Prescribing Temazepam (Restoril)

Why Temazepam Still Matters

Temazepam is a middle-of-the-road benzodiazepine hypnotic that has outlasted its cohort. Of the five benzodiazepines the FDA formally approved for insomnia (flurazepam, temazepam, triazolam, estazolam, and quazepam), temazepam is the one still routinely prescribed. The others have been pushed aside by the z-drugs, by low-dose sedating antidepressants, and by the broad cultural retreat from benzodiazepines. Temazepam survived for two unglamorous reasons: it has a duration of action that actually fits a night of sleep, and it is metabolized by glucuronidation rather than the CYP450 system, which makes it clean, predictable, and unusually forgiving in exactly the patients who tend to be on everything else.

That second point is the whole case for temazepam. It is one of the three "LOT" benzodiazepines (Lorazepam, Oxazepam, Temazepam) that undergo Phase II hepatic glucuronidation with no active metabolites and almost no CYP-mediated drug interactions. For an elderly patient, a patient with cirrhosis, or a patient stacked with interacting medications, that pharmacokinetic profile is an advantage over alprazolam, diazepam, or clonazepam. If you are going to reach for a benzodiazepine hypnotic at all, temazepam is often the most defensible one to reach for.

This is not, though, a guide to a drug you should use freely. Temazepam has a narrow, legitimate place, short-term, situational, or carefully bounded treatment of severe insomnia, wrapped in a much larger set of reasons to be cautious. Benzodiazepine hypnotics suppress the slow-wave sleep that makes sleep restorative, produce dependence within weeks, accumulate cognitive and fall risk that patients and prescribers both routinely fail to notice, and can be lethal when combined with opioids or alcohol. Temazepam is not exempt from any of that.

The thesis of this guide is double-edged: temazepam is the benzodiazepine hypnotic to know because it is the cleanest one pharmacokinetically, but the skill is not in starting it, it's in bounding it, monitoring for the harms that hide in plain sight, and getting patients off it before short-term help becomes long-term dependence.

Part 1: Indications

FDA-Approved Use

• Short-term treatment of insomnia, particularly insomnia characterized by difficulty falling asleep, frequent nocturnal awakenings, and/or early-morning awakening.

That is the entire on-label indication. The labeling frames it as short-term (typically 7–10 days of use, with reassessment if used beyond 2–3 weeks), which reflects both the evidence base and the pharmacology of tolerance and dependence.

Where It Fits in Practice

Acute, situational insomnia. The cleanest use: a death in the family, a move, a new job, a hospitalization, a stretch of acute stress that has wrecked sleep for several nights. A defined stressor, a defined endpoint, a short course.

Insomnia comorbid with a psychiatric disorder, as an adjunct, not a solution. Insomnia and mood/anxiety disorders are tightly intertwined. This matters clinically because treating the depression while ignoring the comorbid insomnia reduces antidepressant effectiveness and predicts relapse. Temazepam can be a legitimate short-term bridge here, covering sleep while the antidepressant takes hold, but it is a bridge, not the destination. The sequencing of insomnia relative to the mood disorder is itself informative: insomnia more often precedes depression (41% vs. 29%) and more often follows anxiety, and a returning insomnia prodrome can be the earliest signal of depressive relapse.

The severely anxious patient with insomnia who has failed everything else. This is a real but narrow niche, and it is second- or third-line by design. As one sleep specialist put it plainly: "Occasionally I've used temazepam in an anxiety patient when nothing else works." That is the correct altitude: an occasional tool for the refractory case, not a routine choice.

Off-label anxiety. Temazepam is sometimes used off-label for anxiety, leaning on the general anxiolytic properties of the benzodiazepine class. But it is a hypnotic by design and dosing; if you want a benzodiazepine for daytime anxiety, other agents are better matched. Don't reach for a bedtime hypnotic to cover a daytime problem.

Who Temazepam Is Not For

• Patients with a current or recent substance use disorder, especially involving alcohol, opioids, or sedatives (Schedule IV controlled substance; real abuse and diversion potential).
• Patients on opioids (see boxed warning).
• Patients with untreated obstructive sleep apnea or significant COPD: temazepam suppresses respiratory drive and worsens apnea.
• Patients for whom you have no plan to stop it. If you cannot articulate the exit, reconsider the entry.

