Research and Clinical Trials on Fluvoxamine (Luvox, Faverin)

By Dr Greg Mulhauser
avatar image

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.

Article Contents

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).

 

Get These Clinical Trials as a Newsfeed

Fluvoxamine:     Get the Fluvoxamine clinical trials feed.    Add the Fluvoxamine clinical trials feed to your My Yahoo! page.    Add the Fluvoxamine clinical trials feed to your MyMSN page.

Current Research Literature on Fluvoxamine (Luvox, Faverin)

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

Some Selective Serotonin Reuptake Inhibitors Inhibit Dynamin I Guanosine Triphosphatase (GTPase).

Biol Pharm Bull. 2008 Aug; 31(8): 1489-95
Otomo M, Takahashi K, Miyoshi H, Osada K, Nakashima H, Yamaguchi N
Neuronal dynamin I plays a critical role in the recycling of synaptic vesicles, and thus in nervous system function. We expressed and purified dynamin I to explore potentially clinically useful endocytosis inhibitors and to examine the mechanism of their action. We estimated the IC(50) of nineteen psychotropic drugs for dynamin I. The IC(50) values of two selective serotonin reuptake inhibitors (sertraline and fluvoxamine) were 7.3+/-1.0 and 14.7+/-1.6 muM, respectively. Kinetic analyses revealed that fluvoxamine is a noncompetitive inhibitor of dynamin I guanosine triphosphatase (GTPase) with respect to guanosine 5'-triphosphate (GTP) and a competitive inhibitor with respect to L-phosphatidylserine (PS). Fluvoxamine may compete with PS for binding to the pleckstrin homology domain of dynamin I. On the other hand, sertraline was a mixed type inhibitor with respect to both GTP and PS. Our results indicate that sertraline and fluvoxamine may regulate the transportation of neurotransmitters by modulating synaptic vesicle endocytosis via the inhibition of dynamin I GTPase.

Co-occurring depressive symptoms in the older patient with schizophrenia.

Drugs Aging. 2008; 25(8): 631-47
Kasckow JW, Zisook S
Clinicians treating older patients with schizophrenia are often challenged by patients presenting with both depressive and psychotic features. The presence of co-morbid depression impacts negatively on quality of life, functioning, overall psychopathology and the severity of co-morbid medical conditions. Depressive symptoms in patients with schizophrenia include major depressive episodes (MDEs) that do not meet criteria for schizoaffective disorder, MDEs that occur in the context of schizoaffective disorder and subthreshold depressive symptoms that do not meet criteria for MDE. Pharmacological treatment of patients with schizophrenia and depression involves augmenting antipsychotic medications with antidepressants. Recent surveys suggest that clinicians prescribe antidepressants to 30% of inpatients and 43% of outpatients with schizophrenia and depression at all ages. Recent trials addressing the efficacy of this practice have evaluated selective serotonin reuptake inhibitors (SSRIs) such as fluoxetine, sertraline, fluvoxamine and citalopram. These trials have included only a small number of subjects and few older subjects participated; furthermore, the efficacy results have been mixed. Although no published controlled psychotherapeutic studies have specifically targeted major depression or depressive symptoms in older patients with schizophrenia, psychosocial interventions likely play a role in any comprehensive management plan in this population of patients.Our recommendations for treating the older patient with schizophrenia and major depression involve a stepwise approach. First, a careful diagnostic assessment to rule out medical or medication causes is important as well as checking whether patients are adherent to treatments. Clinicians should also consider switching patients to an atypical antipsychotic if they are not taking one already. In addition, dose optimization needs to be targeted towards depressive as well as positive and negative psychotic symptoms. If major depression persists, adding an SSRI is a reasonable next step; one needs to start with a low dose and then cautiously titrate upward to reduce depressive symptoms. If remission is not achieved after an adequate treatment duration (8-12 weeks) or with an adequate dose (similar to that used for major depression without schizophrenia), switching to another agent or adding augmenting therapy is recommended.We recommend treating an acute first episode of depression for at least 6-9 months and consideration of longer treatment for patients with residual symptoms, very severe or highly co-morbid major depression, ongoing episodes or recurrent episodes. Psychosocial interventions aimed at improving adherence, quality of life and function are also recommended. For patients with schizophrenia and subsyndromal depression, a similar approach is recommended.Psychosis accompanying major depression in patients without schizophrenia is common in elderly patients and is considered a primary mood disorder; for these reasons, it is an important syndrome to consider in the differential diagnosis of older patients with mood and thought disturbance. Treatment for this condition has involved electroconvulsive therapy (ECT) as well as combinations of antidepressant and antipsychotic medications. Recent evidence suggests that combination treatment may not be any more effective than antidepressant treatment alone and ECT may be more efficacious overall.

Mouse strain differences in immobility and sensitivity to fluvoxamine and desipramine in the forced swimming test: Analysis of serotonin and noradrenaline transporter binding.

