Research and Clinical Trials on Escitalopram (Lexapro, Cipralex)

By Dr Greg Mulhauser
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This list of current clinical research trials on Escitalopram (Lexapro, Cipralex) is followed by a short set of abstracts from the most recent research articles published on the drug.

Article Contents

Escitalopram (Lexapro, Cipralex) Clinical Research Trials

From our searchable database at ClinicalTrialsFeeds.org, this list includes all the latest information about clinical trials involving Escitalopram (Lexapro, Cipralex).

 

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Current Research Literature on Escitalopram (Lexapro, Cipralex)

Here are abstracts for some of the latest research articles to have appeared on Escitalopram (Lexapro, Cipralex):

An open pilot study of the combination of escitalopram and bupropion-SR for outpatients with major depressive disorder.

J Psychiatr Pract. 2008 Sep; 14(5): 271-80
Leuchter AF, Lesser IM, Trivedi MH, Rush AJ, Morris DW, Warden D, Fava M, Wisniewski SR, Luther JF, Perales M, Gaynes BN, Stewart JW
OBJECTIVE: Monotherapy with a selective serotonin reuptake inhibitor (SSRI) is the most common initial treatment for major depressive disorder (MDD), but this monotherapy leads to remission in fewer than a third of patients. The combination of the SSRI escitalopram and bupropion-SR is commonly used for treating patients with MDD who have had an inadequate response to antidepressant monotherapy. This pilot study was conducted to evaluate this combination in the treatment of MDD in patients with chronic or recurrent MDD to estimate safety, tolerability, and remission rates. METHOD: In this study, 51 outpatients with chronic or recurrent non-psychotic MDD were treated with a combination of escitalopram and bupropion-SR for up to 12 weeks. Participants were started on escitalopram at 10 mg/day, and bupropion-SR was then added at week 1, starting at 150 mg/day. The maximum dose of escitalopram was 20 mg/day and the maximum dose of bupropion-SR was 400 mg/day. RESULTS: Rates of response (62%) and remission (50%) at study exit (based on participants for whom at least one post-baseline measure was collected) were significantly higher than is typical for SSRI monotherapy. The level of treatment emergent adverse events was low, and only 3 participants (6%) discontinued treatment due to side effects. The mean maximum dose of escitalopram was 18 mg/day, which was achieved by week 6, and the mean dose at study exit was also 18 mg/day. The mean maximum dose of bupropion-SR was 329 mg/day, which was achieved by week 8, and the mean dose at study exit was 327 mg/day. CONCLUSIONS: These results suggest that the combination of escitalopram and bupropion-SR is effective and well tolerated. Further controlled trials comparing this combination with monotherapy are needed.

Augmenting serotonin neurotransmission with citalopram modulates emotional expression decoding but not structural encoding of moderate intensity sad facial emotional stimuli: an event-related potential (ERP) investigation.

J Psychopharmacol. 2008 Oct 2;
Labuschagne I, Croft R, Phan K, Nathan P
Abstract Antidepressants targeting the serotonergic system have been shown to modulate biases in emotional processing. The effects of serotonergic modulation on the temporal course of emotional processing (accruing within milliseconds) are unknown. Furthermore, it is unknown how serotonin affects different stages of facial emotional processing. The current study investigated the effects of acute serotonin augmentation on event-related potential (ERP) measures associated with 'structural encoding' (N170) and emotion 'expression decoding' (N250 and a late slow-wave positive potential [LPP]) of happy and sad facial stimuli, relative to neutral facial stimuli. The study was a double-blind, placebo-controlled, cross-over design, in which 14 healthy male participants completed a facial recognition task under two acute treatment conditions: 1) placebo (PLB) and 2) 20 mg citalopram (CIT). ERP recording were conducted while subjects viewed neutral, happy and sad facial stimuli. Findings indicated that under PLB, the N170 was not modulated by valence (happy or sad versus neutral), but the N250 and LPP were enhanced for processing happy (relative to neutral) faces. Citalopram had no effect on the N170, but it enhanced the LPP for processing sad (relative to neutral) faces. These findings suggest that serotonin enhancement has selective and temporal effects on emotional face processing, with evidence for modulating processes associated with 'expression decoding' but not 'structural encoding'. The enhanced cortical response to perception of moderately intense sad facial expressions following citalopram administration may relate to the cognitive processing of the social relevance or significance of such ambiguous stimuli.

The pharmacokinetics of standard antidepressants with aripiprazole as adjunctive therapy: studies in healthy subjects and in patients with major depressive disorder.

