Research and Clinical Trials on Fluvoxamine (Luvox, Faverin)

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This list of current clinical research trials on Fluvoxamine (Luvox, Faverin) is followed by a short set of abstracts from the most recent research articles published on the drug.

Fluvoxamine (Luvox, Faverin) Clinical Research Trials

From our searchable database at ClinicalTrialsFeeds.org, this list includes all the latest information about clinical trials involving Fluvoxamine (Luvox, Faverin).

 

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Current Research Literature on Fluvoxamine (Luvox, Faverin)

Here are abstracts for some of the latest research articles to have appeared on Fluvoxamine (Luvox, Faverin):

Meta-analysis of major depressive disorder relapse and recurrence with second-generation antidepressants.

Psychiatr Serv. 2008 Oct; 59(10): 1121-30
Hansen R, Gaynes B, Thieda P, Gartlehner G, Deveaugh-Geiss A, Krebs E, Lohr K
OBJECTIVE: This meta-analysis reviewed data on the efficacy and effectiveness of second-generation antidepressants for preventing major depression relapse and recurrence during continuation and maintenance phases of treatment, respectively. METHODS: MEDLINE, EMBASE, and PsycINFO, the Cochrane Library, and International Pharmaceutical Abstracts were searched for the period of January 1980 through April 2007 for reviews, randomized controlled trials, meta-analyses, and observational studies on the topic. Two persons independently reviewed abstracts and full-text articles using a structured data abstraction form to ensure consistency in appraisal and data extraction. RESULTS: Four comparative trials and 23 placebo-controlled trials that addressed relapse or recurrence prevention were included. Results of comparative trials have not demonstrated statistically significant differences between duloxetine and paroxetine, fluoxetine and sertraline, fluvoxamine and sertraline, and trazodone and venlafaxine. Pooled data for the class of second-generation antidepressants compared with placebo suggested a relatively large effect size that persists over time. For preventing both relapse and recurrence, the number of patients needed to treat is five (95% confidence interval of 4 to 6). Differences in the length of open-label treatment before randomization, drug type, and trial duration did not affect pooled estimates of relapse rates. Across all trials, 7% of patients randomly assigned to receive active treatment and 5% of patients randomly assigned to receive a placebo discontinued treatment because of adverse events. CONCLUSIONS: This review demonstrates the overall benefits of continuation- and maintenance-phase treatment of major depression with second-generation antidepressants and emphasizes the need for additional studies of comparative differences among drugs.

Intracerebroventricular fluvoxamine administration inhibited pain behavior but increased Fos expression in affective pain pathways.

Pharmacol Biochem Behav. 2008 Sep 12;
Hayashi T, Miyata M, Nagata T, Izawa Y, Kawakami Y
Anti-nociceptive effects of fluvoxamine, administered by intracerebroventricular (i.c.v.) injection, include inhibited pain behavior in both formalin-induced acute pain (p

In vitro inhibition of CYP1A2 by model inhibitors, anti-inflammatory analgesics and female sex steroids: predictability of in vivo interactions.

Basic Clin Pharmacol Toxicol. 2008 Aug; 103(2): 157-65
Karjalainen MJ, Neuvonen PJ, Backman JT
The cytochrome P450 enzyme CYP1A2 is crucial for the metabolism of many drugs, for example, tizanidine. As the effects of several non-steroidal anti-inflammatory drugs (NSAID) and female sex steroids on CYP1A2 activity in vitro are unknown, their effects on phenacetin O-deethylation were studied and compared with the effects of model inhibitors in human liver microsomes, followed by prediction of their interaction potential with tizanidine in vivo. In vitro, fluvoxamine, tolfenamic acid, mefenamic acid and rofecoxib potently inhibited CYP1A2 [the 50% inhibitory concentration (IC(50)) < 10 microM]. Ethinyloestradiol, celecoxib, desogestrel and zolmitriptan were moderate (IC(50) 20-200 microM), and etodolac, ciprofloxacin, etoricoxib and gestodene weak inhibitors of CYP1A2 (IC(50) > 200 microM). At 100 microM, the other tested NSAIDs and steroids inhibited CYP1A2 less than 35%. Pre-incubation increased the inhibitory effects of rofecoxib, progesterone and desogestrel. Using the free portal plasma inhibitor concentration and the competitive inhibition model, the effect of fluvoxamine and the lack of effects of tolfenamic acid and celecoxib on tizanidine pharmacokinetics in human beings were well predicted. However, the effects of ciprofloxacin, rofecoxib and oral contraceptives were greatly underestimated even when the predictions were based on their total portal plasma concentration. Besides rofecoxib, and possibly mefenamic acid, other NSAIDs were predicted not to significantly inhibit CYP1A2 in human beings. The type of enzyme inhibition, particularly metabolism-dependent inhibition, free inhibitor concentration and accumulation of the inhibitor into the hepatocytes should be considered in extrapolations of in vitro results to human beings.

Interaction between SERTPR and stressful life events on response to antidepressant treatment.

Eur Neuropsychopharmacol. 2008 Sep 22;
Mandelli L, Marino E, Pirovano A, Calati R, Zanardi R, Colombo C, Serretti A
A polymorphism within the serotonin transporter gene (SERTPR) has been repeatedly associated to mood disorders and response to SSRIs treatment. Recent evidence suggested that influence of genetic effect of SERTPR might be modulated by stress, particularly as regard the development of anxious-depressive symptoms. Nevertheless, there is no information about the role of stressors as potential modulator of SERTPR effects on depressive outcome during pharmacological treatment. In a sample of 159 mood disorder patients treated with fluvoxamine, we found stressors preceding the onset of the illness significantly influencing the genetic effect exerted by SERTPR on response after 6 weeks of treatment. This preliminary finding supports the idea of complex interaction between biological and environmental factors underlying the efficacy of biological treatments, other than liability for mood disorders. Nevertheless, many limitations characterize the present investigation and well-funded studies on larger samples are required.

Inter-Individual Variation in Relative CYP1A2/3A4 Phenotype Influences Susceptibility of Clozapine Oxidation to CYP-Specific Inhibition in Human Hepatic Microsomes.

Drug Metab Dispos. 2008 Sep 22;
Zhang WV, D'Esposito F, Edwards RJ, Ramzan I, Murray M
The atypical antipsychotic drug clozapine (CLZ) is effective in a substantial number of patients who exhibit treatment-resistance to conventional agents. CYP1A2 is generally considered to be the major enzyme involved in the biotransformation of CLZ to its N-demethylated (norCLZ) and N-oxygenated (CLZ N-oxide) metabolites in liver, but several studies have also implicated CYP3A4. The present study assessed the interplay between these CYPs in CLZ biotransformation in a panel of hepatic microsomal fractions from fourteen individuals. The relative activity of CYPs 1A2 and 3A4 in microsomes was found to be a major determinant of the relative susceptibility of norCLZ formation to inhibition by the CYP-selective inhibitors fluvoxamine and ketoconazole. In contrast, the activity of CYP3A4 alone was correlated with the susceptibility of CLZ N-oxide formation to inhibition by these agents. These findings suggest that both CYPs may be dominant CLZ oxidases in patients and that the relative activities of these enzymes may determine clearance pathways. In vivo assessment of CYP1A2 and CYP3A4 activities, perhaps by phenotyping approaches, could assist the optimization of CLZ dosage and minimise pharmacokinetic interactions with coadministered drugs.

 

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

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