Research and Clinical Trials on Fluoxetine (Prozac, Sarafem)

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By Dr Greg Mulhauser

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.

Article Contents

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).

 

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Current Research Literature on Fluoxetine (Prozac, Sarafem)

Here are abstracts for some of the latest research articles to have appeared on Fluoxetine (Prozac, Sarafem):

Association of PDE11A global haplotype with major depression and antidepressant drug response.

Neuropsychiatr Dis Treat. 2009; 5: 163-70
Luo HR, Wu GS, Dong C, Arcos-Burgos M, Ribeiro L, Licinio J, Wong ML
Cyclic nucleotide phosphodiesterases (PDEs) hydrolyze the intracellular second messengers cAMP and cGMP to their corresponding monophosphates. PDEs play an important role in signal transduction by regulating the intracellular concentration of cyclic nucleotides. We have previously shown that the individual haplotype GAACC in the PDE11A gene was associated with major depressive disorder (MDD) based on block-by-block analysis. There are two PDE genes, PDE11A and PDE1A, located in chromosome 2q31-q32. In this study, we have further explored whether the whole region 2q31-q32 contribute to MDD or antidepressant response 278 depressed Mexican-American participants and 321 matched healthy controls. Although there is no significant interaction between the two genes, the remission rate of individual carrying the combination genotype at rs1880916 (AG/AA) and rs1549870 (GG) is significantly increased. We analyzed the global haplotype by examining 16 single-nucleotide polymorphisms (SNPs) in PDE11A and six SNPs in PDE1A. None of the haplotypes consisting of six SNPs in the PDE1A have a significant difference between depressed and control groups. Among haplotypes consisting of 16 SNPs across 440 kb in the PDE11A gene, 18 common haplotypes (with frequency higher than 0.8%) have been found in the studied population. Six haplotypes showed significantly different frequencies between the MDD group and the control group. The phylogenetic network result for the 16 SNPs showed that several historic recombination events have happened in the PDE11A gene. The frequency of one haplotype is significantly lower in the remitter group than in the nonremitter group for the depressed participants treated with either desipramine or fluoxetine. Thus, our data suggest that the PDE11A global haplotype is associated with both MDD and antidepressant drug response.

Vascular Endothelial Growth Factor Signaling is Required for the Behavioral Actions of Antidepressant Treatment: Pharmacological and Cellular Characterization.

Neuropsychopharmacology. 2009 Jun 24;
Greene J, Banasr M, Lee B, Warner-Schmidt J, Duman RS
This study extends earlier work on the role of vascular endothelial growth factor (VEGF) in the actions of antidepressant treatment in two key areas. First, by determining the requirement for VEGF in the actions of a 5-HT selective reuptake inhibitor (SSRI), fluoxetine in behavioral models of depression/antidepressant response; and second, by examining the role of the 5-HT1A receptor subtype in the regulation of VEGF, and the cellular localization of antidepressant regulation of VEGF expression. The results show that pharmacological inhibition of VEGF receptor signaling blocks the behavioral actions of fluoxetine in rats subjected to chronic unpredictable stress. Infusions of SU5416 or SU1498, two structurally dissimilar inhibitors of VEGF-Flk-1 receptor signaling, block the antidepressant effects of fluoxetine on sucrose preference, immobility in the forced swim test, and latency to feed in the novelty suppressed feeding paradigm. We also show that activation of 5-HT1A receptors is sufficient to induce VEGF expression and that a 5-HT1A antagonist blocks both the increase in VEGF and behavioral effects induced by fluoxetine. Finally, double labeling studies show that chronic fluoxetine administration increases VEGF expression in both neurons and endothelial cells in the hippocampus. Taken together these studies show that VEGF is necessary for the behavioral effects of the SSRI fluoxetine, as well as norepinephrine selective reuptake inhibitor, and that these effects may be mediated by 5-HT1A receptors located on neurons and endothelial cells.Neuropsychopharmacology advance online publication, 24 June 2009; doi:10.1038/npp.2009.68.

Pharmacotherapy for cannabis dependence: how close are we?

