Research and Clinical Trials on Citalopram (Celexa, Cipramil, Seropram)

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By Dr Greg Mulhauser

This list of current clinical research trials on Citalopram (Celexa, Cipramil, Seropram) is followed by a short set of abstracts from the most recent research articles published on the drug.

Article Contents

Citalopram (Celexa, Cipramil, Seropram) Clinical Research Trials

From our searchable database at ClinicalTrialsFeeds.org, this list includes all the latest information about clinical trials involving Citalopram (Celexa, Cipramil, Seropram).

 

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Current Research Literature on Citalopram (Celexa, Cipramil, Seropram)

Here are abstracts for some of the latest research articles to have appeared on Citalopram (Celexa, Cipramil, Seropram):

Metabolite identification in rat brain microdialysates by direct infusion nanoelectrospray ionization after desalting on a ZipTip and LTQ/Orbitrap mass spectrometry.

Rapid Commun Mass Spectrom. 2009 Nov 16; 23(24): 4003-4012
Erve JC, Beyer CE, Manzino L, Talaat RE
Analyzing brain microdialysate samples by mass spectrometry is challenging due to the high salt content of the artificial cerebral spinal fluid (aCSF), low analyte concentrations and small sample volumes collected. A drug and its major metabolites can be examined in brain microdialysates by targeted approaches such as selected reaction monitoring (SRM) which provides selectivity and high sensitivity. However, this approach is not well suited for metabolite profiling in the brain which aims to determine biotransformation pathways. Identifying minor metabolites, or metabolites that arise from brain metabolism, remains a challenge and, for a drug in early discovery, identification of metabolites present in the brain can provide useful information for understanding the pharmacological activity and potential toxicological liabilities of the drug. A method is described here for rapid metabolite profiling in brain microdialysates that involves sample clean-up using C18 ZipTips to remove salts followed by direct infusion nanoelectrospray with an LTQ/Orbitrap mass spectrometer using real-time internal recalibration. Full scan mass spectra acquired at high resolving power (100 K at m/z 400) were examined manually and with mass defect filtering. Metabolite identification was aided by sub-parts-per-million mass accuracy and structural characterization was accomplished by tandem mass spectrometry (MS/MS) experiments in the Orbitrap or LTQ depending on the abundance of the metabolite. Using this approach, brain microdialysate samples from rats dosed with one of four CNS drugs (imipramine, reboxetine, citalopram or trazodone) were examined for metabolites. For each drug investigated, metabolites, some of which not previously reported in rat brain, were identified and characterized. Copyright (c) 2009 John Wiley & Sons, Ltd.

Change in cognitive functioning following acute antidepressant treatment in late-life depression.

Am J Geriatr Psychiatry. 2009 Oct; 17(10): 881-8
Culang ME, Sneed JR, Keilp JG, Rutherford BR, Pelton GH, Devanand DP, Roose SP
OBJECTIVE: Selective Serotonin Reuptake Inhibitors (SSRIs) are the most commonly prescribed medications for geriatric depression. The association of late-life depression and cognitive impairment has been well documented. However, there have been few placebo-controlled trials examining the impact of SSRIs on cognitive functioning. DESIGN: Prepost neuropsychological (NP) data collected as part of an 8-week, double-blind, placebo-controlled trial of citalopram in depressed patients aged 75 years and older were used to examine change in cognitive functioning. Setting: University-affiliated outpatient psychiatry clinics. PARTICIPANTS: One hundred seventy-four community-dwelling men and women aged 75 years or older with nonpsychotic unipolar depression. MEASUREMENTS: NP assessments included mental status (Mini-Mental State Examination), psychomotor speed (Wechsler Adult Intelligence Scale-III Digit Symbol Subtest), reaction time (Choice Reaction Time), visual-spatial skill (Judgment of Line Orientation), executive functioning (Stroop Color/Word Test), and memory (Buschke Selective Reminding Test). RESULTS: Differences in the pattern of change by treatment group depended on responder status. Citalopram nonresponders were the only group to decline on verbal learning and psychomotor speed. Citalopram responders showed significant improvement in visuospatial functioning, when compared with nonresponders in either condition, but their improvement was not greater than responders on placebo. Citalopram responders showed greater improvement on psychomotor speed than citalopram nonresponders, but their improvement was not greater than placebo responders or nonresponders. CONCLUSIONS: Medication may have a deleterious effect on some aspects of cognition among patients aged 75 years and older who have not responded. This suggests that patients should not be maintained on a medication if they have not had an adequate response.

