Research and Clinical Trials on Nefazodone (Serzone, Dutonin)

Nefazodone (Serzone, Dutonin) Clinical Research Trials

From our searchable database at ClinicalTrialsFeeds.org, this list includes all the latest information about clinical trials involving Nefazodone (Serzone, Dutonin).

• Effectiveness of Nefazodone and Bupropion in Treating Marijuana Dependent Individuals
  Status: Completed, Condition Summary: Marijuana Abuse
• Nefazodone in the Treatment of Cocaine Dependence and Depression - 4
  Status: Active, not recruiting, Condition Summary: Cocaine-Related Disorders; Substance-Related Disorders
• Nefazodone in the Treatment of Social Phobia
  Status: Completed, Condition Summary: Social Anxiety Disorder (SAD)
• Effect of Nefazodone on Relapse in Females With Cocaine Abuse - 10
  Status: Completed, Condition Summary: Cocaine-Related Disorders
• Effects of Nefazodone on Treatment of Female Cocaine Abusers - 3
  Status: Completed, Condition Summary: Cocaine-Related Disorders

 

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Current Research Literature on Nefazodone (Serzone, Dutonin)

Here are abstracts for some of the latest research articles to have appeared on Nefazodone (Serzone, Dutonin):

High throughput and sensitive determination of trazodone and its primary metabolite, m-chlorophenylpiperazine, in human plasma by liquid chromatography-tandem mass spectrometry.

J Chromatogr B Analyt Technol Biomed Life Sci. 2008 Jul 3;
Patel BN, Sharma N, Sanyal M, Shrivastav PS
A precise, sensitive and high throughput liquid chromatography-tandem mass spectrometry (LC-MS/MS) method for simultaneous determination of trazodone (TRZ) and its primary metabolite, m-chlorophenylpiperazine (mCPP), in human plasma was developed and validated. The analytes and the internal standard-nefazodone were extracted from 500muL aliquots of human plasma via liquid-liquid extraction in n-hexane. Chromatographic separation was achieved in a run time of 2.5min on a Betabasic cyano column (100mmx2.1mm, 5mum) under isocratic conditions. Detection of analytes and IS was done by tandem mass spectrometry, operating in positive ion and multiple reaction monitoring (MRM) acquisition mode. The protonated precursor to product ion transitions monitored for TRZ, mCPP and IS were m/z 372.2-->176.2, 197.2-->118.1 and 470.5-->274.6 respectively. The method was fully validated for its sensitivity, selectivity, accuracy and precision, matrix effect, stability study and dilution integrity. A linear dynamic range of 10.0-3000.0ng/mL for TRZ and 0.2-60.0ng/mL for mCPP was evaluated with mean correlation coefficient (r) of 0.9986 and 0.9990 respectively. The intra-batch and inter-batch precision (%CV) across five validation runs (LLOQ, lower limit of quantitation; LQC, low quality control; MQC, middle quality control; HQC, high quality control and ULOQ, upper limit of quantitation) was

What moderator characteristics are associated with better prognosis for depression?

Neuropsychiatr Dis Treat. 2005 Mar; 1(1): 51-7
Trivedi MH, Morris DW, Pan JY, Grannemann BD, John Rush A
A retrospective data analysis was conducted to evaluate the usefulness of baseline characteristics in predicting treatment response to antidepressant medication in 97 outpatients with nonpsychotic major depression treated for up to sixteen weeks with nefazodone. Baseline demographics (gender), illness features (symptom severity, length of illness, length of current episode, number of episodes, age of onset, longitudinal subtype, endogenicity, melancholia, family history of mood disorders), and social features (living status) were evaluated. Response to treatment was defined as a >/= 50% reduction in the 17-item Hamilton Rating Scale for Depression (HRSD(17)) score. The results of a survival analysis indicated that patients with shorter histories of illness (< 4 years), a negative family history of depression, and those who were either married or were living with someone were more likely to have a positive outcome during the acute phase treatment of depression. The main findings are consistent with extensive previous literature indicating a better short-term outcome of depression where illness is shorter, where there is no family history, and where there is better social support.

Cellular Imaging Predictions of Clinical Drug-Induced Liver Injury.

