Research and Clinical Trials on Alprazolam (Xanax)

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By Dr Greg Mulhauser

This list of current clinical research trials on Alprazolam (Xanax) is followed by a short set of abstracts from the most recent research articles published on the drug.

Article Contents

Alprazolam (Xanax) Clinical Research Trials

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

 

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Current Research Literature on Alprazolam (Xanax)

Here are abstracts for some of the latest research articles to have appeared on Alprazolam (Xanax):

The efficacy of pregabalin and benzodiazepines in generalized anxiety disorder presenting with high levels of insomnia.

Int Clin Psychopharmacol. 2009 Jul; 24(4): 214-22
Montgomery SA, Herman BK, Schweizer E, Mandel FS
The objective of this study was to assess the impact of high levels of insomnia on response to pregabalin (PGB) in patients with generalized anxiety disorder (GAD). Pooled data were analyzed from six double-blind, placebo-controlled, 4- to 6-week trials of outpatients who met the Diagnostic and Statistical Manual of Mental Disorders (fourth edition) criteria for GAD with a minimum Hamilton Rating Scale for Anxiety (HAM-A) score = 18. Response was evaluated for three fixed-dose PGB groups (150, 300-450, 600 mg/day), and for a benzodiazepine group (alprazolam or lorazepam). A 'high-insomnia' subgroup was defined by a baseline HAM for Depression (HAM-D) insomnia factor score greater than 3 (maximum = 6). At baseline, 1002 (54%) patients met the criteria for the high-insomnia subgroup, and 852 (46%) for the low-insomnia subgroup. Mean baseline HAM-A scores were 1-2 points higher in high-insomnia versus low-insomnia patients. In high-insomnia patients, PGB produced significantly greater improvement in HAM-A total scores at last observation carried forward endpoint on 300-450 mg (-13.1+/-0.6) and 600 mg (-11.2+/-0.5) dose groups compared with placebo (-8.3+/-0.5; P

Microemulsion based intranasal delivery system for treatment of insomnia.

Drug Deliv. 2009 Apr; 16(3): 128-34
Porecha S, shah T, Jogani V, Naik S, Misra A
The aim of this investigation was to prepare and characterize microemulsions/mucoadhesive microemulsions of Diazepam (D), Lorazepam (L) and Alprazolam (A), evaluate their pharmacodynamic performances by performing comparative sleep induction studies in male albino rats to assess their role in effective management of insomnia patients. Microemulsions of Diazepam (DME), Lorazepam (LME) and Alprazolam (AME) were prepared by titration method and characterized for drug content, globule size distribution and zeta potential, nasal toxicity and sleep induction. DME, LME and AME were transparent and stable with mean globule size and zeta potential in the range of 95.6 nm to 141.7 nm and -2.205 to -0.111 mV respectively. The prepared microemulsions exhibited reversible nasal toxicity. Onset of sleep and duration of sleep were observed in the following order: Lorazepam > Alprazolam>Diazepam. Faster onset of sleep following intranasal administration of microemulsions (45 min) for all three drugs suggested selective nose-to-brain transport of drug(s). Intranasal administration of microemulsion based formulations resulted in even faster onset of sleep (

Caffeine augments Alprazolam induced cytotoxicity in human cell lines.

Toxicol In Vitro. 2009 May 31;
Saha B, Mukherjee A, Samanta S, Saha P, Ghosh AK, Santra CR, Karmakar P
Combined effects of alprazolam (Alp), a member of benzodiazepine group of drugs and caffeine on human cell lines, HeLa and THP1 were investigated in this study. Alp mediated cytotoxicity was enhanced while caffeine was present. The cell death was confirmed by observing morphological changes, LDH assay and membrane anisotropic study. Also such combined effects induced elevated level of ROS and depletion of GSH. The mechanism of cell death induced by simultaneous treatment of Alp and caffeine was associated with the calcium-mediated activation of mu-calpain, release of lysosomal protease cathepsin B, activation of PARP and cleavage of caspase 3. Our results indicate that, Alp alone induces apoptosis in human cells but in the presence of caffeine it augments necrosis in a well-regulated pathway. Thus our observations strongly suggest that, alprazolam and caffeine together produce severe cytotoxicity in human cell lines.