Part 2: Candidacy and Workup

Temazepam does not require the lab workup lithium does; there is no therapeutic level to draw and no organ to surveil chronically. The "workup" here is a candidacy assessment: the questions that determine whether a benzodiazepine hypnotic is safe for this patient.

Screen deliberately for:

Useful baseline tool: a sleep diary kept for more than 5 nights. It documents the true baseline (sleep latency, awakenings, total sleep time), anchors your assessment, and gives you an objective measure of response so you're not titrating on impression alone. It also frequently reveals a treatable sleep-hygiene or circadian problem that makes the hypnotic unnecessary.

There is no chronic lab monitoring requirement for temazepam. What replaces the lab draw is repeated clinical reassessment: is it still working, is it still needed, and are the quiet harms (cognitive dulling, morning sedation, falls) accumulating?

Part 3: How to Start and Dose

Formulation and doses

Temazepam is available as oral capsules, most commonly 7.5 mg, 15 mg, 22.5 mg, and 30 mg.

• Usual adult dose: 15 mg at bedtime.
• Range: 7.5 mg to 30 mg at bedtime.
• Start low, 7.5 mg or 15 mg, and use the lowest dose that works. 30 mg is the top of the range and buys more next-day hangover and more accumulation risk; reserve it for patients who have clearly failed lower doses.
• Elderly or debilitated patients: start at 7.5 mg. Go up only if needed and tolerated.

How to dose it

• Take immediately before getting into bed, or within a few minutes of it. Temazepam's onset is moderate rather than fast (some effect within roughly 30 minutes, but peak levels not until about 1.2–1.6 hours), so plan to be in bed when it takes hold. The single most effective way to prevent the rare-but-real complex sleep behaviors (sleep-walking, sleep-eating) is to make sure the patient is in bed by the time it works, not up wandering the kitchen.
• Allow a full night's opportunity for sleep, ideally 7–8 hours, before the patient needs to be up and functional. The duration of effect can run up to roughly 8 hours, and cutting the night short is a recipe for next-morning impairment.
• Avoid taking it on a full stomach if a fast onset is wanted; food slows benzodiazepine absorption and delays onset.
• Do not combine with alcohol or other sedatives, and counsel explicitly against it.

Duration of the prescription

More than the milligrams, this is the part of dosing that takes discipline. Prescribe for the shortest clinically necessary period: for acute situational insomnia, that is often just a handful of nights. Physiologic dependence begins to develop within several weeks of nightly use, so an open-ended nightly prescription manufactures the dependence you'll later have to taper.

Practical approaches:

• Limit the quantity dispensed and avoid automatic refills. A small quantity with a planned reassessment beats a 90-day supply on autopilot.
• Consider intermittent rather than nightly dosing where clinically appropriate (e.g., a few nights per week), which reduces tolerance and dependence, though for some patients this trades steady relief for unpredictability.
• Set the endpoint out loud at the first visit. "This is to get you through the next couple of weeks; then we reassess and, if you're still struggling, we address the underlying cause rather than just refilling this."

Part 4: Monitoring: No Labs, but Not "Set and Forget"

Temazepam has no specific laboratory monitoring parameters. But "no labs" is not "no monitoring": the surveillance is clinical, and the things you're watching for are precisely the ones patients don't report spontaneously.

At each contact, actively ask about:

• Efficacy and ongoing need. Is it still helping? For insomnia, tolerance to the hypnotic effect develops relatively fast, faster than tolerance to the anxiolytic effect, so a drug that worked in week one may be doing little by month three while still producing dependence and cognitive cost.
• Next-day sedation / "hangover." Especially in the elderly, morning grogginess is a red flag for accumulation or too high a dose. The classic tells: "I feel exhausted when I wake up," "it takes me three hours to get dressed," "I go right back to bed after breakfast." Treat those complaints as possible drug toxicity, not as the illness.
• Cognitive impairment. This is insidious. Benzodiazepine cognitive effects (memory, processing speed, attention) accumulate over months and are frequently invisible to both patient and prescriber. Family members often notice before either of you do.
• Falls. Fall risk is real and peaks early in treatment; in older adults benzodiazepines raise fall risk by roughly 50%. Ask specifically.
• Escalation / early refills. Requests for higher doses or early refills usually signal tolerance, dependence, or misuse; reassess rather than reflexively increase.

