or placebo (N = 25) in a 12-week tr
169 y (n = 24) and supportive psychotherapy with imipramine (n = 26) had significantly greater improvemen
170 ssigned to treatment with paroxetine (N=35), imipramine (N=39), or placebo (N=43) for 10 weeks.
171 ) only (n=77); placebo only (n=24); CBT plus imipramine (n=65); or CBT plus placebo (n=63).
172 (either cognitive behavior therapy [N=36] or imipramine [N=22]).
173                            When treated with imipramine, neither Per3(-/-) nor WT mice exhibited an a
174 erozygotes were prolonged in forced swim and imipramine normalized this behavior.
175 MeCP2 is required for the effects of chronic imipramine on depressive-like behaviors induced by chron
176  phenelzine and the tricyclic antidepressant imipramine on HPA activity and forebrain GR gene express
177                Uptake was greatly reduced by imipramine or KB-R7943 if these were added when [fMg2+]i
178  sensitive to temperature, is insensitive to imipramine or KB-R7943, but is inactivated by depolariza
179  adult stress, antidepressant treatment with imipramine or ketamine, and assessed for treatment respo
180 licated in depression and its treatment with imipramine or ketamine.
181 ocampal neurogenesis, whereas treatment with imipramine or minocycline had minimal or no anti-depress
182 sed patients with HIV infection responded to imipramine or paroxetine at a higher rate than to placeb
183  2 years' duration and who had improved with imipramine or phenelzine were stabilized for 6 months an
184 he inhibition of its binding by desipramine, imipramine, or citalopram.
185 ere randomly assigned to receive fluoxetine, imipramine, or placebo for a 10-week clinical trial.
186 domized prospective fashion with sertraline, imipramine, or placebo.
187 eeks of acute-phase therapy with sertraline, imipramine, or placebo.
188 ed to 12 weeks of treatment with sertraline, imipramine, or placebo.
189 compounds hydroxyzine pamoate (Vistaril) and imipramine pamoate (Tofranil-PM); and the peptide hormon
190                                  Compared to imipramine, paroxetine resulted in a lower incidence of
191           Results showed that Amitriptyline, Imipramine, Paroxetine, and Sertraline had potential ant
192 ol, phenobarbital, pargyline, D-amphetamine, imipramine, piracetam or N-methyl-D-aspartate (NMDA) inc
193 er heart failure, induced with a propranolol-imipramine-plasma expansion treatment.
194 ne of four maintenance treatment conditions: imipramine plus interpersonal psychotherapy, imipramine
195                            Among responders, imipramine produced a response of higher quality.
196 e hypothesis that maintenance treatment with imipramine protects patients with panic disorder and ago
197 d mutagenesis as primary determinants of the imipramine response.
198  Moreover, coadministration of rolipram with imipramine resulted in a more rapid induction of CREB th
199 nt with either cognitive behavior therapy or imipramine; results obtained with emotion-focused psycho
200                                      Chronic imipramine reversed this downregulation and increased hi
201  chemically diverse antidepressants, such as imipramine, rolipram, phenelzine, ketamine, and its meta
202 highest disproportionality for IFIS included imipramine (ROR = 251.66, 95% confidence interval [CI] =
203 8-1.03), carbamazepine (RR 0.68, 0.44-1.06), imipramine (RR 0.95, 0.66-1.36), and paliperidone (RR 0.
204 C5 overexpression in the hippocampus blocked imipramine's ability to reverse depression-like behavior
205                    Our findings suggest that imipramine's proposed activities on forebrain GR functio
206 ; this replicates acute trials demonstrating imipramine's relative ineffectiveness in patients with a
207 ial defeat stress, chronic administration of imipramine significantly improved social interaction in
208 r all antidepressants, except paroxetine and imipramine, started to rise again.
209 tly greater proportion of patients receiving imipramine than those receiving sertraline or placebo di
210  more likely to show a favorable response to imipramine than to sertraline.
211  more patients dropped out of treatment with imipramine than with fluoxetine.
