Research and Clinical Trials on Fluvoxamine (Luvox, Faverin)
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).
- Developing Adaptive Treatment Strategies for Children and Adolescents With Obsessive-compulsive Disorder.
Status: Recruiting, Condition Summary: Obsessive-Compulsive Disorder
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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):
Clinically relevant drug interactions in anxiety disorders.
Hum Psychopharmacol. 2012 Feb 7;
Muscatello MR, Spina E, Bandelow B, Baldwin DS
OBJECTIVE: Certain drugs used in the treatment of patients with anxiety disorders can interact with other psychotropic drugs and with pharmacological treatments for physical illnesses. There is a need for an updated comparative review of clinically relevant drug interactions in this area. DESIGN: Relevant literature on drug interactions with medications used in the treatment of anxiety disorders was identified through a search in MEDLINE and EMBASE. RESULTS: Drug interactions involving medications used to treat anxiety disorders may be pharmacokinetic, such as enzyme inhibition or induction in the cytochrome P450 system and transporter-mediated drug interactions, or pharmacodynamic, such as additive effects in causing drowsiness or additive effects at neurotransmitter receptors. Certain selective serotonin reuptake inhibitors (fluoxetine, fluvoxamine, and paroxetine) are particularly liable to be potentially involved in untoward pharmacokinetic interactions. CONCLUSIONS: The potential for drug interactions with medications used in anxiety disorders should be the cause of clinical concern, particularly in elderly individuals. However, the liability for harmful drug interactions may be anticipated, and the risk reduced. Although not all interactions are clinically relevant, careful monitoring of clinical response and possible interactions is essential. Copyright © 2012 John Wiley & Sons, Ltd.
Biochim Biophys Acta. 2012 Jan 27;
Fu Y, Yu S, Guo X, Li X, Li T, Li H, Dong Y
Emerging evidence from therapeutic trials in humans and animal models suggests that in the treatment of depression, antidepressants play a role by targeting the glutamatergic system. Fluvoxamine is one of the widely used SSRIs which has been considered to target monoamine neurotransmitter reuptake mechanisms. However, whether fluvoxamine has an effect on the glutamate release is still unclear. The present experiment studied the effect of fluvoxamine on presynaptic glutamate release in prelimbic cortex, both in control C57BL/6 mice and chronic restraint stress C57BL/6 mice, and further investigated the mechanism underlying this effect by using patch clamp, on-line fluorimetry, pharmacological approaches combined with other techniques. The results showed that fluvoxamine increased the glutamate release in the depression model mice but it had no effect on the glutamate release in the control mice. The mechanism underlying these effects in depression model mice was that, fluvoxamine firstly activated presynaptic 5-HT(3) receptors, which transiently increased the Ca(2+) concentration. The increase of Ca(2+) concentration via 5-HT(3) receptors caused the activation of sigma-1 receptors, which were activated by fluvoxamine. The activation of sigma-1 receptors increased the intrasynaptosomal Ca(2+) concentration significantly through the outflow of endoplasmic reticulum calcium and finally activated PKC. These results suggested that fluvoxamine may have a selective effect and different mechanism based on the condition of animal.
Obsessive compulsive disorder.
Clin Evid (Online). 2012; 2012:
Soomro GM
Obsessions or compulsions that cause personal distress or social dysfunction affect about 1% of adult men and 1.5% of adult women. About half of adults with obsessive compulsive disorder (OCD) have an episodic course, whereas the other half have continuous problems. Prevalence in children and adolescents is 2.7%. The disorder persists in about 40% of children and adolescents at mean follow-up of 5.7 years. METHODS AND OUTCOMES: We conducted a systematic review and aimed to answer the following clinical questions: What are the effects of initial treatments for obsessive compulsive disorder in adults? What are the effects of initial treatments for obsessive compulsive disorder in children and adolescents? What are the effects of maintenance treatment for obsessive compulsive disorder in adults? What are the effects of maintenance treatment for obsessive compulsive disorder in children and adolescents? What are the effects of treatments for obsessive compulsive disorder in adults who have not responded to initial treatment with serotonin reuptake inhibitors (SRIs)? We searched: Medline, Embase, The Cochrane Library, and other important databases up to April 2011 (Clinical Evidence reviews are updated periodically; please check our website for the most up-to-date version of this review). We included harms alerts from relevant organisations such as the US Food and Drug Administration (FDA) and the UK Medicines and Healthcare products Regulatory Agency (MHRA).We found 43 systematic reviews, RCTs, or observational studies that met our inclusion criteria. We performed a GRADE evaluation of the quality of evidence for interventions.In this systematic review we present information relating to the effectiveness and safety of the following interventions: addition of antipsychotics to serotonin reuptake inhibitors, behavioural therapy alone or with serotonin reuptake inhibitors, cognitive therapy or cognitive behavioural therapy (CBT) (alone or with serotonin reuptake inhibitors), electroconvulsive therapy, optimum duration of maintenance treatment, psychosurgery, serotonin reuptake inhibitors (citalopram, clomipramine, fluoxetine, fluvoxamine, paroxetine, or sertraline), and transcranial magnetic stimulation.
