Research and Clinical Trials on Fluoxetine (Prozac, Sarafem)
This list of current clinical research trials on Fluoxetine (Prozac, Sarafem) is followed by a short set of abstracts from the most recent research articles published on the drug.
Fluoxetine (Prozac, Sarafem) Clinical Research Trials
From our searchable database at ClinicalTrialsFeeds.org, this list includes all the latest information about clinical trials involving Fluoxetine (Prozac, Sarafem).
- Developing Adaptive Treatment Strategies for Children and Adolescents With Obsessive-compulsive Disorder.
Status: Recruiting, Condition Summary: Obsessive-Compulsive Disorder - Safety and Efficacy of F2695 SR in Adults With Fatigue Associated With Major Depressive Disorder
Status: Recruiting, Condition Summary: Major Depressive Disorder - A Study for Assessing Treatment of Patients Ages 10-17 With Bipolar Depression
Status: Recruiting, Condition Summary: Bipolar Depression - A Study Of DVS SR In Treatment Of Children And Adolescent Outpatients With MDD
Status: Recruiting, Condition Summary: Major Depressive Disorder - Fluoxetine Essay in Children With Autism
Status: Withdrawn, Condition Summary: Autism - Evaluation of Stepped Care for Chronic Pain in Iraq/Afghanistan Veterans (ESCAPE)
Status: Active, not recruiting, Condition Summary: Low Back Pain; Pain; Pain, Intractable - Omega-3 and Therapy Study for Depression
Status: Recruiting, Condition Summary: Childhood Depression
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Fluoxetine: 
Current Research Literature on Fluoxetine (Prozac, Sarafem)
Here are abstracts for some of the latest research articles to have appeared on Fluoxetine (Prozac, Sarafem):
Neuropsychopharmacology. 2012 Feb 8;
Baj G, D'Alessandro V, Musazzi L, Mallei A, Sartori CR, Sciancalepore M, Tardito D, Langone F, Popoli M, Tongiorgi E
Brain-derived neurotrophic factor (BDNF) is encoded by multiple BDNF transcripts, whose function is unclear. We recently showed that a subset of BDNF transcripts can traffic into distal dendrites in response to electrical activity, while others are segregated into the somatoproximal domains. Physical exercise and antidepressant treatments exert their beneficial effects through upregulation of BDNF, which is required to support survival and differentiation of newborn dentate gyrus (DG) neurons. While these DG processes are required for the antidepressant effect, a role for CA1 in antidepressant action has been excluded, and the effect on CA3 neurons remains unclear. Here, we show for the first time that physical exercise and antidepressants induce local increase of BDNF in CA3. Voluntary physical exercise for 28 consecutive days, or 2-week treatment with 10 mg/kg per day fluoxetine or reboxetine, produced a global increase of BDNF mRNA and protein in the neuronal somata of the whole hippocampus and a specific increase of BDNF in dendrites of CA3 neurons. This increase was accounted for by BDNF exon 6 variant. In cultured hippocampal neurons, application of serotonin or norepinephrine (10-50 μM) induced increase in synaptic transmission and targeting of BDNF mRNA in dendrites. The increased expression of BDNF in CA3 dendrites following antidepressants or exercise further supports the neurotrophin hypothesis of antidepressants action and confirms that the differential subcellular localization of BDNF mRNA splice variants provides a spatial code for a selective expression of BDNF in specific subcellular districts. This selective expression may be exploited to design more specific antidepressants.Neuropsychopharmacology advance online publication, 8 February 2012; doi:10.1038/npp.2012.5.
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.
Antidepressants differentially modify the extinction of an aversive memory task in female rats.
Prog Neuropsychopharmacol Biol Psychiatry. 2012 Jan 28;
Melo TG, Izídio GS, Ferreira LS, Silveira DS, Macedo PT, Cabral A, Ribeiro AM, Silva RH
Treatment of major depression, posttraumatic stress disorder and other psychopathologies with antidepressants can be associated with improvement of the cognitive deficits related to these disorders. Although the mechanisms of these effects are not completely elucidated, alterations in the extinction of aversive memories are believed to play a role in these psychopathologies. We have recently verified that female rats present low levels of extinction when submitted to the plus-maze discriminative avoidance task. In the present study, female rats were treated long term with clinically used antidepressants (fluoxetine, nortriptyline or mirtazapine) and subjected to the plus-maze discriminative avoidance task to evaluate learning, memory, extinction and anxiety-related behaviors as well as behavioral despair in the forced swimming test. All groups learned the task and exhibited retrieval. Chronic treatment with fluoxetine (but not with the other antidepressants tested) increased extinction of the discriminative task. In the forced swimming test, the animals treated with fluoxetine and mirtazapine showed decreased immobility duration. In conclusion, fluoxetine potentiated extinction, while both fluoxetine and mirtazapine were effective in ameliorating depressive-like behavior in the forced swimming test, suggesting a possible dissociation between the effects on mood and the extinction of aversive memories in female rats.