212                                     Doses of imipramine that inhibit 5-HT uptake neither reduce aggre
213 80%) prevented by the amine uptake inhibitor imipramine, the MAO inhibitor pargyline and the MEK inhi
214   Similar findings were not demonstrated for imipramine; this replicates acute trials demonstrating i
215 city exists between IL-10 and IL-12 and that imipramine tips the balance toward an increased IL-12/IL
216 with the substance P antagonist L-760,735 or imipramine to block this response were examined in gerbi
217 rain microsomes were capable of metabolizing imipramine to both hydroxylated and N-demethylated produ
218 n of imipramine, 47% for those switched from imipramine to placebo, and 87% for placebo-treated patie
219 lower relapse rates than those switched from imipramine to placebo.
220  imipramine (mean dosage, 221 mg/d) and from imipramine to sertraline (mean dosage, 163 mg/d) resulte
221 t nonresponders benefited from a switch from imipramine to sertraline, or vice versa, despite a high
222  serves as a "gatekeeper" limiting access of imipramine to the cavity.
223  (d) inhibits binding of [(3)H]TCP and [(3)H]imipramine to the desensitized/carbamylcholine-bound Tor
224 d by antidepressants, e.g., S-citalopram and imipramine, to alleviate symptoms of depression and anxi
225 in the saline treated animals but not in the imipramine treated animals.
226 ine were more chronically depressed than the imipramine-treated patients.
227 ssed rats, similar to classic antidepressant imipramine treatment (10 mg/kg, i.p.).
228 of prophylactic effectiveness of maintenance imipramine treatment and demonstrate that relapse, altho
229 ypes remains unclear, both are alleviated by imipramine treatment during dim night-time light.
230                                              Imipramine treatment is effective for primary depression
231 andomized trial that compared sertraline and imipramine treatment of 531 patients with chronic depres
232  performance, and this effect was rescued by imipramine treatment over the last two weeks.
233                                              Imipramine treatment was safe and associated with improv
234 s in gene expression are reversed by chronic imipramine treatment, and that resilient mice-those resi
235 sponders and nonresponders after ketamine or imipramine treatment.
236 at overlap dramatically with those seen with imipramine treatment.
237 ffects of chronic MAOI (phenelzine) and TCA (imipramine) treatment on neural corticosteroid receptor
238                                              Imipramine typically increased and phenelzine decreased
239   Patients were randomly assigned to receive imipramine, up to 300 mg/d, only (n=83); cognitive-behav
240                               Patients given imipramine, venlafaxine, and duloxetine had more discont
241 suggesting both common and unique effects of imipramine versus ketamine.
242 2 for sertraline vs placebo and P < .001 for imipramine vs placebo).
243 sion (P = .04 and P = .01 for sertraline and imipramine vs placebo, respectively), the Montgomery-Asb
244                                              Imipramine was an effective antidepressant in patients r
245             This hyperacetylation by chronic imipramine was associated with a selective downregulatio
246                                              Imipramine was included because its known efficacy for t
247 e monohydroxylated metabolite (m/z 297.2) of imipramine was observed following chip-based monolithic
248 ps, the effectiveness of both fluoxetine and imipramine was significantly better than that of placebo
249 ween the responses of rabbit and pig FMO1 to imipramine was studied by random chimeragenesis and site
250 ects who completed the trial (for them, only imipramine was superior to placebo at week 12).
251                                              Imipramine was superior to placebo on some self-reported
252                      Another antidepressant, imipramine, was without any effect on allopregnanolone o
253 a human urine sample spiked with 1 microg/mL imipramine were loaded onto eight different monolithic c
254 tely treated patients, 57% (24/42) receiving imipramine were rated as responders compared with 7% (3/
255                               Sertraline and imipramine were significantly better than placebo in imp
256                 However, both paroxetine and imipramine were superior to placebo for patients with lo
257 ysate showed N-demethylation activity toward imipramine, whereas another brain P-450 CYP4F6-expressed
258                                          1e (imipramine), which was a duplicate of Fig.
259 ors, as well as the tricyclic antidepressant imipramine, which inhibits MAO activity and reduces oxid
260 such as chlorpromazine, trifluoperazine, and imipramine, which mimic the effect of cholesterol.
261  receptor, confers significant resistance to imipramine while leaving the responses to 5HT or fluoxet
262 ed the efficacy and safety of paroxetine and imipramine with that of placebo in the treatment of bipo
263 ith the TCAs nortriptyline, clomipramine, or imipramine, with clinical follow-up of 7 weeks.
264 fferences in time to response were seen with imipramine, with women responding significantly more slo
265 e therefore hypothesized that phenelzine and imipramine would also affect brainstem GR gene expressio

 
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