Top Gene Interactions
- Metabolism: Extensively metabolized in the liver via decarboxylation (major pathway), demethylation, and side chain oxidation. Metabolites include an N-oxide derivative (weakly active; approximately 12% of a dose) and an N-desmethyl metabolite (inactive; approximately 16%). Approximately 50% of a dose is converted to other inactive metabolites via decarboxylation. Hepatic microsomal enzymes are apparently not involved in zopiclone clearance. Half Life: Elimination half life is approximately 5 hours (range 3.8 to 6.5 hours) and is prolonged to 11.9 hours in patients with hepatic insufficiency.
- Uses/Sources: For the short-term treatment of insomnia.
- Health Effects: They cause slurred speech, disorientation and "drunken" behavior. They are physically and psychologically addictive.
- Symptoms: Rare individual instances of fatal outcomes following overdose with racemic zopiclone have been reported in European postmarketing reports, most often associated with overdose with other CNS-depressant agent. Signs and symptoms of overdose effects of CNS depressants can be expected to present as exaggerations of the pharmacological effects noted in preclinical testing.
- Route of Exposure: Rapidly absorbed following oral administration.
Mechanism of Action
|Target Name||Mechanism of Action||References|
Gamma-aminobutyric acid receptor subunit alpha-1
Gamma-aminobutyric acid receptor subunit alpha-2
Gamma-aminobutyric acid receptor subunit alpha-3
Gamma-aminobutyric acid receptor subunit alpha-5
|Translocator protein||Zopiclone exerts its action by binding on the benzodiazepine receptor complex and modulation of the GABABZ receptor chloride channel macromolecular complex.||