The therapeutic pharmacological properties of<unk>  include hypnotic, anxiolytic, anticonvulsant, and myorelaxant properties.<unk>  and benzodiazepines bind to the same sites on GABAA receptors, causing an enhancement of the actions of GABA to produce the therapeutic and adverse effects of<unk> . The metabolite of<unk>  called desmethylzopiclone is also pharmacologically active, although it has predominately anxiolytic properties. One study found some slight selectivity for<unk>  on α1 and α5 subunits, although it is regarded as being unselective in its binding to GABAA receptors containing α1, α2, α3, and α5 subunits. Desmethylzopiclone has been found to have partial agonist properties, unlike the parent drug<unk> , which is a full agonist. The mechanism of action of<unk>  is similar to benzodiazepines, with similar effects on locomotor activity and on dopamine and serotonin turnover. A meta-analysis of randomised controlled clinical trials that compared benzodiazepines to<unk>  or other Z drugs such as zolpidem and zaleplon has found few clear and consistent differences between<unk>  and the benzodiazepines in sleep onset latency, total sleep duration, number of awakenings, quality of sleep, adverse events, tolerance, rebound insomnia, and daytime alertness.<unk>  is in the cyclopyrrolone family of drugs. Other cyclopyrrolone drugs include suriclone.<unk> , although molecularly different from benzodiazepines, shares an almost identical pharmacological profile as benzodiazepines, including anxiolytic properties. Its mechanism of action is by binding to the benzodiazepine site and acting as a full agonist, which in turn positively modulates benzodiazepine-sensitive GABAA receptors and enhances GABA binding at the GABAA receptors to produce<unk> 's pharmacological properties. In addition to<unk> 's benzodiazepine pharmacological properties, it also has some barbiturate-like properties. Pharmacokinetics Two major<unk>  metabolites. After oral administration,<unk>  is rapidly absorbed, with a bioavailability around 75–80%. Time to peak plasma concentration is 1–2 hours. A high-fat meal preceding<unk>  administration does not change absorption (as measured by AUC), but reduces peak plasma levels and delays its occurrence, thus may delay the onset of therapeutic effects. The plasma protein-binding of<unk>  has been reported to be weak, between 45 and 80% (mean 52–59%). It is rapidly and widely distributed to body tissues, including the brain, and is excreted in urine, saliva, and breast milk.<unk>  is partly extensively metabolized in the liver to form an active N-demethylated derivative (N-desmethylzopiclone) and an inactive<unk> -N-oxide. Hepatic enzymes playing the most significant role in<unk>  metabolism are CYP3A4 and CYP2E1. In addition, about 50% of the administered dose is decarboxylated and excreted via the lungs. In urine, the N-demethyl and N-oxide metabolites account for 30% of the initial dose. Between 7 and 10% of<unk>  is recovered from the urine, indicating extensive metabolism of the drug before excretion. The terminal elimination half-life of<unk>  ranges from 3.5 to 6.5 hours (5 hours on average). The pharmacokinetics of<unk>  in humans are stereoselective. After oral administration of the racemic mixture, Cmax (time to maximum plasma concentration), area under the plasma time-concentration curve (AUC) and terminal elimination half-life values are higher for the dextrorotatory enantiomers, owing to the slower total clearance and smaller volume of distribution (corrected by the bioavailability), compared with the levorotatory enantiomer. In urine, the concentrations of the dextrorotatory enantiomers of the N-demethyl and N-oxide metabolites are higher than those of the respective antipodes. The pharmacokinetics of<unk>  are altered by aging and are influenced by renal and hepatic functions. In severe chronic kidney failure, the area under the curve value for<unk>  was larger and the half-life associated with the elimination rate constant longer, but these changes were not considered to be clinically significant. Sex and race have not been found to interact with pharmacokinetics of<unk> .
Zopiclone
Eszopiclone
Chloropicrin
Flumetasone
Budesonide
Clobetasone
Mibolerone
Fluticasone furoate