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):

Discriminative stimulus properties of the "atypical" antidepressant, mirtazapine, in rats: a pharmacological characterization.

Psychopharmacology (Berl). 2008 Aug 16;
Dekeyne A, Millan MJ
RATIONALE: Though interoceptive properties of antidepressants have been described, discriminative stimulus (DS) properties of mirtazapine, which does not affect monoamine reuptake, remain uncharacterized. OBJECTIVES: The objectives of the study are to train rats to recognize a mirtazapine DS, then perform substitution studies with other antidepressants and drugs acting at sites occupied by mirtazapine. MATERIALS AND METHODS: Using a two-lever, fixed-ratio 10 schedule, rats were trained to discriminate mirtazapine (2.5 mg/kg, i.p.) from saline. RESULTS: Sessions, 63 +/- 8, were necessary to reach the criterion for 14 rats that all subsequently recognized (100%) mirtazapine at the training dose. Mirtazapine blocks serotonin (5-HT)(2C) receptors, and the 5-HT(2C) antagonists, SB242,084, SB243,213 and S32006, revealed dose-dependent and full (>/=80%) substitution at doses of 2.5, 2.5, and 0.63 mg/kg, respectively. By contrast, the 5-HT(2A) antagonists, MDL100,907 and SR46349-B, the 5-HT(2B) antagonist, SB204,741, and the 5-HT(3) antagonist, ondansetron, showed no significant substitution. Though mirtazapine indirectly recruits 5-HT(1A) receptors, the 5-HT(1A) agonists, buspirone and 8-OH-DPAT, did not substitute. Mirtazapine blocks alpha(2)-adrenoceptors, but several alpha(2)-adrenoceptor antagonists (yohimbine, RX821,002 and atipamezole) failed to substitute. Despite blockade by mirtazapine of histamine H(1) receptors, no substitution was seen with the selective H(1) antagonist, pyrilamine. Finally, the selective noradrenaline reuptake inhibitor, reboxetine (0.16), fully substituted for mirtazapine, whereas the 5-HT/noradrenaline reuptake inhibitors, duloxetine and S33005, several 5-HT reuptake inhibitors (citalopram, fluvoxamine, and paroxetine) and the dopamine reuptake inhibitors, bupropion and GBR12,935, did not substitute. CONCLUSION: Mirtazapine elicits a DS in rats for which selective antagonists at 5-HT(2C) receptors display dose-dependent substitution, whereas drugs acting at other sites recognized by mirtazapine are ineffective.

Impact of escitalopram treatment on Quality of Life Enjoyment and Satisfaction Questionnaire scores in major depressive disorder and generalized anxiety disorder.

Int Clin Psychopharmacol. 2008 Sep; 23(5): 276-86
Demyttenaere K, Andersen HF, Reines EH
Administration of the same Quality of Life Enjoyment and Satisfaction Questionnaire (Q-LES-Q) in major depressive disorder (MDD) and in generalized anxiety disorder (GAD) before and after treatment allowed us to compare quality of life enjoyment and satisfaction in these two disorders and to compare outcome based on symptoms versus functioning. Q-LES-Q and symptom-specific Montgomery-Asberg Depression Rating Scale (MADRS) and Hamilton Anxiety Scale (HAMA) data from eight randomized, 8-week, double-blind, placebo-controlled clinical trials with escitalopram were used. MDD (n=1140) or GAD (n=1045) patients report a substantial degree of quality of life enjoyment and satisfaction impairment (baseline scores 64% and 76% of community norm, respectively). Treatment resulted in statistically and clinically significant improvement in quality of life enjoyment and satisfaction. The improvement was greater in patients treated with escitalopram than with placebo. In MDD, the majority of remitters (MADRS

Escitalopram in the treatment of obsessive-compulsive disorder: a double blind placebo control trial.

J Ayub Med Coll Abbottabad. 2007 Oct-Dec; 19(4): 58-63
Khan MN, Hotiana UA, Ahmad S
BACKGROUND: The tolerability and efficacy for patients with obsessive-compulsive disorder (OCD) in a large, sample on Escitalopram was studied. METHODS: A total of 100 adults with a confirmed diagnosis of OCD were included. The percentage of patients with an adequate drug trial, defined as 42 days of continuous treatment with a serotonin- reuptake inhibitor or placebo at dosages at or above established minimal effective dosages. RESULTS: Ninety-six percent of the adults who were newly diagnosed with OCD in the index year had an adequate trial of medication after their first visit for OCD. By the second half of 42 days the patient who were responding to the treatment were randomly allocated to two groups. One group received the same drug and other group was given placebo. The results were complied at the end of three months of each patient treatment. No additional psychotherapy was offered to these patients during this time period. CONCLUSIONS: Despite the typically chronic course of OCD, many patients with OCD responded to the Esciatolpram at the dosage of twenty milligram per day.

