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1 th AD109 2.5/75 mg (P < 0.05 vs. placebo and atomoxetine).
2 to-striatal effective connectivity following atomoxetine.
3 energic state in determining the response to atomoxetine.
4 improvement of response inhibition following atomoxetine.
5 0 mg of the noradrenaline reuptake inhibitor atomoxetine.
6  was not significant for methylphenidate and atomoxetine.
7 rt-term benefits of stimulant medication and atomoxetine.
8 herapy), but this connection was restored by atomoxetine.
9 thesis of an important pharmaceutical agent, atomoxetine.
10 y used ADHD therapeutics methylphenidate and atomoxetine.
11 sign, following either placebo or 40-mg oral atomoxetine.
12 id not use methylphenidate, amphetamines, or atomoxetine.
13 motically released methylphenidate than with atomoxetine.
14 sed methylphenidate was superior to that for atomoxetine.
15 henidate, 30 (43%) subsequently responded to atomoxetine.
16 is of ezetimibe, dapoxetine, duloxetine, and atomoxetine.
17 on to establish the therapeutic potential of atomoxetine.
18 6 to 0.69; amphetamines, 0.40, 0.22 to 0.72; atomoxetine, 0.45, 0.35 to 0.58).
19 ns of the aryloxypropanamine template (e.g., atomoxetine, 2) led to a novel series of 1-(3-amino-2-hy
20  years) with ADHD were randomized to receive atomoxetine (20-50 mg BID, N = 220) or placebo (N = 225)
21 g twice daily (BID) or the active comparator atomoxetine (40 mg BID) vs placebo for 28 days.
22                  The response rates for both atomoxetine (45%) and methylphenidate (56%) were markedl
23 CALL2, which could be rescued by tomoxetine (atomoxetine), a clinical medication for ADHD.
24 rformed a biomarker-driven phase II trial of atomoxetine, a clinically-approved norepinephrine transp
25                                  Response to atomoxetine, a nonstimulant norepinephrine-specific reup
26 compulsivity or under chronic treatment with atomoxetine, a noradrenergic reuptake inhibitor used to
27           To this end, we administered 40 mg atomoxetine, a selective noradrenaline re-uptake inhibit
28 eclinical and clinical studies suggests that atomoxetine, a selective noradrenaline reuptake inhibito
29                  We test this approach using atomoxetine, a selective noradrenaline reuptake inhibito
30 ed four compounds that matched the effect of atomoxetine: aceclofenac, amlodipine, doxazosin, and mox
31  to receive 6 weeks of treatment with either atomoxetine (administered once daily) or placebo.
32  authors assessed the efficacy of once-daily atomoxetine administration in the treatment of children
33 ability were significant only for the use of atomoxetine (aHR, 0.89; 95% CI, 0.82-0.97), especially a
34 rom 19.0 (11.8-28.8) to 11.8 (5.5-21.5) with atomoxetine alone (-38.8%; P < 0.01 vs. placebo).
35 naptic catecholamine levels by administering atomoxetine, an NE transporter blocker, and examined the
36 there was no overall behavioral benefit from atomoxetine, analyses of individual differences revealed
37                  Dropout rates were 5.1% for atomoxetine and 2.7% for placebo, with no significant di
38 using the norepinephrine transporter blocker atomoxetine and demonstrate consistent, causal effects o
39  However, newer non-stimulant drugs, such as atomoxetine and guanfacine, suggest that targeting the n
40 ed only by methylphenidate, relative to both atomoxetine and placebo.
41 ly released methylphenidate with response to atomoxetine and placebo.
42 ated to gains in task-related activation for atomoxetine and reductions in activation for methylpheni
43 e a simple behavioral phenotype generated by atomoxetine and screened the 1200 compound Prestwick Che
44 eported offspring outcomes in pregnancy with atomoxetine and/or methylphenidate and in mothers with A
45 tion of a norepinephrine reuptake inhibitor (atomoxetine) and an antimuscarinic (oxybutynin) on OSA s
46  design of the influence of methylphenidate, atomoxetine, and citalopram on error awareness in 27 hea
47 ethylphenidate and amphetamine formulations, atomoxetine, and extended-release guanfacine to improve
48 esign after single doses of methylphenidate, atomoxetine, and placebo in functional magnetic resonanc
49 such as methylphenidate, dexamphetamine, and atomoxetine, and psychosocial interventions, to those se
50 hat for control medications (alpha agonists, atomoxetine, antidepressants, and mood stabilizers).
51 mulant methylphenidate and the non-stimulant atomoxetine are used in the pharmacotherapy of attention
52                Fluorodeoxyglucose-PET showed atomoxetine-associated increased uptake in hippocampus,
53 iptions for methylphenidate, amphetamine, or atomoxetine at baseline.
