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    Flurazepam molecular structure

    Flurazepam Stats & Data

    Dalmane Dalmadorm
    Chemical Class Benzodiazepine
    Psychoactive Class Depressant
    Half-Life Parent: ~2–4 h; active metabolite N‑desalkylflurazepam: ~47–100 h (wide interindividual range; accumulation with repeated use is expected).

    Pharmacology

    DrugBank
    Protein binding 83% State Solid

    Description

    A benzodiazepine derivative used mainly as a hypnotic.

    Mechanism of Action

    Flurazepam binds to an allosteric site on GABA-A receptors. Binding potentiates the action of GABA on GABA-A receptors by opening the chloride channel within the receptor, causing chloride influx and hyperpolarization.

    Pharmacodynamics

    Flurazepam, a benzodiazepine derivative, is a hypnotic agent which does not appear to decrease dream time as measured by rapid eye movements (REM). Furthermore, it decreases sleep latency and number of awakenings for a consequent increase in total sleep time.

    Metabolism

    Flurazepam is rapidly metabolized and is excreted primarily in the urine. Both hydroxyethyl flurazepam (the major metabolite) and N-desalkyl flurazepam are active. The N-desalkyl metabolite is slowly excreted in the urine as the conjugated form

    Absorption

    Flurazepam hydrochloride is rapidly (30 minutes) absorbed from the gastrointestinal tract

    Toxicity

    Coma, confusion, low blood pressure, sleepiness

    Indication

    For short-term and intermittent use in patients with recurring insomnia and poor sleeping habits

    Half-life

    The mean apparent half-life of flurazepam is 2.3 hours. The half life of elimination of N1-des-alkyl- flurazepam ranged from 47 to 100 hours

    Elimination

    Flurazepam is rapidly metabolized and is excreted primarily in the urine. Less than 1% of the dose is excreted in the urine as N1-desalkyl-flurazepam.

    Receptor Profile

    Receptor Actions

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

    Receptor Binding

    Translocator protein modulator

    Effect Profile

    Curated + 11 Reports
    Benzodiazepine 6.6

    Strong anxiolysis and cognitive impairment with moderate euphoria, mild sedation

    Anxiolysis×3
    10
    Sedation / Relaxation×2
    5
    Motor / Cognitive Impairment×1
    10
    Euphoria / Mood Lift×1
    6

    Tolerance & Pharmacokinetics

    drugs.wiki
    Half-Life
    Parent: ~2–4 h; active metabolite N‑desalkylflurazepam: ~47–100 h (wide interindividual range; accumulation with repeated use is expected).
    Addiction Potential
    Moderate to high; benzodiazepine-type dependence may develop with regular use. Abrupt cessation after prolonged or high-dose use risks severe withdrawal (including seizures).

    Experience Report Analysis

    Erowid
    11 Reports
    2007–2017 Date Range
    6 With Age Data
    3 Effects Detected

    Demographics

    Gender Distribution

    Age Distribution

    Reports Over Time

    Effect Analysis

    Erowid

    Effects aggregated from 11 experience reports (11 Erowid)

    11 Reports
    3 Effects Detected
    3 Positive
    0 Adverse
    0 Neutral

    Effect Sentiment Distribution

    Confidence Distribution

    Positive Effects 3

    Sedation 54.5% 70%
    Anxiety Suppression 36.4% 70%
    Stimulation 27.3% 70%

    Adverse Effects 0

    Real-World Dose Distribution

    62K Doses

    From 11 individual dose entries

    Oral (n=11)

    Median: 30.0mg 25th: 30.0mg 75th: 45.0mg 90th: 60.0mg
    mg/kg median: 0.372 mg/kg 75th: 0.64

    Form / Preparation

    Most common forms and preparations reported

    Benzodiazepine Equivalence

    mg Flurazepam = mg Diazepam
    Bioavailability Oral 83%

    Flurazepam - 15-30mg's ~=10mg Diazepam.

    All other CNS depressants.

    Harm Reduction

    drugs.wiki

    Flurazepam is rapidly absorbed but acts as a prodrug to N-desalkylflurazepam, which has a very long elimination half-life (roughly 47–100 hours), so effects can accumulate across nights and significantly impair next-day cognition, coordination, and reaction time. Driving impairment and increased accident risk are documented with benzodiazepines in general, and risk rises sharply if alcohol is also used; avoid driving or operating machinery not only the night of dosing but also the next day if residual sedation is present. Older adults eliminate benzodiazepines more slowly and face higher risks of falls, confusion, and amnesia; use the lowest dose possible and avoid long-acting hypnotics in this group where alternatives exist. Combining flurazepam with opioids or alcohol greatly increases the risk of life‑threatening respiratory depression; if any opioids are in use, do not take flurazepam and ensure naloxone availability in the household. Avoid combining with other CNS depressants such as GHB/GBL, barbiturates, or sedating antihistamines; even cannabis can meaningfully increase psychomotor impairment. People with pre‑existing respiratory disorders (e.g., OSA, COPD) are more susceptible to hypoventilation at sedative doses; medical oversight is advised, and flurazepam is generally a poor choice in these settings. Physical dependence can develop within weeks; never stop abruptly after repeated use—coordinate a slow, individualized taper with a clinician to mitigate severe withdrawal and seizure risk. In breastfeeding, flurazepam is generally not preferred due to long-acting metabolites and a report of infant sedation during multi‑drug exposure; if used, infants should be monitored for excessive drowsiness and poor feeding. In overdose, supportive care is first-line; flumazenil is typically avoided outside select scenarios because it can precipitate seizures—particularly in benzodiazepine‑tolerant patients or mixed TCA overdoses. Due to widespread circulation of counterfeit ‘benzodiazepine’ tablets (sometimes containing potent nitazene opioids), avoid non‑pharmacy sources; if exposure is possible, use drug‑checking services where available and never mix with depressants. Space doses by at least 24–48 hours and avoid ‘booster’ redoses at night; apparent early wear‑off can reflect redistribution, while the active metabolite persists and will compound next-day effects.

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