Toxicol Sci. 2008 Jun 3;
Xu JJ, Henstock PV, Dunn MC, Smith AR, Chabot JR, de Graaf D
Drug-induced liver injury (DILI) is the most common adverse event causing drug non-approvals and drug withdrawals. Using drugs as test agents and measuring a panel of cellular phenotypes that are directly linked to key mechanisms of hepatotoxicity, we have developed an in vitro testing strategy that is predictive of many clinical outcomes of DILI. Mitochondrial damage, oxidative stress, and intracellular glutathione, all measured by high content cellular imaging in primary human hepatocyte cultures, are the three most important features contributing to the hepatotoxicity prediction. When applied to over 300 drugs and chemicals including many that caused rare and idiosyncratic liver toxicity in humans, our testing strategy has a true-positive rate of 50-60% and an exceptionally low false-positive rate of 0-5%. These in vitro predictions can augment the performance of the combined traditional preclinical animal tests by identifying idiosyncratic human hepatotoxicants such as nimesulide, telithromycin, nefazodone, troglitazone, tetracycline, sulindac, zileuton, labetalol, diclofenac, chlorzoxazone, dantrolene, and many others. Our findings provide insight to key DILI mechanisms, and suggest a new approach in hepatotoxicity testing of pharmaceuticals.

The impact of mental illness on sexual dysfunction.

Adv Psychosom Med. 2008; 29: 89-106
Zemishlany Z, Weizman A
Sexual dysfunction is prevalent among psychiatric patients and may be related to both the psychopathology and the pharmacotherapy. The negative symptoms of schizophrenia limit the capability for interpersonal and sexual relationships. The first-generation antipsychotics cause further deterioration in erectile and orgasmic function. Due to their weak antagonistic activity at D2 receptors, second-generation antipsychotics are associated with fewer sexual side effects, and thus may provide an option for schizophrenia patients with sexual dysfunction. Depression and anxiety are a cause for sexual dysfunction that may be aggravated by antidepressants, especially selective serotonin reuptake inhibitors (SSRIs). SSRI-induced sexual dysfunction may be overcome by lowering doses, switching to an antidepressant with low propensity to cause sexual dysfunction (bupropion, mirtazapine, nefazodone, reboxetine), addition of 5HT2 antagonists (mirtazapine, mianserin) or coadministration of 5-phosphodiesterase inhibitors. Eating disorders and personality disorders, mainly borderline personality disorder, are also associated with sexual dysfunction. Sexual dysfunction in these cases stems from impaired interpersonal relationships and may respond to adequate psychosexual therapy. It is mandatory to identify the specific sexual dysfunction and to treat the patients according to his/her individual psychopathology, current pharmacotherapy and interpersonal relationships.

In vitro assessment of mitochondrial dysfunction and cytotoxicity of nefazodone, trazodone, and buspirone.

Toxicol Sci. 2008 Jun; 103(2): 335-45
Dykens JA, Jamieson JD, Marroquin LD, Nadanaciva S, Xu JJ, Dunn MC, Smith AR, Will Y
Mitochondrial toxicity is increasingly implicated in a host of drug-induced organ toxicities, including hepatotoxicity. Nefazodone was withdrawn from the U.S. market in 2004 due to hepatotoxicity. Accordingly, we evaluated nefazodone, another triazolopyridine trazodone, plus the azaspirodecanedione buspirone, for cytotoxicity and effects on mitochondrial function. In accord with its clinical disposition, nefazodone was the most toxic compound of the three, trazodone had relatively modest effects, whereas buspirone showed the least toxicity. Nefazodone profoundly inhibited mitochondrial respiration in isolated rat liver mitochondria and in intact HepG2 cells where this was accompanied by simultaneous acceleration of glycolysis. Using immunocaptured oxidative phosphorylation (OXPHOS) complexes, we identified Complex 1, and to a lesser amount Complex IV, as the targets of nefazodone toxicity. No inhibition was found for trazodone, and buspirone showed 3.4-fold less inhibition of OXPHOS Complex 1 than nefazodone. In human hepatocytes that express cytochrome P450, isoform 3A4, after 24 h exposure, nefazodone and trazodone collapsed mitochondrial membrane potential, and imposed oxidative stress, as detected via glutathione depletion, leading to cell death. Our results suggest that the mitochondrial impairment imposed by nefazodone is profound and likely contributes to its hepatotoxicity, especially in patients cotreated with other drugs with mitochondrial liabilities.