54 ved either placebo or a single dose of 40 mg atomoxetine at each session.
55 d amphetamine derivatives, a-2-agonists, and atomoxetine) at baseline assessment.
56        The effects of methylphenidate (MPH), atomoxetine (ATMX), and/or physical exercise (EX) on ori
57 ects of the selective NE re-uptake inhibitor atomoxetine (ATO) and the mixed DA/NE re-uptake inhibito
58                                              Atomoxetine (ATO), a selective noradrenaline reuptake in
59 amphetamine (AMPH; 0.25, 1.0, or 4.0mug), or atomoxetine (ATO; 1.0, 4.0, or 16.0mug) into either medi
60 samples from an AD phase 2 clinical trial of atomoxetine (ATX) demonstrated that abnormal elevations
61 nted by the noradrenaline reuptake inhibitor atomoxetine (ATX) in highly impulsive vulnerable rats.
62 ethylphenidate (MPH), a psychostimulant, and atomoxetine (ATX), a selective norepinephrine reuptake i
63            Treatment with methylphenidate or atomoxetine based on prescription data.
64  increased inter-network connectivity due to atomoxetine between the insula and the hippocampus.
65 rom the pre-supplementary motor cortex; (ii) atomoxetine can enhance downstream modulation of frontal
66 s using the noradrenergic reuptake inhibitor atomoxetine can improve response inhibition in some pati
67           Here we tested the hypotheses that atomoxetine can restore functional brain networks for re
68 lack of sensitivity, as both amphetamine and atomoxetine changed the kinetics of sub-second release.
69  male participants received methylphenidate, atomoxetine, citalopram or placebo during four separate
70 examphetamine, lisdexamphetamine, modafinil, atomoxetine, clonidine) during pregnancy and children of
71    No associations were found for modafinil, atomoxetine, clonidine, and guanfacine.
72                                   In adults, atomoxetine, cognitive behavioural therapy, methylphenid
73 reduced stop-signal reaction time) following atomoxetine correlated with structural connectivity as m
74 e selective noradrenaline reuptake inhibitor atomoxetine could improve response inhibition, gambling
75                                      Rather, atomoxetine decreased V(max) and DAT cell surface expres
76                                The effect of atomoxetine depended on locus coeruleus integrity: parti
77                                 By contrast, atomoxetine did not affect impulsivity in control partic
78                                              Atomoxetine did not alter DAT kinetic parameters or loca
79 ve previously shown that methylphenidate and atomoxetine, drugs widely used for the treatment of atte
80  receiving treatment with methylphenidate or atomoxetine during pregnancy compared with unexposed off
81 ggests the maintenance of methylphenidate or atomoxetine during pregnancy is safe, given that congeni
82 e catecholamine agonists methylphenidate and atomoxetine effectively treat attention-deficit/hyperact
83                                              Atomoxetine enhanced stop-related RIFG activation in pro
84 inically effective drugs methylphenidate and atomoxetine enhanced stopping abilities.
85 pharmaceutical agents, including duloxetine, atomoxetine, fluoxetine and tolterodine.
86                Both the 4 mg BID ABT-894 and atomoxetine groups demonstrated significant improvement
87 %) of the 69 patients who did not respond to atomoxetine had previously responded to osmotically rele
88           Methylphenidate, amphetamines, and atomoxetine had worse tolerability than placebo (methylp
89 dual differences in behavioural responses to atomoxetine highlight the need for patient stratificatio
90 improvements in symptoms with stimulants and atomoxetine; however, data on long-term benefits and ris
91 lphenidate hydrochloride vs the nonstimulant atomoxetine hydrochloride.
92                The principal result was that atomoxetine improved stop-signal reaction times in those
93                                              Atomoxetine improved stopping accuracy on the Stop Signa
94 s in future investigations on the effects of atomoxetine in Parkinson's disease and support the hypot
95 l translational evidence for the efficacy of atomoxetine in remediating decisional impulsivity in CUD
96 in and the norepinephrine reuptake inhibitor atomoxetine, in the treatment of OSA.