Part 5: Side Effects and How to Manage Them

Most acute side effects are mild, dose-dependent, and transient, but the serious harms of benzodiazepine hypnotics are the quiet, cumulative ones (cognition, falls, dependence, and sleep-architecture damage), not the obvious ones. Manage the acute effects, but keep your eye on the cumulative ones.

Central nervous system (the common, usually mild cluster)

Drowsiness, headache, dizziness, lightheadedness, and difficulty with concentration and memory. These arise from the non-specific GABA-A modulation that produces temazepam's effect in the first place. Daytime sedation is usually mild and often eases within a few days as tolerance develops.

Management:

• Lower the dose (drop 30 → 15, or 15 → 7.5).
• Confirm the timing: the patient needs a full 7–8 hour sleep window; morning impairment is often just too short a night.
• Reassess need if sedation persists.

Next-morning impairment and driving

Reaction time and processing speed are most impaired around the peak (roughly 30–60 minutes after dosing), but meaningful impairment can carry into the next morning, and affected patients are typically unaware of it.

Management:

• Counsel explicitly: do not drive or operate machinery if there is any residual grogginess, and never drive at peak effect.
• Use the lowest effective dose and the full sleep window.

Cognitive impairment (the important one)

Covered in Monitoring, worth repeating here because it is the harm most likely to be missed. It is dose- and duration-dependent, insidious, partially reversible after discontinuation (with some deficits detectable up to a year out), and a legitimate reason on its own to keep courses short and to run periodic taper trials.

Falls

Dose-dependent, highest early in treatment, and serious in the elderly (hip fractures can be life-altering or fatal). Switching to a z-drug does not reliably reduce fall risk. The real mitigation is lowest effective dose, shortest duration, and honest reassessment of whether the drug is needed at all.

Sleep architecture: the effect patients don't feel but should know about

This is a downside of benzodiazepine hypnotics that is easy to overlook, because the patient feels like they slept. Temazepam:

• Suppresses slow-wave (deep) sleep, pushing patients toward lighter Stage II sleep.
• Little effect on REM sleep at hypnotic doses; the sleep-laboratory studies in the label found REM unchanged.

The result is more time asleep but arguably less restorative sleep, and it sets up rebound insomnia on discontinuation. This is part of why abrupt stopping feels so bad and why some patients conclude they "can't sleep without it" when they are really experiencing withdrawal.

Respiratory suppression

Temazepam suppresses respiratory drive and blunts arousal responses, clinically important in obstructive sleep apnea and COPD, where it can worsen nocturnal hypoxemia, and catastrophic in combination with opioids or alcohol (see Toxicity).

Paradoxical / behavioral effects

Uncommon but documented across the class: disinhibition, agitation, and complex sleep behaviors (sleep-walking, sleep-eating, sleep-driving). Restoril's label carries the same complex-behaviors warning the z-drug labels carry. What it does not carry is the boxed warning and contraindication the z-drugs picked up in 2019, which is the one place temazepam compares favorably to zolpidem here. Counsel every patient to get into bed immediately after dosing, which prevents most cases. Be especially vigilant for disinhibition in the elderly, in dementia, and in personality-disordered patients.

The dementia question

Observational studies have linked benzodiazepine use to a 1.5–1.8-fold increased risk of Alzheimer's dementia, with risk rising with duration, higher dose, and longer half-lives. The signal is confounded by indication (benzodiazepines get prescribed to people with early, as-yet-undiagnosed cognitive or prodromal symptoms), and better-controlled recent studies weaken but do not fully erase the association. You don't need to resolve the causality debate to justify caution: the other, well-established cognitive and fall harms already argue for short courses and lowest effective doses, especially in the elderly.

Part 6: Toxicity, Overdose, and the Boxed Warning

Benzodiazepine overdose alone

Taken by itself, temazepam, like the benzodiazepine class, is comparatively safe in overdose. Even at high doses, respiratory depression from a benzodiazepine alone is usually limited; the picture is deep sedation, ataxia, slurred speech, and confusion, with breathing typically preserved. This is a major safety advantage over the barbiturates the class replaced.

The lethal combinations

The danger is synergistic CNS and respiratory depression when temazepam is combined with other depressants:

• Opioids: the most dangerous, and the subject of an FDA boxed warning. Benzodiazepines and opioids suppress breathing by different mechanisms (benzos via GABA-A, opioids in the medulla), so the combination is additive-to-synergistic and can be fatal. Concomitant use carries a 2–4 fold increased risk of overdose death.
• Alcohol: synergistic depression; potentially fatal at high combined levels, and a clear driver of accident risk even at moderate levels.
• Other sedative-hypnotics: muscle relaxants, sedating antihistamines/antipsychotics, other benzodiazepines and z-drugs all add to the depressant load.