A link between oxytocin and serotonin in humans: Supporting evidence from peripheral markers.
Eur Neuropsychopharmacol. 2012 Jan 30;
Marazziti D, Baroni S, Giannaccini G, Betti L, Massimetti G, Carmassi C, Catena-Dell'osso M
Pharmacological studies indicate a functional interaction between the serotonergic and oxytocinergic systems. In particular, some selective serotonin (5-HT) reuptake inhibitors, such as citalopram and fluvoxamine, seem to exert part of their antidepressant effects through oxytocin (OT) release. Further, the administration of fenfluramine, a serotonergic agonist, to healthy subjects increases plasma OT levels. Interestingly, immunocytochemical and double-immunofluorescent techniques revealed a high degree of overlap between 5-HT transporter (SERT)-labeled fibers and OT-containing cells in the paraventricular and supraoptic nuclei of primate hypothalamus. These findings suggest that the influence of 5-HT on OT system might be mediated by SERT. In this study, we explored the possible existence of a link between OT and SERT in human subjects, by means of two peripheral markers, the platelet SERT, as measured by [(3)H]-paroxetine ([(3)H]-Par) binding, and plasma OT levels. As far as [(3)H]-Par binding parameters are concerned, the Bmax (mean±SD, fmol/mg protein) was 1155+130 and the Kd (mean±SD, nM) was 1.31±0.61. The OT plasma levels (mean±SD, pg/ml) were 1.14±1.07. A significant and positive correlation was found between plasma OT levels and Kd values (correlation coefficient: r: 0.466, p=.038). This result represents the first evidence of an interaction between OT and SERT, as measured by [(3)H]-Par binding, at peripheral levels in humans. Given the several activities mediated by both OT and 5-HT, such a relationship might provide new perspectives and insights into psychiatric disorders and/or social relationship disturbances, as well as novel treatment strategies overcoming and/or integrating the serotonergic paradigm.
Cardioprotective effect of fluvoxamine, sigma-1 receptor high affinity agonist.
Yakugaku Zasshi. 2012; 132(2): 167-72
Tagashira H, Fukunaga K
Selective serotonin reuptake inhibitors (SSRIs) are known to reduce post-myocardial infarction (MI)-induced morbidity and mortality. However, the molecular mechanism underlying SSRI-induced cardioprotection remains unclear. Here, we investigated the role of sigma-1 receptor (Sig-1R) stimulation with fluvoxamine on myocardial hypertrophy and cardioprotection. Male ICR mice were subjected to transverse aortic constriction (TAC) in the cardiac aortic arch. To confirm the cardioprotective role of Sig-1R stimulation by fluvoxamine, we treated mice with fluvoxamine (0.5 or 1 mg/kg) orally once a day for 4 weeks after onset of aortic banding. Interestingly, in untreated mice, Sig-1R expression in the left ventricle (LV) markedly decreased over 4 weeks with increased hypertrophy. By contrast, fluvoxamine administration significantly attenuated TAC-induced myocardial hypertrophy concomitant with recovery of Sig-1R expression in LV. Fluvoxamine also attenuated hypertrophy-induced impaired LV fractional shortening. The fluvoxamine cardioprotective effect was nullified by treatment with a Sig-1R antagonist, NE-100 (1 mg/kg). Importantly, another SSRI with very low affinity for Sig-1R, paroxetine, did not exhibit antihypertrophic effects in TAC mice and in cultured cardiomyocyte treated with angiotensin II. Fluvoxamine treatment significantly restored TAC-induced impaired Akt and eNOS phosphorylation in LV. Our findings suggest that fluvoxamine protects heart against TAC-induced cardiac dysfunction via upregulation of Sig-1R and stimulation of Sig-1R-mediated Akt-eNOS signaling in mice. This is the first report of a potential role of Sig-1R stimulation by fluvoxamine in preventing cardiac hypertrophy and myocardial injury in TAC mice.
