Research and Clinical Trials on Zolpidem (Ambien, Stilnoct)

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By Dr Greg Mulhauser

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

Article Contents

Zolpidem (Ambien, Stilnoct) Clinical Research Trials

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

 

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Current Research Literature on Zolpidem (Ambien, Stilnoct)

Here are abstracts for some of the latest research articles to have appeared on Zolpidem (Ambien, Stilnoct):

Development of a homogeneous immunoassay for the detection of zolpidem in urine.

J Anal Toxicol. 2009 Oct; 33(8): 486-90
Huynh K, Wang G, Moore C, Barhate R, Coulter C, Rodrigues W, Catbagan P, Soares J
Sleep disorders are common conditions that affect about 40 million people in the U.S every year, the most common of which is insomnia, which is characterized by difficulty falling or staying asleep. Zolpidem (Ambien) is a non-benzodiazepine prescription drug that is used to treat insomnia and is often preferred over the commonly used benzodiazepines due to a lesser side effect profile. This is because the non-benzodiazepine binding is more selective to GABA-A receptors versus the non-selective binding of benzodiazepines. With the increasing popularity of non-benzodiazepines, drug abuse and driving-while-impaired cases involving sleep-inducing drugs have risen. Therefore, a highly sensitive and rapid homogeneous immunoassay (EMIT-type assay) has been developed for the detection of zolpidem in urine. The zolpidem antibody is highly specific and does not cross-react with other newer sleep aids such as zopiclone and zaleplon. This assay has a detection limit of 5 ng/mL for zolpidem in urine. Further evaluation of this assay using liquid chromatography-tandem mass spectrometry (LC-MS-MS) analysis of authentic urine samples demonstrated that the accuracy of the assay is greater than 90%. Because this assay is designed to measure the non-conjugated drug in urine, it resulted in simplification for gas chromatography-MS or LC-MS-MS confirmation methods that do not require urine hydrolysis before solid-phase extraction or liquid-liquid extraction.

The paradox of caffeine-zolpidem interaction: a network analysis.

Curr Drug Targets. 2009 Oct; 10(10): 1009-20
Myslobodsky M
A widely prescribed and potent short-acting hypnotic, zolpidem has become the mainstay for the treatment of middle-of-the-night sleeplessness. It is expected to be antagonized by caffeine. Paradoxically, in some cases caffeine appears to slightly enhance zolpidem sedation. The pharmacokinetic and pharmacodynamic nature of this odd effect remains unexplored. The purpose of this study is to reproduce a hypothetical molecular network recruited by caffeine when co-administered with zolpidem using Ingenuity Pathway Analysis. Thus generated, network drew attention to several possible contributors to caffeine sedation, such as tachykinin precursor 1, cannabinoid, and GABA receptors. The present overview is centered on the possibility that caffeine potentiation of zolpidem sedation does not involve a centralized interaction of specific neurotransmitters, but rather is contributed by its antioxidant capacity. It is proposed that by modifying the cellular redox state, caffeine ultimately reduces the pool of reactive oxygen species, thereby increasing the bioavailability of endogenous melatonin for interaction with zolpidem. This side effect of caffeine encourages further studies of multiple antioxidants as an attractive way to potentially increasing somnolence.

Discriminative stimulus effects of L-838,417 (7-tert-butyl-3-(2,5-difluoro-phenyl)-6-(2-methyl-2H-[1,2,4]triazol-3-ylmethoxy)-[1,2,4]triazolo[4,3-b]pyridazine): Role of GABA(A) receptor subtypes.

Neuropharmacology. 2009 Oct 22;
Licata SC, Platt DM, Rüedi-Bettschen D, Atack JR, Dawson GR, Van Linn ML, Cook JM, Rowlett JK
Previous reports suggest that gamma-aminobutyric acid type A (GABA(A)) receptors containing alpha1 subunits may play a pivotal role in mediating the discriminative stimulus effects of benzodiazepines (BZs). L-838,417 (7-tert-Butyl-3-(2,5-difluoro-phenyl)-6-(2-methyl-2H-[1,2,4]triazol-3-ylmethoxy)-[1,2,4]triazolo[4,3-b]pyridazine) is a GABA(A) receptor modulator with intrinsic efficacy in vitro at alpha2, alpha3, and alpha5 subunit-containing GABA(A) receptors, and little demonstrable intrinsic efficacy in vitro at alpha1 subunit-containing GABA(A) receptors. The present study evaluated the discriminative stimulus effects of L-838,417 in order to determine the extent to which the alpha2, alpha3, and alpha5 subunit-containing GABA(A) receptors contribute to the interoceptive effects of BZ-type drugs. Squirrel monkeys (Saimiri sciureus) were trained to discriminate L-838,417 (0.3 mg/kg, i.v.) from vehicle under a 5-response fixed-ratio schedule of food reinforcement. Under test conditions, L-838,417 administration resulted in dose-dependent increases in drug-lever responding that were antagonized by the BZ-site antagonist, flumazenil. Administration of non-selective BZs, compounds with 10-fold greater affinity for alpha1 subunit-containing GABA(A) receptors compared to alpha2, alpha3, and alpha5 subunit-containing GABA(A) receptors, barbiturates and ethanol (which modulate the GABA(A) receptor via a non-BZ site), all resulted in a majority of responses on the L-838,417-paired lever (65-100% drug-lever responding). betaCCT, an antagonist that binds with 20-fold greater affinity for alpha1 subunit-containing GABA(A) receptors relative to alpha2, alpha3, and alpha5-containing GABA(A) receptors, had no significant effect on the discriminative stimulus effects of L-838,417 or the L-838,417-like effects of diazepam or zolpidem. These data suggest that efficacy at alpha2, alpha3, and/or alpha5 subunit-containing GABA(A) receptors likely are sufficient for engendering BZ-like discriminative stimulus effects.

Zolpidem-induced sleep-related eating disorder.

J Neurol Sci. 2009 Oct 10;
Yun CH, Ji KH
An association between zolpidem administration and sleep-related eating disorder (SRED) has been suggested. The authors observed zolpidem-induced SRED in restless legs syndrome (RLS). With the review of previous reports, we identified a common occurrence of RLS in zolpidem-induced SRED.

Zolpidem dependence in a geriatric patient: a case report.

J Am Geriatr Soc. 2009 Oct; 57(10): 1962-3
Spyridi S, Diakogiannis I, Nimatoudis J, Iacovides A, Kaprinis G

 

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

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