Flumazenil

The benzodiazepine antagonist flumazenil can reverse temazepam in a monitored setting, but it is not for routine or home use: in a chronic benzodiazepine user it can precipitate withdrawal seizures, and it carries arrhythmia risk. Management of pure benzodiazepine overdose is usually supportive care (airway, breathing, circulation, monitoring for aspiration), not antagonist reversal.

Part 7: Drug Interactions

Interactions are where temazepam has its clearest advantage, and the main reason to prefer it over other benzodiazepines.

The pharmacokinetic advantage: glucuronidation, not CYP450

Temazepam is metabolized almost entirely by hepatic glucuronidation (Phase II / UGT), not by the CYP450 system, and it produces no active metabolites. The consequences:

• It is largely free of the CYP-mediated drug interactions that plague other benzodiazepines. Alprazolam, diazepam, and clonazepam are CYP substrates whose levels are raised by CYP3A4/2C19 inhibitors (fluoxetine, fluvoxamine, oral contraceptives, grapefruit juice), sometimes requiring dose reduction. Temazepam sidesteps this.
• No active metabolites means no accumulation of long-lived downstream compounds, a real advantage in the elderly and the hepatically impaired.

This is exactly why temazepam (with lorazepam and oxazepam) is the benzodiazepine of choice in complex polypharmacy, cirrhosis, and old age: predictable kinetics and few interaction landmines.

The interactions that do matter: pharmacodynamic, not pharmacokinetic

The dangerous interactions with temazepam are additive CNS/respiratory depression, not enzyme effects:

• Opioids: boxed warning; potentially fatal (see Part 6).
• Alcohol: synergistic depression; counsel explicitly against mixing.
• Other sedative-hypnotics: z-drugs, other benzodiazepines, sedating antihistamines/antipsychotics, muscle relaxants, gabapentinoids all add depressant load.

The clinical rule: with temazepam, stop worrying about the CYP interaction table and start worrying about the total sedative/respiratory-depressant burden the patient is carrying.

Part 8: Special Populations

Elderly (≥65)

Temazepam's profile matters most in older adults, and so does caution.

• The upside: glucuronidation metabolism means no CYP interactions and no accumulating active metabolites, so temazepam (like lorazepam/oxazepam) is better tolerated than long-acting or CYP-metabolized agents in this group. Avoid clonazepam and diazepam, which accumulate and drive fall risk.
• The downside: older adults are more sensitive to all benzodiazepine harms (falls with fractures, delirium, cognitive impairment, and daytime sedation), and the Beers Criteria advise against benzodiazepines in older adults generally.
• Practically: start at 7.5 mg, keep courses short, watch actively for morning grogginess and functional decline, and have a low threshold to taper. If a hypnotic is truly needed and a benzodiazepine is the choice, temazepam is a reasonable one, but the safest benzodiazepine is still one used briefly, at the lowest dose, with a plan to stop.

Pregnancy

Benzodiazepines cross the placenta. The historical concern was a first-trimester oral cleft association (strongest in older data on diazepam); more recent data have softened but not eliminated this signal. Late-pregnancy exposure risks neonatal sedation, "floppy infant" hypotonia, and neonatal withdrawal.

• Prefer non-pharmacologic management of pregnancy-related insomnia (sleep hygiene, CBT-I) first.
• If a benzodiazepine is necessary, some sources view occasional, intermittent, low-dose use, especially after the first trimester, as relatively lower-risk, but this is a shared-decision, case-by-case judgment, and short-acting agents are preferred to minimize fetal accumulation.
• Weigh against the real harms of untreated maternal illness and severe insomnia; don't reflexively stop a needed medication without a plan.

Lactation

Benzodiazepines enter breast milk in small amounts; the concern is infant sedation and lethargy, particularly with chronic dosing and with long-half-life, accumulating agents. Among benzodiazepines, short-acting agents with no active metabolites (lorazepam, oxazepam) are generally preferred for breastfeeding; temazepam is intermediate and best limited rather than used chronically. If used, monitor the infant for sedation, poor feeding, and lethargy, and favor the lowest dose and intermittent use.