Arch Gen Psychiatry. 2012 Feb 9;
Gibbons RD, Brown CH, Hur K, Davis JM, Mann JJ
CONTEXT: The US Food and Drug Administration issued a black box warning for antidepressants and suicidal thoughts and behavior in children and young adults. OBJECTIVE: To determine the short-term safety of antidepressants by standard assessments of suicidal thoughts and behavior in youth, adult, and geriatric populations and the mediating effect of changes in depressive symptoms. DATA SOURCES: All intent-to-treat person-level longitudinal data of major depressive disorder from 12 adult, 4 geriatric, and 4 youth randomized controlled trials of fluoxetine hydrochloride and 21 adult trials of venlafaxine hydrochloride. STUDY SELECTION: All sponsor-conducted randomized controlled trials of fluoxetine and venlafaxine. DATA EXTRACTION: The suicide items from the Children's Depression Rating Scale-Revised and the Hamilton Depression Rating Scale as well as adverse event reports of suicide attempts and suicide during active treatment were analyzed in 9185 patients (fluoxetine: 2635 adults, 960 geriatric patients, 708 youths; venlafaxine: 2421 adults with immediate-release venlafaxine and 2461 adults with extended-release venlafaxine) for a total of 53 260 person-week observations. DATA SYNTHESIS: Suicidal thoughts and behavior decreased over time for adult and geriatric patients randomized to fluoxetine or venlafaxine compared with placebo, but no differences were found for youths. In adults, reduction in suicide ideation and attempts occurred through a reduction in depressive symptoms. In all age groups, severity of depression improved with medication and was significantly related to suicide ideation or behavior. CONCLUSIONS: Fluoxetine and venlafaxine decreased suicidal thoughts and behavior for adult and geriatric patients. This protective effect is mediated by decreases in depressive symptoms with treatment. For youths, no significant effects of treatment on suicidal thoughts and behavior were found, although depression responded to treatment. No evidence of increased suicide risk was observed in youths receiving active medication. To our knowledge, this is the first research synthesis of suicidal thoughts and behavior in depressed patients treated with antidepressants that examined the mediating role of depressive symptoms using complete longitudinal person-level data from a large set of published and unpublished studies.
Understanding the molecular pharmacology of the serotonergic system: using fluoxetine as a model.
J Pharm Pharmacol. 2012 Mar; 64(3): 317-25
Sghendo L, Mifsud J
Objectives Serotonin is a monoamine neurotransmitter that is widely distributed in the body and plays an important role in a variety of psychological and other body functions such as mood, sexual desire and function, appetite, sleep, memory and learning, temperature regulation and social behaviour. This review will assess the use of fluoxetine, one of the most commonly used selective serotonin reuptake inhibitors, as a model for understanding the molecular pharmacology of the serotoninergic system. Key findings Seven serotonin receptor families have been discovered to date. All serotonin receptors, except 5-HT(3) , are G-protein coupled, seven transmembrane receptors that activate an intracellular second messenger cascade. The 5-HT(3) receptor is a ligand-gated ion channel. Furthermore, 5-HT(1A) receptors are known as autoreceptors since their stimulation inhibits the release serotonin in nerve terminals. A transporter protein found in the plasma membrane of serotonergic neurones is responsible for the reuptake of this neurotransmitter. Selective serotonin reuptake inhibitors, such as fluoxetine, act primarily at the serotonin transporter protein and have limited, if any, reaction with other neurotransmitter systems. Selective serotonin reuptake inhibitors appear to bind with the serotonin transporter with different rates of occupancy, duration and potency. Summary The following review focuses on the interaction of serotonin with this membrane transporter in the body and assesses the use of fluoxetine as a reference drug in the understanding of this interaction.