J Psychopharmacol. 2008 Oct 2;
Boulton D, Balch A, Royzman K, Patel C, Berman R, Mallikaarjun S, Reeves R
Abstract Possible effects of the atypical antipsychotic aripiprazole on the pharmacokinetics of standard antidepressant therapies (ADTs) were assessed in two open-label, non-randomised studies in healthy subjects (Studies 1 and 2) and two placebo-controlled studies in patients with major depressive disorder (MDD) (Studies 3 and 4). Healthy subjects received venlafaxine 75 mg/day (Study 1; N = 38) or escitalopram 10 mg/day (Study 2; N = 25) with the addition of aripiprazole 10-20 mg/day (10 mg/day fixed dose in Study 2) for 14 days. Patients with MDD (N = 498; Studies 3 and 4) received escitalopram (10-20 mg/day), fluoxetine (20-40 mg/day), paroxetine controlled-release (37.5-50 mg/day), sertraline (100-150 mg/day) or venlafaxine extended-release (150-225 mg/day) for 8 weeks plus placebo. Incomplete responders were randomised (1:1) to placebo or adjunctive aripiprazole 2-20 mg/day. Blood samples were collected for pharmacokinetic analysis of ADTs. Plasma concentration-time data from Studies 3 and 4 were combined for statistical analysis. In healthy subjects, point estimates [90% CI] for the ratios of geometric means of Cmax (venlafaxine 1.148 [1.083-1.217]; escitalopram 1.04 [0.99-1.09]) and AUCTAU (venlafaxine 1.183 [1.130-1.238]; escitalopram 1.07 [1.04-1.11]) indicated no meaningful increase in ADT exposure in the presence of aripiprazole. In patients, point estimates for mean plasma concentration ratios indicated no substantial effect of aripiprazole on any ADT escitalopram 0.970 [0.911-1.033], fluoxetine 1.177 [1.049-1.321], paroxetine 0.730 [0.598-0.892], sertraline 0.958 [0.887-1.035] or venlafaxine 0.966 [0.887-1.051]. Aripiprazole had no meaningful effects on the pharmacokinetics of standard ADTs in either healthy subjects or patients with MDD.

Neurokinin(1) Antagonists Potentiate Antidepressant Properties of Serotonin Reuptake Inhibitors, Yet Blunt Their Anxiogenic Actions: A Neurochemical, Electrophysiological, and Behavioral Characterization.

Neuropsychopharmacology. 2008 Oct 1;
Gobert A, Brocco M, Dekeyne A, Di Cara B, Bouchez G, Lejeune F, Gannon RL, Millan MJ
Though neurokinin(1) (NK(1)) receptor antagonists are active in experimental models of depression, clinical efficacy has proven disappointing. This encourages interest in association of NK(1) receptor blockade with inhibition of serotonin (5-HT) reuptake. The selective NK(1) antagonist, GR205171, dose-dependently enhanced citalopram-induced elevations of extracellular levels of 5-HT in frontal cortex, an action expressed stereospecifically vs its less active distomer, GR226206. Further, increases in 5-HT levels in dorsal hippocampus, basolateral amygdala, nucleus accumbens, and striatum were likewise potentiated, and GR205171 similarly facilitated the influence of fluoxetine upon levels of 5-HT, as well as dopamine and noradrenaline. In parallel electrophysiological studies, the inhibitory influence of citalopram and fluoxetine upon raphe-localized serotonergic neurones was stereospecifically blunted by GR205171. Antidepressant actions of citalopram in a forced-swim test in mice were stereospecifically potentiated by GR205171, and it also enhanced attenuation by citalopram of stress-related ultrasonic vocalizations in rats. Further, GR205171 and citalopram additively abrogated the advance in circadian rhythms provoked by exposure to light in hamsters. By contrast, GR205171 stereospecifically blocked anxiogenic actions of citalopram in social interaction procedures in rats and gerbils, and stereospecifically abolished facilitation of fear-induced foot tapping by fluoxetine in gerbils. By analogy to GR205171, a further NK(1) antagonist, RP67580, enhanced the influence of citalopram upon frontocortical levels of 5-HT and potentiated its actions in the forced swim test. In conclusion, NK(1)receptor blockade differentially modulates functional actions of SSRIs: antidepressant properties are reinforced, whereas anxiogenic effects are attenuated. Combined NK(1) receptor antagonism/5-HT reuptake inhibition may offer advantages in the management of depressed and anxious states.Neuropsychopharmacology advance online publication, 1 October 2008; doi:10.1038/npp.2008.176.

Evidence for modulation of facial emotional processing bias during emotional expression decoding by serotonergic and noradrenergic antidepressants: an event-related potential (ERP) study.

Psychopharmacology (Berl). 2008 Sep 30;
Kerestes R, Labuschagne I, Croft RJ, O'Neill BV, Bhagwagar Z, Phan KL, Nathan PJ
RATIONALE: Serotonergic (SSRI) and noradrenergic (NRI) antidepressants modulate biases in emotional processing such that perceptual bias is shifted away from negative and towards positive emotional material. However, the effects of serotonergic and noradrenergic modulation on the temporal course (occurring in milliseconds) of emotional processing, and in particular, the rapid physiological changes associated with the different stages of emotional processing, are unknown. OBJECTIVE: The current study assessed the effects of acute serotonergic (i.e. with citalopram) and noradrenergic (i.e. with reboxetine) augmentation on event-related potential (ERP) measures associated with 'structural encoding' (N170) and emotion expression decoding (N250 and late positive potential [LPP]) for positive (happy) and negative (sad) facial stimuli relative to neutral facial stimuli. MATERIALS AND METHODS: This study employed a double-blind, placebo-controlled, cross-over design in which 12 healthy male participants completed a facial expression recognition task tested under three acute conditions: (a) placebo, (b) citalopram (20 mg) and (c) reboxetine (4 mg). RESULTS: Both citalopram and reboxetine had no effect on the N170 ERP component associated with structural encoding, but potentiated the N250 associated with happy (relative to neutral) emotional facial expression decoding. Both drugs had no valence effects on later ERP measures of emotion expression decoding (LPP). CONCLUSIONS: Citalopram and reboxetine have selective effects on the temporal course of emotional processing with evidence to suggest specific effects on emotion expression decoding of positive (happy) emotional facial stimuli as evidenced by changes in the attention-modulated N250 but not structural encoding. These findings provide physiological evidence that antidepressants may shift perceptual biases in emotional processing away from negative and towards positive stimuli.

 

This page was last reviewed by Dr Greg Mulhauser, Friday, 4 July 2008.

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