Physiologically based predictions of the impact of inhibition of intestinal and hepatic metabolism on human pharmacokinetics of CYP3A substrates.

J Pharm Sci. 2009 May 28;
Fenneteau F, Poulin P, Nekka F
The first objective of the present study was to predict the pharmacokinetics of selected CYP3A substrates administered at a single oral dose to human. The second objective was to predict pharmacokinetics of the selected drugs in presence of inhibitors of the intestinal and/or hepatic CYP3A activity. We developed a whole-body physiologically based pharmacokinetics (WB-PBPK) model accounting for presystemic elimination of midazolam (MDZ), alprazolam (APZ), triazolam (TRZ), and simvastatin (SMV). The model also accounted for concomitant administration of the above-mentioned drugs with CYP3A inhibitors, namely ketoconazole (KTZ), itraconazole (ITZ), diltiazem (DTZ), saquinavir (SQV), and a furanocoumarin contained in grape-fruit juice (GFJ), namely 6',7'-dihydroxybergamottin (DHB). Model predictions were compared to published clinical data. An uncertainty analysis was performed to account for the variability and uncertainty of model parameters when predicting the model outcomes. We also briefly report on the results of our efforts to develop a global sensitivity analysis and its application to the current WB-PBPK model. Considering the current criterion for a successful prediction, judged satisfied once the clinical data are captured within the 5th and 95th percentiles of the predicted concentration-time profiles, a successful prediction has been obtained for a single oral administration of MDZ and SMV. For APZ and TRZ, however, a slight deviation toward the 95th percentile was observed especially for C(max) but, overall, the in vivo profiles were well captured by the PBPK model. Moreover, the impact of DHB-mediated inhibition on the extent of intestinal pre-systemic elimination of MDZ and SMV has been accurately predicted by the proposed PBPK model. For concomitant administrations of MDZ and ITZ, APZ and KTZ, as well as SMV and DTZ, the in vivo concentration-time profiles were accurately captured by the model. A slight deviation was observed for SMV when coadministered with ITZ, whereas more important deviations have been obtained between the model predictions and in vivo concentration-time profiles of MDZ coadministered with SQV. The same observation was made for TRZ when administered with KTZ. Most of the pharmacokinetic parameters predicted by the PBPK model were successfully predicted within a two-fold error range either in the absence or presence of metabolism-based inhibition. Overall, the present study demonstrated the ability of the PBPK model to predict DDI of CYP3A substrates with promising accuracy. (c) 2009 Wiley-Liss, Inc. and the American Pharmacists Association J Pharm Sci.

A fatal case of benzodiazepine withdrawal.

Am J Forensic Med Pathol. 2009 Jun; 30(2): 177-9
Lann MA, Molina DK
Medical examiners often receive cases with limited medical history. Sometimes the medical history received is slightly skewed, or even incorrect. Here we describe a case which was initially referred to the Bexar County Medical Examiner's Office from a large community hospital as a case of zolpidem overdose. The deceased presented to the hospital with hypertension, elevated temperature, worsening bizarre behavior, and movement irregularities. While in the hospital, the decedent developed seizure-like activity and died approximately 15 hours after admission. A complete autopsy was performed and yielded no significant gross or histologic abnormalities. A full toxicologic analysis revealed therapeutic levels of citalopram and phenytoin. Zolpidem was not present. Further review of the decedent's medical history as well as information provided by the next of kin revealed that the deceased had been taking diazepam for several years but had recently been switched to alprazolam. The decedent had abruptly stopped taking the alprazolam approximately 4 days before admission when she ran out of the medication, after taking approximately 200 mg in a 6-day period. Given the inconsistent clinical presentation and the findings at autopsy, we suspect that she suffered from benzodiazepine withdrawal and not an overdose as initially reported. Although it is possible that the zolpidem, reportedly taken in the 12 hours before admission, masked the initial symptoms of withdrawal, the constellation of symptoms and signs at presentation are more consistent with benzodiazepine withdrawal than of zolpidem overdose. In this report, we emphasize to the forensic community that one must maintain a high index of suspicion for alternative explanations if the initial report does not seem to fit the presentation or autopsy findings. This case illustrates that although it may take some extra time and effort, further investigation into clinical history can prove crucial to obtaining the correct cause of death and manner of death. This is only the second case within the English literature of death because of benzodiazepine withdrawal.

 

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

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