Alprazolam

Benzodiazepine, Triazolobenzodiazepine, Anxiolytic

Alprazolam

Xanax

Alprazolam, marketed as Xanax, is the second most widely prescribed psychiatric medicine in the United States, accounting for approximately 30.5 million prescriptions in 2024. It is a high-potency, fast-acting triazolobenzodiazepine first synthesized in 1969 by the medicinal chemist Jackson B. Hester Jr. at the Upjohn Company in Kalamazoo, Michigan, patented in 1976, and approved by the United States Food and Drug Administration on 16 October 1981. Alprazolam is FDA-approved for generalized anxiety disorder and for panic disorder with or without agoraphobia; it is widely prescribed off-label for short-term symptomatic anxiety. Its short half-life relative to other benzodiazepines, distinctive triazolobenzodiazepine structure, and rapid onset shaped both its rise to dominance in the 1980s and 1990s and its central role in the modern story of benzodiazepine dependence and misuse. The medicine carries two distinct boxed warnings: the 2016 warning concerning the life-threatening risks of concomitant opioid use, and the 2020 class-wide warning concerning abuse, misuse, addiction, physical dependence, and withdrawal reactions inherent to the benzodiazepine class.

History

The history of alprazolam begins not at Upjohn but at Hoffmann-La Roche in Nutley, New Jersey, where the Polish-American chemist Leo Sternbach discovered the benzodiazepine class by accident. Sternbach, born in 1908 in Abbazia (now Opatija) in what was then Austria-Hungary, had completed his doctorate in organic chemistry at the Jagiellonian University in Krakow and joined Roche in Basel in the 1940s before being relocated to the Nutley laboratories during the war. Through the early 1950s he led a research program seeking new tranquilizers; the program produced a long series of heptoxdiazines that showed no useful pharmacology, and management told him to abandon the work. In 1957, during a general laboratory cleanup, an assistant came across an uncharacterized compound that had been set aside two years earlier and asked whether it should be discarded; Sternbach instead sent it for pharmacological screening as a final effort. The compound, eventually named chlordiazepoxide, showed potent sedative, muscle-relaxant, and anticonvulsant activity in animal testing, and on chemical re-evaluation proved to belong to a new ring system, the 1,4-benzodiazepines. Roche marketed chlordiazepoxide as Librium in 1960 and the more potent and shorter-acting diazepam as Valium in 1963; by the 1970s diazepam was the most widely prescribed medicine in the world.

Upjohn entered the benzodiazepine field as the patents on the Roche compounds approached expiration. Jackson B. Hester Jr., a medicinal chemist at the Upjohn laboratories in Kalamazoo, Michigan, undertook a structure-activity exploration of compounds that fused a triazole ring to the benzodiazepine skeleton. The triazolobenzodiazepines were a structurally distinct subclass with greater potency at the GABA-A receptor and, in some derivatives, properties suggestive of antidepressant activity not seen with the simple 1,4-benzodiazepines. Hester filed the patent on alprazolam on 29 October 1969; the patent (US 3,987,052) was granted on 19 October 1976. He had also developed triazolam, which Upjohn marketed as the hypnotic Halcion, in the same series.

The medicine's clinical positioning was shaped by the psychiatrist David V. Sheehan, who in the late 1970s argued that panic disorder was both more common than the field had recognized and pharmacologically responsive to benzodiazepines, contrary to the prevailing view that panic was rare and treatable only with tricyclic antidepressants. Sheehan worked with Upjohn to design and conduct what became the largest psychiatric drug trial of its era, the Cross-National Collaborative Panic Study, a multicenter randomized controlled trial published in the Archives of General Psychiatry in 1988 comparing alprazolam, imipramine, and placebo for panic disorder. The trial established alprazolam's efficacy for panic and supplied the regulatory basis for the FDA's 1990 expansion of alprazolam's indication to include panic disorder. Sheehan's framing of panic disorder as a discrete and treatable condition reshaped the diagnostic landscape; the Upjohn marketing campaign was so closely associated with the diagnosis that insiders sometimes referred to panic disorder as "the Upjohn illness."