Differential inhibitory effects of drugs acting at the noradrenaline and 5-hydroxytrptamine transporters in rat and human neocortical synaptosomes.

Br J Pharmacol. 2009 Nov 12;
Mantovani M, Dooley D, Weyerbrock A, Jackisch R, Feuerstein T
Background and purpose: Although the amino acid sequences of rat and human 5-hydroxytryptamine (5-HT) and noradrenaline (NA) transporters (i.e. SERT and NET) are highly homologous, species differences exist in the inhibitory effects of drugs acting at these transporters. Therefore, comparison of the potencies of drugs acting at SERT and NET in native human and rat neocortex may serve to more accurately predict their clinical profile. Experimental approach: Synaptosomes prepared from fresh human and rat neocortical tissues were used for [(3)H]-5-HT and [(3)H]-NA saturation and competition uptake experiments. The drugs tested included NA reuptake inhibitors (desipramine, atomoxetine and (S,S)-reboxetine), 5-HT reuptake blockers (citalopram, fluoxetine and fluvoxamine) and dual 5-HT/NA reuptake inhibitors (duloxetine and milnacipran). Key results: In saturation experiments on synaptosomal [(3)H]-5-HT and [(3)H]-NA uptake, the dissociation constants did not indicate species differences although a smaller density of both SERT and NET was observed in human tissues. In competition experiments with the various drugs, marked species differences in their potencies were observed, especially at SERT. The rank order of selectivity ratios (SERT/NET) in human neocortex was as follows: citalopram >/= duloxetine = fluvoxamine >/= fluoxetine > milnacipran > desipramine = atomoxetine > (S,S)-reboxetine. Significant species differences in these ratios were observed for duloxetine, atomoxetine and desipramine. Conclusions and implications: This study provides the first compilation of drug potency at native human neocortical SERT and NET. The significant species differences (viz., human vs. rat) in drug potency suggest that the general use of rodent data should be limited to predict clinical efficacy or profile.

Effects of Selective Serotonin Reuptake Inhibitors on Timolol Metabolism in Human Liver Microsomes and Cryo-Preserved Hepatocytes.

Basic Clin Pharmacol Toxicol. 2009 Nov 11;
Volotinen M, Korjamo T, Tolonen A, Turpeinen M, Pelkonen O, Hakkola J, Mäenpää J
Timolol has been widely used in the treatment of glaucoma. Topically applied, timolol may cause adverse cardiovascular effects due to systemic absorption through the nasolacrimal duct. Timolol is mainly metabolized by cytochrome P450 2D6 (CYP2D6) in the liver. The aim of the present study was to characterize further the metabolism of timolol in vitro. Especially the effect of several drugs such as selective serotonin reuptake inhibitors on the metabolism of timolol was evaluated. In human liver microsomes, four timolol metabolites were identified, in cryo-preserved hepatocytes nine. In both in vitro experiments, the hydroxy metabolite M1 was the main metabolite. The in vivo half-life predicted for timolol was 3.7 hr. in cryo-preserved hepatocytes, corresponding to the half-life of timolol in humans in vivo. Fluoxetine, paroxetine, sertraline, citalopram and fluvoxamine inhibited the formation of M1 in microsomes with IC(50) values of 1.4, 2.0, 3.5, 21 and 20 muM, respectively. In human cryo-preserved hepatocytes, the IC(50) values for fluoxetine, paroxetine and fluvoxamine were 0.7, 0.5 and 5.9 muM, respectively. In conclusion, compounds known to be potent CYP2D6 inhibitors inhibited timolol metabolism in in vitro experiments. The present results strongly suggest that fluoxetine and paroxetine may significantly affect the metabolism of timolol also in vivo and may thus potentiate the adverse cardiovascular effects of topically administered timolol.

Drug fails to subdue repetitive behavior in children with autism spectrum disorders.

Harv Ment Health Lett. 2009 Oct; 26(4): 7

 

This page was last reviewed by Dr Greg Mulhauser, Monday, 1 June 2009.

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