Clinically relevant pharmacokinetic drug interactions with second-generation antidepressants: An update.

Clin Ther. 2008 Jul; 30(7): 1206-27
Spina E, Santoro V, D'Arrigo C
Background: The second-generation antidepressants include selective serotonin reuptake inhibitors (SSRIs), serotonin and norepinephrine reuptake inhibitors (SNRIs), and other compounds with different mechanisms of action. All second-generation antidepressants are metabolized in the liver by the cytochrome P450 (CYP) enzyme system. Concomitant intake of inhibitors or inducers of the CYP isozymes involved in the biotransformation of specific antidepressants may alter plasma concentrations of these agents, although this effect is unlikely to be associated with clinically relevant interactions. Rather, concern about drug interactions with second-generation antidepressants is based on their in vitro potential to inhibit >/=1 CYP isozyme. Objective: The goal of this article was to review the current literature on clinically relevant pharmacokinetic drug interactions with second-generation antidepressants. Methods: A search of MEDLINE and EMBASE was conducted for original research and review articles published in English between January 1985 and February 2008. Among the search terms were drug interactions, second-generation antidepressants, newer antidepressants, SSRIs, SNRIs, fluoxetine, paroxetine, fluvoxamine, sertraline, citalopram, escitalopram, venlafaxine, duloxetine, mirtazapine, reboxetine, bupropion, nefazodone, pharmacokinetics, drug metabolism, and cytochrome P450. Only articles published in peerreviewed journals were included, and meeting abstracts were excluded. The reference lists of relevant articles were hand-searched for additional publications. Results: Second-generation antidepressants differ in their potential for pharmacokinetic drug interactions. Fluoxetine and paroxetine are potent inhibitors of CYP2D6, fluvoxamine markedly inhibits CYP1A2 and CYP2C19, and nefazodone is a substantial inhibitor of CYP3A4. Therefore, clinically relevant interactions may be expected when these antidepressants are coadministered with substrates of the pertinent isozymes, particularly those with a narrow therapeutic index. Duloxetine and bupropion are moderate inhibitors of CYP2D6, and sertraline may cause significant inhibition of this isoform, but only at high doses. Citalopram, escitalopram, venlafaxine, mirtazapine, and reboxetine are weak or negligible inhibitors of CYP isozymes in vitro and are less likely than other second-generation antidepressants to interact with co-administered medications. Conclusions: Second-generation antidepressants are not equivalent in their potential for pharmacokinetic drug interactions. Although interactions may be predictable in specific circumstances, use of an antidepressant with a more favorable drug-interaction profile may be justified.

Serotonin transporter gene polymorphisms in patients with chronic tension-type headache: A preliminary study.

Neurol India. 2008 Apr-Jun; 56(2): 156-60
Akcali A, Tataroglu C, Erdal E, Aydin N, Pehlivan S
Background and Objectives: This study is designed to understand the pathophysiology of one of the most serious health problems, chronic tension-type headache (CTTH). Two polymorphic sites in serotonin transporter protein gene attracted much interest. These are: the variable number of tandem repeats (VNTR) and 5'-flanking promoter region (5-HTTLPR). Materials and Methods: VNTR and 5-HTTLPR polymorphisms were investigated in 126 CTTH patients and 138 healthy control subjects. The patients were being treated with amitripytyline or citalopram or sertraline (SSRI). The polymerase chain reaction (PCR) method was used to investigate the polymorphisms in the serotonin transporter protein gene. Results: There were no statistically significant results based on the 5-HTTLPR gene alleles, however, STin 2.12/12 genotype and STin 2.12 allele were seen to predominate the control group. In order to investigate the combined effect of the two polymorphic loci on the 5-HTT gene expression, samples were separated into nine groups. Genotypes (S/S-12/10) and (L/S-12/10) displayed statistically significant frequency in the CTTH group than in the control group. No significant differences were noticed between the 5-HTTLPR and VNTR haplotype groups and success in treatment. Conclusion: It is possible to make reliable comparisons and hypothesis about the homozygous and/or heterozygous presence of S and STin 12/10 alleles which may be in interaction with CTTH. On the other hand, the presence of homozygous L and STin12 alleles may play a protective role against CTTH. It is also possible that heterogeneity among diseases showing the same clinical research will require a lot of effort for individual identification.

 

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

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