Hepatic impairment

A relative strength. Because temazepam undergoes glucuronidation rather than hepatic oxidation and has no active metabolites, it is one of the safer benzodiazepines in liver disease, alongside lorazepam and oxazepam. The oxidatively metabolized agents (diazepam, alprazolam, chlordiazepoxide) accumulate in cirrhosis and should be avoided. Even so, use the lowest effective dose: hepatic patients are often encephalopathy-prone and sensitive to any sedative.

Renal impairment

Temazepam is not level-monitored and does not require the renal vigilance lithium does, but the glucuronide metabolite is renally cleared, so use conservative dosing and watch for oversedation in significant renal impairment. As with all these populations, lowest effective dose, shortest course.

Substance use disorder

Temazepam is a Schedule IV controlled substance with real abuse and diversion potential.

• Active alcohol, opioid, sedative, or stimulant use disorder is a contraindication. Benzodiazepines potentiate the opioid high and can reignite an abuse cycle.
• Remote, stable recovery (e.g., a long-sober alcoholic active in support) may permit cautious, structured, monitored use, naturalistic data suggest this can be done without relapse, but this is a deliberate, documented decision, not a default.
• Monitor for early refills, dose escalation, and use as an intoxicant.

Children and adolescents

Benzodiazepine hypnotics are not a standard treatment for pediatric insomnia; data are limited and the risk/benefit is unfavorable relative to behavioral approaches. Manage pediatric insomnia behaviorally and by treating underlying causes; reserve pharmacology for specialist settings.

Part 9: Discontinuation and Tapering

Every benzodiazepine, temazepam included, produces physiologic dependence after several weeks of regular use. Dependence is not addiction, it simply means abrupt cessation triggers withdrawal, but it means you never stop temazepam abruptly in a regular user.

What withdrawal looks like

• Common: rebound insomnia (often worse than baseline, driven partly by slow-wave rebound), rebound anxiety, tremor, headache, sweating (including night sweats, which patients rarely connect to withdrawal), perceptual changes, and irritability.
• Serious but rare at therapeutic doses without concurrent alcohol/other drugs: seizures, delirium, psychosis, and withdrawal akathisia (a severe inner restlessness linked to increased suicide risk).
• Post-acute withdrawal syndrome (PAWS): in some patients, anxiety, cognitive fog, paresthesias, tinnitus, and mood lability persist for months beyond the acute phase. Recognize it, it is frequently misread as relapse or a new disorder, which leads to the drug being restarted unnecessarily.

The rebound insomnia deserves special emphasis: it is the reason so many patients conclude they "can't sleep without it." Reframe it for them: this is temporary withdrawal, not proof of need.

How to taper

• Go slow, and slow down further near the end. A workable general rule for benzodiazepines is roughly a 25% reduction every 1–2 weeks early, tapering to smaller steps (≈12.5% or less) in the final stretch; another common framing is ~5% every few days for sensitive patients. The unifying principle: the first half of the dose comes off faster than the second half.
• Total duration ranges from a few weeks for short-course users to several months (occasionally a year or more) for long-term users. Match the taper length to the exposure length.
• Do not "skip nights" as a taper strategy: intermittent skipping causes blood-level swings and withdrawal, especially with a relatively short-acting agent. Reduce the dose steadily instead.
• Write the schedule down. Patients follow a concrete, dated, step-by-step taper far better than a verbal "cut back slowly." A written schedule measurably improves compliance and reduces the panic that drives patients back to full dose.
• Use the tools for fine reductions when needed near the end: smaller-strength capsules, and where necessary compounding-pharmacy custom doses.

The therapeutic alliance

The most important predictor of a successful taper is not the schedule, it's the therapeutic alliance. If the prescriber wants discontinuation and the patient doesn't, anxiety rises and the taper fails. Frame it as a joint project with a shared rationale (better cognition, fewer falls, clearer mornings), offer the patient control over pace ("Good month? Want to hold here two more weeks before the next step?"), and pair it with behavioral support: CBT-I is as effective as the drug for sleep and gives the patient something to replace it with.

