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    Zopiclone molecular structure

    Zopiclone Stats & Data

    Imovane Zimovane
    Chemical Class Benzodiazepine
    Psychoactive Class Depressant
    Half-Life ~5 hours in healthy adults (3.5–6.5 h); prolonged to ~12 h in hepatic impairment.

    Pharmacology

    DrugBank
    Protein binding Approximately 45% State Solid

    Description

    Zopiclone is a novel hypnotic agent used in the treatment of insomnia. Its mechanism of action is based on modulating benzodiazepine receptors. In addition to zopiclone's benzodiazepine pharmacological properties it also has some barbiturate-like properties.

    Mechanism of Action

    Zopiclone exerts its action by binding on the benzodiazepine receptor complex and modulation of the GABABZ receptor chloride channel macromolecular complex. Both zopiclone and benzodiazepines act indiscriminately at the benzodiazepine binding site on α1, α2, α3 and α5 GABAA containing receptors as full agonists causing an enhancement of the inhibitory actions of GABA to produce the therapeutic (hypnotic and anxiolytic) and adverse effects of zopiclone.

    Pharmacodynamics

    Zopiclone is a nonbenzodiazepine hypnotic from the pyrazolopyrimidine class and is indicated for the short-term treatment of insomnia. While Zopiclone is a hypnotic agent with a chemical structure unrelated to benzodiazepines, barbiturates, or other drugs with known hypnotic properties, it interacts with the gamma-aminobutyric acid-benzodiazepine (GABABZ) receptor complex. Subunit modulation of the GABABZ receptor chloride channel macromolecular complex is hypothesized to be responsible for some of the pharmacological properties of benzodiazepines, which include sedative, anxiolytic, muscle relaxant, and anticonvulsive effects in animal models. Zopiclone binds selectively to the brain alpha subunit of the GABA A omega-1 receptor.

    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.

    Absorption

    Rapidly absorbed following oral administration.

    Toxicity

    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.

    Indication

    For the short-term treatment of insomnia.

    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.

    Receptor Profile

    Receptor Actions

    Agonists
    full agonist at benzodiazepine binding site
    Modulators
    GABA-A receptor positive allosteric modulator (benzodiazepine site)

    Receptor Binding

    Gamma-aminobutyric acid receptor subunit alpha-1 potentiator
    Gamma-aminobutyric acid receptor subunit alpha-2 potentiator
    Gamma-aminobutyric acid receptor subunit alpha-3 potentiator
    Gamma-aminobutyric acid receptor subunit alpha-5 potentiator
    Translocator protein agonist

    History & Culture

    Zopiclone was developed by the French pharmaceutical company Rhône-Poulenc S.A. and first introduced to the market in 1986. Rhône-Poulenc has since become part of Sanofi, which remains the primary global manufacturer. Upon its release, zopiclone was marketed as offering improvements over benzodiazepines for treating insomnia, though subsequent meta-analyses have found it comparable to benzodiazepines across all assessed parameters. The substance remained unscheduled in the United States until April 4, 2005, when the Drug Enforcement Administration placed it under Schedule IV of the Controlled Substances Act, citing evidence of addictive properties similar to those of benzodiazepines. Zopiclone as marketed globally is a racemic mixture containing two stereoisomers, of which only one possesses pharmacological activity. In 2005, the same year as federal scheduling, the Massachusetts-based pharmaceutical company Sepracor began marketing the active stereoisomer separately as eszopiclone under the brand name Lunesta in the United States. This development effectively placed what functions as a generic medication in most countries under new patent protection within the American market. In France, zopiclone ranks among the ten most commonly obtained medications through fraudulent prescriptions, indicating significant diversion from legitimate pharmaceutical channels.

    Subjective Effect Notes

    physical: The physical effects of zopiclone can be broken down into several components which progressively intensify proportional to dosage.

    cognitive: The general head space of zopiclone is described by many as one of intense sedation and decreased inhibition. It contains a large number of typical depressant cognitive effects.

    Effect Profile

    Curated + 44 Reports
    Benzodiazepine 8.6

    Strong anxiolysis, sedation, cognitive impairment, and euphoria

    Anxiolysis×3
    10
    Sedation / Relaxation×2
    107.5
    Motor / Cognitive Impairment×1
    109.0
    Euphoria / Mood Lift×1
    104.8
    Catalog Erowid

    Tolerance & Pharmacokinetics

    drugs.wiki
    Half-Life
    ~5 hours in healthy adults (3.5–6.5 h); prolonged to ~12 h in hepatic impairment.
    Addiction Potential
    Moderate. Zopiclone can produce tolerance, dependence, and a benzodiazepine‑like withdrawal syndrome, including risk of seizures after abrupt cessation at high or prolonged doses.

    Tolerance Decay

    Full tolerance 14d Half tolerance 14d Baseline ~28d

    Hypnotic tolerance to sleep‑inducing effects can develop within days to weeks of daily use; functional tolerance to impairment is incomplete (driving deficits persist despite regular use). Return toward baseline generally occurs over 2–4+ weeks of abstinence but varies widely. Data are a synthesis of clinical guidance for benzodiazepine‑site agonists and limited zopiclone‑specific studies; confidence moderate to low.

