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    Chloral Hydrate Stats & Data

    Noctec Somnos Somnote Welldorm Mickey finn chloral-hydrate aquachloral
    Chemical Class medicine
    Psychoactive Class Depressant
    Half-Life Trichloroethanol (active): ~8–13 hours; Trichloroacetic acid: ~4–5 days (enterohepatic recirculation can prolong apparent effects).

    Pharmacology

    DrugBank
    State Solid

    Description

    A hypnotic and sedative used in the treatment of insomnia. The safety margin is too narrow for chloral hydrate to be used as a general anesthetic in humans, but it is commonly used for that purpose in animal experiments. It is no longer considered useful as an anti-anxiety medication.

    Metabolism

    Metabolized by the liver and erythrocytes to form trichloroethanol, an active metabolite. This reaction is catalyzed by alcohol dehydrogenase and other enzymes. Oxidation of chloral hydrate and trichloroethanol to trichloroacetic acid in the liver and kidneys also occurs to a lesser extent. Trichloroethanol also undergoes glucuronidation to produce an inactive metabolism.

    Absorption

    Rapidly absorbed in the GI tract following oral or rectal administration. Chloral hydrate and its active metabolite, trichloroethanol, have been detected in CSF, umbilical cord blood, fetal blood, and amniotic fluid.

    Indication

    Mainly used as a hypnotic in the treatment of insomnia; however, it is only effective as a hypnotic for short-term use. May be used as a routine sedative preoperatively to decrease anxiety and cause sedation and/or sleep with respiration depression or cough reflex.

    Elimination

    Trichloroethanol, trichloroethanol glucuronide, and trichloroacetic acid are excreted in the urine. Some trichloroethanol glucuronide may be secreted into bile and excreted in the feces.

    Receptor Profile

    Receptor Actions

    Modulators
    GABA-A receptor positive allosteric modulator (non-benzodiazepine site)

    Tolerance & Pharmacokinetics

    drugs.wiki
    Half-Life
    Trichloroethanol (active): ~8–13 hours; Trichloroacetic acid: ~4–5 days (enterohepatic recirculation can prolong apparent effects).
    Addiction Potential
    Moderate to high with repeated frequent use. Tolerance builds within days; dependence and a sedative-hypnotic–type withdrawal (agitation, insomnia; severe cases delirium) can occur with regular dosing.

    Experience Report Analysis

    Erowid
    10 Reports
    2005–2013 Date Range
    5 With Age Data
    4 Effects Detected

    Demographics

    Gender Distribution

    Age Distribution

    Reports Over Time

    Effect Analysis

    Erowid

    Effects aggregated from 10 experience reports (10 Erowid)

    10 Reports
    4 Effects Detected
    3 Positive
    0 Adverse
    1 Neutral

    Effect Sentiment Distribution

    Confidence Distribution

    Positive Effects 3

    Sedation 60.0% 70%
    Stimulation 60.0% 70%
    Anxiety Suppression 50.0% 70%

    Adverse Effects 0

    Real-World Dose Distribution

    62K Doses

    From 10 individual dose entries

    Oral (n=9)

    Median: 1000.0mg 25th: 500.0mg 75th: 1000.0mg 90th: 1600.0mg
    mg/kg median: 12.738 mg/kg 75th: 13.937

    Form / Preparation

    Most common forms and preparations reported

    Harm Reduction

    drugs.wiki

    Lethal dose margin is narrow: deaths have occurred with ingestions as low as ~4–10 g; overdose presents with profound CNS depression, respiratory suppression, and risk of cardiac arrhythmias. Co-ingestion with alcohol or other depressants (opioids, benzodiazepines, GHB/GBL) markedly increases risk of loss of consciousness, respiratory depression, aspiration, and death—avoid these combinations entirely and place any unresponsive person in the recovery position while seeking emergency care. Chloral hydrate is metabolized primarily by alcohol dehydrogenase to trichloroethanol (active) and further to trichloroacetic acid; genetic variation and concurrent alcohol use can meaningfully alter both potency and duration between individuals. In cirrhosis or hepatic decompensation, chloral hydrate can precipitate or worsen hepatic encephalopathy; avoid use in significant liver disease and in untreated sleep apnea. Cardiac irritability/arrhythmia can occur in overdose and in susceptible individuals; those with structural heart disease or on other QT-/rhythm‑affecting drugs should avoid nonmedical use. Residual psychomotor impairment may persist into the next day due to metabolite half-lives; do not drive or operate machinery for at least a full night after dosing. Repeated frequent use rapidly builds tolerance and can cause dependence; withdrawal may begin within 12–24 hours after cessation in heavy users and may resemble alcohol/barbiturate withdrawal (including delirium)—medical supervision is strongly advised for dependent users. Oral and rectal routes can irritate mucosa; always dilute liquids and avoid concentrated solutions to reduce GI irritation; injection is strongly discouraged due to vein and tissue irritation. Products and syrups may vary in concentration; use an accurate milligram scale or clearly labeled pharmaceutical preparations to avoid dosing errors. Breast milk transfer occurs and may sedate infants; avoid during pregnancy and lactation unless medically supervised. If severe vomiting, chest pain, palpitations, confusion, or shallow breathing occur after use, seek emergency help immediately and avoid giving more depressants while awaiting care.

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