The FDA approved alprazolam on 16 October 1981 for the treatment of anxiety disorders. Upjohn launched the medicine as Xanax in late 1981 and within two years it had become the most prescribed psychiatric medicine in the United States, a position it held through most of the 1980s. The 1990 expansion to include panic disorder, the 2003 introduction of the extended-release formulation (Xanax XR), and the patent expiration in 1993 with the entry of generic competitors shaped the next two decades of prescribing. The patent expired in September 1993; generic alprazolam reached the market the same year. Upjohn merged with Pharmacia in 1995 and was subsequently acquired by Pfizer in 2003; Pfizer spun the Upjohn business off in 2020 to form Viatris, which now holds the Xanax brand.

The efficacy literature on alprazolam for panic disorder has been complicated by publication bias. A meta-analysis by Ahn-Horst and Turner, published online in late 2023 and in print in Psychological Medicine in 2024, examined the five FDA-submitted regulatory trials of alprazolam extended-release for panic disorder, of which only one demonstrated a positive efficacy outcome; three of the trials were subsequently published in the peer-reviewed literature, all reporting positive outcomes, but the analysis found that two of the three published positive reports represented inappropriate spin of underlying negative results. The effect size based on the complete FDA-submitted trial set was small (Hedges's g 0.33); based on the published literature alone it was moderate (g 0.47), a difference reflecting the selective publication and framing of the data. The Australian Therapeutic Goods Administration rescheduled alprazolam to Schedule 8 in 2014 specifically because of concerns about tolerance, dependence, and abuse, and Pfizer Australia withdrew the Xanax brand from that market the same year.

The dominant modern story about alprazolam is dependence and misuse, and the regulatory response has come in two stages. On 31 August 2016, in response to a citizen petition from public health officials representing more than thirty states, cities, medical schools, and health organizations, the FDA required a boxed warning on all benzodiazepine and all opioid products describing the life-threatening risk of respiratory depression, coma, and death when the two classes are used together. Four years later, on 23 September 2020, the FDA required a second, distinct boxed warning on all benzodiazepines describing the class-inherent risks of abuse, misuse, addiction, physical dependence, and withdrawal reactions. Alprazolam remains a Schedule IV controlled substance in the United States and is similarly controlled under the 1971 United Nations Convention on Psychotropic Substances. United States benzodiazepine prescribing as a whole declined from approximately 110 million prescriptions in 2017 to 81 million in 2023, while Medicare Part D benzodiazepine prescribing rose by approximately 80% over the same period, reflecting a redistribution from younger to older patients, precisely the demographic most vulnerable to the harms.

The pharmacology of alprazolam has been the subject of two comprehensive clinical reviews worth noting: Verster and Volkerts 2004 (a clinical pharmacology and behavioral toxicity review that remains the standard reference for the medicine's behavioral effects), and Ait-Daoud and colleagues 2018 (a review of use, misuse, and withdrawal). The contemporary deprescribing literature is anchored by the Maudsley Deprescribing Guidelines (Horowitz and Taylor 2024), which provides the operational framework for hyperbolic tapering of benzodiazepines and which has reshaped UK and increasingly international practice on safe discontinuation.

Experience

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Problems

Anxiety disorders broadly★★★★★★★★★★★★★★★—××

FDA-approved for generalized anxiety disorder and panic disorder.

Panic disorder★★★★★★★★★★★★★★★—××

FDA-approved for panic disorder with or without agoraphobia (approved 1990). Some national guidelines (notably Australia's) recommend against alprazolam for panic disorder because of dependence and abuse concerns; the WFSBP recommends alprazolam for treatment-resistant panic disorder only in patients without a history of tolerance or dependence.

Generalized Anxiety Disorder★★★★★★★★★★★★★★★—××

FDA-approved for generalized anxiety disorder. Improvement classically within a week, distinguishing the benzodiazepine onset from the weeks-to-months timeline of SSRIs and SNRIs.

Anxiety★★★★★★★★★★★★★★★—××

Widely prescribed off-label for short-term symptomatic anxiety, procedural anxiety (MRI, dental procedures), and fear of flying. Use limited to as-needed dosing in patients without a history of substance use disorder.

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Titration strategies

Standard adult: anxiety▲0▼×

Start at 0.25-0.5 mg three times daily. Titrate gradually every 3-4 days based on response and tolerability; typical effective range is 0.5-4 mg daily in divided doses. Use the lowest effective dose for the shortest necessary duration.

Panic disorder▲0▼×

Start at 0.5 mg three times daily. Titrate every 3-4 days by no more than 1 mg daily increments. Typical effective dose for panic is 1-4 mg daily in divided doses; some patients require up to 10 mg daily (the FDA maximum), though doses above 4 mg carry substantially increased dependence risk.