When the taper fails

There is no medication with strong evidence to treat benzodiazepine withdrawal. CBT-I is the evidence-based backbone; some clinicians trial trazodone or melatonin for sleep, or propranolol/hydroxyzine for anxiety, though the evidence is thin. If repeated taper attempts fail and withdrawal is intolerable, maintaining the patient on the lowest tolerable dose is a legitimate harm-reduction strategy, not the goal, but safer than a forced, destabilizing withdrawal. Note too that large recent data caution against reflexively forcing benzodiazepines off high-risk patients: attempted withdrawal has been associated with increased mortality in some cohorts, a reminder that untreated illness carries its own risk and that the decision is a risk-benefit calculus.

Part 10: Temazepam vs. the Alternatives

For insomnia, temazepam competes against several classes, and the honest read is that the measured gains are small: a well-known AHRQ meta-analysis (Buscemi et al.) found that on polysomnography, benzodiazepines cut sleep latency by about 10 minutes and added about 33 minutes of total sleep time over placebo. Keep expectations, and the patient's, modest. There is also no evidence that FDA hypnotic approval confers any efficacy advantage; the approved benzodiazepines probably all work about equally well.

vs. z-drugs (zolpidem, zaleplon, eszopiclone). Z-drugs bind selectively to the alpha-1 GABA-A subunit, giving sedation with fewer anxiolytic/muscle-relaxant effects, generally faster onset, and less next-day hangover. But the z-drugs carry a boxed warning and a contraindication for complex sleep behaviors that temazepam's label does not, even though Restoril's label warns about the same behaviors. Z-drugs are the more common modern first-line, but temazepam wins when you specifically want a benzodiazepine's broader effect, or want to stay clear of the z-drug boxed warning, or need the glucuronidation kinetics.

vs. the melatonin agonist ramelteon (Rozerem). Ramelteon doesn't touch GABA at all, so it has no GABAergic side effects, no abuse potential, and is safe in the elderly and in respiratory disease. The trade-off: it doesn't deliver the subjective "knockout" patients expect, has a slower/subtler effect, and won't help daytime anxiety. Prefer it in exactly the patients where temazepam is riskiest (elderly, OSA, substance-use history) when its gentler effect is acceptable.

vs. sedating antidepressants. Trazodone (half-life ~7–8 hours) is a common off-label sleep agent that keeps patients asleep but can cause next-day sedation; low-dose doxepin (Silenor, 3–6 mg) is well-suited to early-morning awakening; mirtazapine helps sleep but drives weight gain. These carry no controlled-substance status or dependence liability and are often preferred for chronic insomnia, especially with comorbid depression.

vs. sedating antipsychotics (quetiapine, olanzapine). Effective sedatives but reserved for the most refractory cases given cost, weight gain, hyperglycemia, and tardive dyskinesia risk, generally the wrong tool for uncomplicated insomnia.

vs. other benzodiazepine hypnotics. Triazolam is shorter-acting and more amnestic; flurazepam and quazepam are long-acting with next-day hangover and accumulation. Temazepam's intermediate duration and clean glucuronidation metabolism are why it's the benzodiazepine hypnotic that endured. Among benzodiazepines generally, it shares the "LOT" advantage with lorazepam and oxazepam.

And the alternative that isn't a drug: CBT-I. For chronic insomnia, cognitive behavioral therapy for insomnia is as effective as a benzodiazepine, is durable after treatment ends, and has none of the dependence, cognitive, or fall liabilities. It belongs first-line for chronic insomnia, with temazepam as a short-term bridge at most.

Mechanism

Temazepam is a positive allosteric modulator of the GABA-A receptor. It binds at the benzodiazepine modulatory site on the receptor complex and enhances the effect of the brain's own GABA, "turbocharging" native GABA to increase the opening of chloride ion channels, hyperpolarizing neurons and slowing their firing. The net effect is the benzodiazepine class quartet: anxiolytic, hypnotic/sedative, anticonvulsant, and muscle-relaxant.

Because temazepam (like all classic benzodiazepines) binds non-selectively across GABA-A subtypes, including both the alpha-1 subunit that mediates sedation and the alpha-2 subunit that mediates anxiolysis, it produces sedation and anxiolysis (unlike the alpha-1-selective z-drugs, which are mostly just sedating). That non-selectivity also explains the broad CNS side-effect profile.

Onset is moderate (some effect within ~30 minutes, but Tmax ~1.2–1.6 hours), and clinical duration, governed more by lipophilicity than by the ~8–15 hour elimination half-life, covers roughly a night's sleep. Its defining pharmacologic feature is metabolic: glucuronidation with no active metabolites, the source of nearly every clinical advantage described in this guide.

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