    Cross-Tolerances

    Benzodiazepines
    70% ●○○
    Other Z‑drugs (zolpidem, zaleplon, eszopiclone)
    60% ●○○

    Experience Report Analysis

    Erowid
    44 Reports
    2001–2025 Date Range
    18 With Age Data
    20 Effects Detected

    Demographics

    Gender Distribution

    Age Distribution

    Reports Over Time

    Effect Analysis

    Erowid

    Effects aggregated from 44 experience reports (44 Erowid)

    44 Reports
    20 Effects Detected
    9 Positive
    7 Adverse
    4 Neutral

    Effect Sentiment Distribution

    Confidence Distribution

    Positive Effects 9

    Sedation 50.0% 70%
    Stimulation 47.7% 70%
    Anxiety Suppression 38.6% 70%
    Euphoria 31.8% 70%
    Tactile Enhancement 20.5% 70%
    Color Enhancement 18.2% 70%
    Empathy 11.4% 70%
    Music Enhancement 11.4% 70%
    Focus Enhancement 9.1% 70%

    Adverse Effects 7

    Memory Suppression 34.1% 70%
    Motor Impairment 25.0% 70%
    Confusion 15.9% 70%
    Nausea 15.9% 70%
    Muscle Tension 6.8% 70%
    Headache 6.8% 70%
    Psychosis 6.8% 70%

    Dose-Response Correlation

    How effect frequency changes across dose levels

    View data table
    Effect Heavy (n=13)
    Stimulation 61.5%
    Memory Suppression 46.2%
    Sedation 38.5%
    Color Enhancement 30.8%
    Euphoria 30.8%
    Visual Distortions 30.8%
    Motor Impairment 30.8%
    Tactile Enhancement 30.8%
    Auditory Effects 23.1%
    Open-Eye Visuals 23.1%
    Anxiety Suppression 23.1%
    Confusion 15.4%
    Nausea 15.4%
    Psychosis 15.4%
    Introspection 15.4%

    Dose–Effect Mapping

    Experience Reports

    How reported effects shift across dose tiers, based on 44 experience reports.

    Limited tier coverage — most reports fall within the Heavy range. Effects at other dose levels may not be represented.

    Oral dose range: 7.5–15.0 mg (median 15.0 mg)
    Effect Heavy (n=13)
    stimulation
    62%
    memory suppression
    46%
    sedation
    38%
    color enhancement
    31%
    euphoria
    31%
    visual distortions
    31%
    motor impairment
    31%
    tactile enhancement
    31%
    auditory effects
    23%
    open-eye visuals
    23%
    anxiety suppression
    23%
    confusion
    15%
    nausea
    15%
    psychosis
    15%
    introspection
    15%
    empathy
    15%

    Dosage Distribution

    Dose distribution from experience reports

    Median: 15.0 mg IQR: 7.5–15.0 mg n=24

    Real-World Dose Distribution

    62K Doses

    From 62 individual dose entries

    Oral (n=47)

    Median: 7.5mg 25th: 7.5mg 75th: 15.0mg 90th: 23.5mg
    mg/kg median: 0.144 mg/kg 75th: 0.264

    Common Combinations

    Most co-occurring substances in experience reports

    Form / Preparation

    Most common forms and preparations reported

    Body-Weight Dosing

    Dose relative to body weight from reports with weight data

    Median: 0.2 mg/kg IQR: 0.106–0.265 mg/kg n=22

    Redose Patterns

    Redosing behavior across 35 reports

    14.3% Redosed
    1.2 Avg Doses
    60m Median Interval

    Legal Status

    Country Status Notes
    Canada Approved prescription medication Approved for medical use and marketed since the mid-1990s. Multiple brand name products (Imovane, Act Zopiclone, M-zopiclone) and generic formulations (Apo-zopiclone, Ag-zopiclone) are available by prescription.
    United Kingdom Prescription only medicine Available as a prescription medication, commonly dispensed in 3.75mg and 7.5mg tablet formulations for the treatment of insomnia.
    United States Scheduled controlled substance Became a federally scheduled controlled substance in 2005. Prior to scheduling, it was available but not specifically controlled under the Controlled Substances Act.

    Harm Reduction

    drugs.wiki

    Zopiclone acts at the benzodiazepine site of the GABAA receptor and should be reserved for short‑term insomnia; longer courses increase tolerance, dependence, and withdrawal risks. Complex sleep‑related behaviors (e.g., sleep‑eating, sleep‑driving) and anterograde amnesia can occur, especially with higher doses, redosing, or use while not immediately going to bed. Residual psychomotor impairment can persist 9–11+ hours; avoid driving or hazardous tasks the next morning and allow a full 8+ hours time in bed. Bitter/metallic taste (dysgeusia) and dry mouth are common and may persist into the next day. Co‑use with other depressants (alcohol, opioids, gabapentinoids, sedating antipsychotics/antihistamines) markedly increases risk of respiratory depression, blackouts, falls, and crashes; avoid such combinations. Hepatic impairment prolongs half‑life and increases next‑day effects; lower doses and extra caution are indicated. Redosing during the same night increases amnesia and disinhibition; due to memory gaps, some users unintentionally redose—pre‑plan a single dose and secure the remainder. If dependence has developed, avoid abrupt cessation; a supervised, gradual taper is safer due to seizure risk. Do not confuse racemic zopiclone dosing (commonly 7.5 mg) with eszopiclone (Lunesta; 1–3 mg)—they are related but not dose‑equivalent.

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