CNS Drugs. 2009; 23(7): 543-53
Vandrey R, Haney M
Cannabis is the most widely used illicit drug in the world. Treatment admissions for cannabis use disorders have risen considerably in recent years, and the identification of medications that can be used to improve treatment outcomes among this population is a priority for researchers and clinicians. To date, several medications have been investigated for indications of clinically desirable effects among cannabis users (e.g. reduced withdrawal, attenuation of subjective or reinforcing effects, reduced relapse). Medications studied have included those: (i) known to be effective in the treatment of other drug use disorders; (ii) known to alleviate symptoms of cannabis withdrawal (e.g. dysphoric mood, irritability); or (iii) that directly affect endogenous cannabinoid receptor function. Results from controlled laboratory studies and small open-label clinical studies indicate that buspirone, dronabinol, fluoxetine, lithium and lofexidine may have therapeutic benefit for those seeking treatment for cannabis-related problems. However, controlled clinical trials have not been conducted and are needed to both confirm the potential clinical efficacy of these medications and to validate the laboratory models being used to study candidate medications. Although the recent increase in research towards the development of pharmacotherapy for cannabis use disorders has yielded promising leads, well controlled clinical trials are needed to support broad clinical use of these medications to treat cannabis use disorders.

Neurosteroids modulate compulsive and persistent behavior in rodents: Implications for obsessive-compulsive disorder.

Prog Neuropsychopharmacol Biol Psychiatry. 2009 Jun 20;
Umathe SN, Vaghasiya JM, Jain NS, Dixit PV
Neurosteroids are reported to modulate GABAergic and glutamatergic pathways that then influence serotonin and dopamine, the neurotransmitters implicated in pathophysiology of obsessive-compulsive disorder (OCD). Fluoxetine, a selective serotonin reuptake inhibitor clinically used in OCD is reported to increase the levels of neurosteroids like allopregnanolone, whereas OCD patients exhibit higher plasma levels of dehydroepiandrosterone 3-sulphate (DHEAS), a neuroactive steroid having opposite effects to that of allopregnanolone. Hence, it was contemplated that neurosteroids may influence obsessive-compulsive behavior. To test this possibility we studied the influence of various neurosteroids on two behavioral models of OCD, namely marble-burying behaviour in mice and spontaneous alternation behavior in rats. The results revealed that allopregnanolone (1 microg/mouse, i.c.v) and progesterone (20 mg/kg, s.c.) reduced the marble-burying behavior in mice, whereas dehydroisoandrosterone 3-sulphate (DHAS) (5 mg/kg, i.p.) exacerbated the same. The effects of allopregnanolone were comparable to that of fluoxetine (10 mg/kg, i.p.). In view of the report that restraint stress increases the levels of allopregnanolone and isolation stress decreases the same, we studied the effect of these stressors on marble-burying behavior; wherein it was found to be less in restraint stress exposed mice, and higher in socially isolated mice. Restrain stress-induced attenuation of marble-burying behavior was blocked by finasteride, a neurosteroid biosynthesis blocker. In spontaneous alternation behavior of rat model, acute and chronic treatment with allopregnanolone (1 microg/mouse, i.c.v.) reduced 8-OH-DPAT-induced persistent behavior, whereas treatment with DHAS (5 mg/kg, i.p.) had an opposite effect. In conclusion, the studies indicate that neurosteroids can modulate obsessive-compulsive behavior in bidirectional manner, and could serve as an effective target in management of OCD.

Use of latency to immobility improves detection of antidepressant-like activity in the behavioral despair test in the mouse.

Eur J Pharmacol. 2009 Jun 20;
Castagné V, Porsolt RD, Moser P
The behavioral despair test (BDT), also called the forced swim test, is an economic, reliable and sensitive test for the detection of potential antidepressant-like activity of new test substances. The vast majority of clinically active antidepressants are active in the BDT, although substances specifically acting on serotonin transmission are generally reported to be less easily detected. Substances active in the BDT decrease the duration of immobility at doses considered as relatively high. In contrast, some psychostimulants are considered as potential false positives since they are also active in the BDT although they are not recognized as clinically active antidepressants. In the present study we have evaluated the usefulness of latency to the first immobility period as an additional parameter in the BDT to further evaluate the effects of antidepressants and psychostimulants administered intraperitoneally in the mouse. The results show that this measure increases the sensitivity of the test for detecting the effects of tricyclic antidepressants (imipramine, desipramine) and selective serotonin/norepinephrine reuptake inhibitors (duloxetine and venlafaxine) but not of serotonin reuptake inhibitors (fluoxetine and escitalopram). In contrast with previous reports, psychostimulants (amphetamine and modafinil) did not affect the duration or the latency to immobility in the BDT. The mouse strain used in the BDT seems to be an important parameter to discriminate between antidepressants and psychostimulants. These results suggest the measure of the latency to the first immobility improves the predictive validity of the BDT.

 

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

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