Eur J Pharmacol. 2008 Jul 10;
Sugimoto Y, Kajiwara Y, Hirano K, Yamada S, Tagawa N, Kobayashi Y, Hotta Y, Yamada J
Strain differences in immobility time in the forced swimming test were investigated in five strains of mice, namely, ICR, ddY, C57BL/6, DBA/2 and BALB/c mice. There were significant strain differences. The immobility times of ICR, ddY and C57BL/6 mice were longer than those of DBA/2 and BALB/c mice. Immobility times were not significantly related to locomotor activity in these strains. There were also differences in sensitivity to the selective serotonin reuptake inhibitor (SSRI) fluvoxamine. In ICR, ddY and C57BL/6 mice, fluvoxamine did not affect immobility time, while it reduced the immobility time of DBA/2 and BALB/c mice dose-dependently. The noradrenaline reuptake inhibitor desipramine decreased immobility time in all strains of mice. Serotonin (5-HT) transporter binding in the brains of all five strains of mice was also investigated. Analysis of 5-HT transporter binding revealed significant strain differences, being lower in DBA/2 and BALB/c mice than in other strains of mice. The amount of 5-HT transporter binding was correlated to baseline immobility time. However, there was no significant relation between noradrenaline transporter binding and immobility time. These results suggest that the duration of baseline immobility depends on the levels of 5-HT transporter binding, leading to apparent strain differences in immobility time in the forced swimming test. Furthermore, differences in 5-HT transporter binding may cause variations in responses to fluvoxamine.

Automated analysis of fluvoxamine in rat plasma using a column-switching system and ion-pair high-performance liquid chromatography.

Biomed Chromatogr. 2008 Jul 25;
Liu S, Shinkai N, Kakubari I, Saitoh H, Noguchi KI, Saitoh T, Yamauchi H
We have established a robust, fully automated analytical method for the analysis of fluvoxamine in rat plasma using a column-switching ion-pair high-performance chromatography system. The plasma sample was injected onto a precolumn packed with Shim-pack MAYI-ODS (50 microm), where the drug was automatically purified and enriched by on-line solid-phase extraction. After elution of the plasma proteins, the analyte was back-flushed from the precolumn and then separated isocratically on a reversed-phase C18 column (L-column ODS) with a mobile phase (acetonitrile-0.1% phosphoric acid, 36:64, v/v) containing 2 mm sodium 1-octanesulfonate. The analyte was monitored by a UV detector at a wavelength of 254 nm. The calibration line for fluvoxamine showed good linearity in the range of 5-5000 ng/mL (r > 0.999) with the limit of quantification of 5 ng/mL (RSD = 6.51%). Accuracy ranged from -2.94 to 4.82%, and the within- and between-day precision of the assay was better than 8% across the calibration range. The analytical sensitivity and accuracy of this assay is suitable for characterization of the pharmacokinetics of orally-administered fluvoxamine in rats. Copyright (c) 2008 John Wiley & Sons, Ltd.

Is co-administration of bupropion with SSRIs and SNRIs in forced swimming test in mice, predictive of efficacy in resistant depression?

Behav Brain Res. 2008 Jul 4;
Prica C, Hascoet M, Bourin M
The monoamine hypothesis based on the deficiency of one or several monoamines is commonly evoked to explain the physiopathology of depression. This hypothesis initially based on noradrenalin and serotonin deficiency has been extended to dopamine. The animal models of depression also suggest an implication of dopamine in the physiopathology of depression. The forced swimming test is an animal model used to predict the antidepressant activity of drugs. OBJECTIVES: The scope of this study was to investigate the antidepressant-like effect of a dopamine re-uptake inhibitor, bupropion, when combined with conventional antidepressants drugs SSRIs (selective serotonin re-uptake inhibitors), SNRI (selective serotonin-noradrenalin re-uptake inhibitors) and a NRI (selective noradrenalin inhibitor). METHODS: This study assessed the effects of co-administration of bupropion with SSRIs: sertraline, paroxetine, citalopram, fluvoxamine, SNRIs: venlafaxine and milnacipran and NRI: desipramine, using an animal model of depression, the forced swimming test in mice. Subactive doses of bupropion (4 and 8mg/kg) and antidepressants: sertraline (2mg/kg), paroxetine, citalopram, fluvoxamine, venlafaxine, milnacipran and desipramine (4mg/kg) were given i.p. 45 and 30min, respectively, before the test. RESULTS: Bupropion (4 and 8mg/kg) combined with inactive doses of antidepressants, decreased immobility time in the mice FST except with sertraline and desipramine. In conclusion, the antidepressant-enhancing effects of bupropion, in the present study, are in agreement with preliminary clinical evidence suggesting that bupropion may enhance the efficacy of therapeutic effect of SSRIs and SNRIs but not the therapeutic effect of NRI. These results suggest that bupropion enhances only the serotonergic system.

 

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

The URL of this page is:
http://counsellingresource.com/medications/trials-and-research/fluvoxamine-research.html