97                                              Atomoxetine increased connectivity from the right IFG to
98                  The catecholaminergic agent atomoxetine increased overall arousal and shifted the en
99               These results suggest that (i) atomoxetine increases sensitivity of the inferior fronta
100                             In addition, the atomoxetine-induced change in connectivity from right IF
101 sion of the noradrenaline reuptake inhibitor atomoxetine into these same regions also reduced social
102                 Once-daily administration of atomoxetine is an effective treatment for children and a
103                             Further study of atomoxetine is warranted for repurposing the drug to slo
104 gh donepezil) and catecholaminergic (through atomoxetine) levels in humans performing a visuo-spatial
105 ity in compulsive disorders and suggest that atomoxetine may be a useful treatment for patients suffe
106 ctivation and frontostriatal connectivity by atomoxetine may improve response inhibition in Parkinson
107      The results support the hypothesis that atomoxetine may restore prefrontal networks related to e
108  short term, alpha-2 agonists, amphetamines, atomoxetine, methylphenidate, and viloxazine showed medi
109 f treatment with methylphenidate (n = 18) or atomoxetine (n = 18) using a parallel-groups design.
110 assigned to receive 0.8-1.8 mg/kg per day of atomoxetine (N=222), 18-54 mg/day of osmotically release
111                                      Neither atomoxetine nor oxybutynin reduced the AHI when administ
112 atments that augment noradrenergic activity (atomoxetine; norepinephrine reuptake inhibitor) during e
113  compared the effects of methylphenidate and atomoxetine on brain function in ADHD, and none during t
114               We investigated the effects of atomoxetine on decisional impulsivity in patients with C
115 e selective noradrenaline reuptake inhibitor atomoxetine on response inhibition in a stop-signal para
116 he inhibitory effects of methylphenidate and atomoxetine on social play are mediated through a distri
117    A single dose of methylphenidate, but not atomoxetine or citalopram, significantly improved the ab
118  31, 2023, with the following search terms: (atomoxetine OR methylphenidate) AND (pregnancy).
119 ce of Alzheimer's disease were randomized to atomoxetine or placebo treatment.
120                      Patients received 40 mg atomoxetine or placebo, orally.
121 pharmacological challenge with 40 mg of oral atomoxetine or placebo.
122           Twenty-one patients received 40 mg atomoxetine or placebo.
123 , crossover trial comparing 1 night of 80 mg atomoxetine plus 5 mg oxybutynin (ato-oxy) to placebo ad
124 NCLUSIONS Treatment with methylphenidate and atomoxetine produces symptomatic improvement via both co
125       This study investigates the effects of atomoxetine ((R)-N-methyl-gamma-(2-methylphenoxy)-benzen
126                                       First, atomoxetine reduced the strength of inter-regional corre
127  received prescribed stimulant medication or atomoxetine relative to the risk during months in which
128  placebo were reduced by methylphenidate and atomoxetine, respectively, but neither survived rigorous
129 nts who received methylphenidate followed by atomoxetine responded better to one or the other, sugges
130                                              Atomoxetine robustly increased plasma and CSF norepineph
131                                              Atomoxetine selectively reduced decisional impulsivity i
132                                              Atomoxetine significantly reduced CSF Tau and pTau, norm
133 1) was similar to those observed in previous atomoxetine studies that used twice-daily dosing.
134                                              Atomoxetine taken alone decreased total sleep time (P <
135 re for Evidence-Based Medicine criteria) and atomoxetine than for the extended-release alpha2-adrener
136 he individual differences in the response to atomoxetine: the reduction in stop-signal reaction time
137 the way to new stratified clinical trials of atomoxetine to treat impulsivity in selected patients wi
138                               Outcomes among atomoxetine-treated patients were superior to those of t
139 ined the effects of daily methylphenidate or atomoxetine treatment across 7 days on circadian clock g
140                                              Atomoxetine treatment also significantly altered CSF abu
141                                              Atomoxetine treatment both decreased impulsivity and pre
142                                        Prior atomoxetine treatment did not augment cocaine self-admin
143 HR OFC, indicating that inhibition of NET by atomoxetine treatment during adolescence indirectly redu
144                                  In summary, atomoxetine treatment was safe, well tolerated and achie
145 reated with methylphenidate were switched to atomoxetine under double-blind conditions.
146                                        Thus, atomoxetine, unlike methylphenidate, does not enhance vu
147 as observed in young adults with ADHD in the atomoxetine versus placebo group as measured by changes
148 tly greater mean reductions were seen in the atomoxetine versus placebo group for the BRIEF-A Global
149 wed a greater increase in prior weighting on atomoxetine versus placebo.
150                                              Atomoxetine was associated with a significant reduction
151    RESULTS Treatment with methylphenidate vs atomoxetine was associated with comparable improvements
152 evealed that enhanced response inhibition by atomoxetine was associated with increased RIFG activatio
153 herapy, dexamphetamine, methylphenidate, and atomoxetine were associated with decreased risk of nonps
154 dol, olanzapine, mirtazapine, bupropion, and atomoxetine were associated with increased odds of OUD r
155 eas, improved behavioral performance whereas atomoxetine, which increases dopamine and noradrenaline

 
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