Extended-release (Xanax XR)▲0▼×

Start at 0.5-1 mg once daily, typically in the morning. Titrate every 3-4 days by up to 1 mg daily. Typical effective range is 3-6 mg once daily. The extended-release form is preferred when continuous coverage is the goal; it produces less inter-dose anxiety than immediate-release dosing.

Elderly▲0▼×

Start at 0.25 mg twice or three times daily. Elderly patients have increased sensitivity to benzodiazepines, slower clearance, and substantially elevated risk of falls, confusion, and dependence. Use only when alternative treatments have been tried or are contraindicated; the American Geriatrics Society Beers Criteria list benzodiazepines as medicines to avoid in older adults.

Hepatic impairment▲0▼×

Start at 0.25 mg twice or three times daily. Alprazolam clearance is reduced approximately twofold in patients with alcoholic cirrhosis. Use with caution; avoid in moderate-to-severe hepatic impairment.

Discontinuation taper▲0▼×

Alprazolam's short half-life and high potency make it one of the more difficult benzodiazepines to discontinue safely. Patients on alprazolam for more than 3-4 weeks should be assumed to have developed physiological dependence; abrupt discontinuation can produce severe withdrawal including seizures and delirium.

The contemporary standard of care is hyperbolic tapering, as operationalized in the Maudsley Deprescribing Guidelines. The principle is that receptor occupancy declines hyperbolically with linear dose reduction, so equal absolute dose decrements produce progressively larger reductions in effect at lower doses; safe tapering therefore requires proportional reductions of the current dose with intervals lengthening as the dose falls. Practical implementation:

• Reduce by approximately 5-10% of the current dose every 2-4 weeks, slowing further if withdrawal symptoms emerge.
• For long-term users (more than 6 months of daily use), consider substitution to an equivalent dose of diazepam before tapering, since diazepam's long half-life produces more stable plasma levels and a more tolerable withdrawal trajectory. Approximate equivalence: 1 mg alprazolam to 20 mg diazepam.
• Use compounded liquid preparations or tablet splitting for the final low-dose steps, where the smallest commercial tablet (0.25 mg) represents a disproportionately large fraction of the residual dose.
• Expect months to years for long-term users, with long-term alprazolam users among the slowest to complete a taper.

The legacy FDA-label pace (reduction of 0.5 mg every three days) is appropriate only as an upper bound for short-duration low-dose users (less than 4-6 weeks of use, daily doses below 1 mg) and should not be applied to established users; for any patient who has taken alprazolam regularly for more than a few weeks, the slow hyperbolic taper is the safer default.

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Effects

• Anxiolysis👤 no reports yet⚕️ no reports yetRate×

  Onset within 30-60 minutes; near-immediate relief of acute anxiety symptoms.
• Somnolence / sedation👤 no reports yet⚕️ no reports yetRate×

  Common, particularly early in treatment; partial tolerance develops over days to weeks.
• Muscle relaxation👤 no reports yet⚕️ no reports yetRate×
• Anterograde amnesia👤 no reports yet⚕️ no reports yetRate×

  Dose-dependent impairment of new memory formation; clinically meaningful at higher doses and a particular concern in elderly patients.
• Ataxia👤 no reports yet⚕️ no reports yetRate×
• Dysarthria👤 no reports yet⚕️ no reports yetRate×
• Cognitive impairment👤 no reports yet⚕️ no reports yetRate×

  Demonstrable impairment in attention, working memory, and psychomotor speed; partial recovery on discontinuation but evidence suggests some persistent neuropsychological effects with long-term use.
• Disinhibition👤 no reports yet⚕️ no reports yetRate×

  Paradoxical reactions including aggression, rage, agitation, and rarely mania can occur; more common in patients with borderline personality disorder.
• Respiratory depression👤 no reports yet⚕️ no reports yetRate×

  Modest at therapeutic doses in benzodiazepine-naive patients; markedly increased when combined with opioids, alcohol, or other CNS depressants.
• Dependence / misuse👤 no reports yet⚕️ no reports yetRate×

  Physiological dependence develops with regular use; clinically significant in many patients after as little as 3-4 weeks of daily dosing. The short half-life and high potency of alprazolam produce dependence more rapidly than longer-acting benzodiazepines such as diazepam or clonazepam.
• Withdrawal/Discontinuation Syndrome👤 no reports yet⚕️ no reports yetRate×

  Anxiety rebound, insomnia, irritability, tremor, sweating, and at higher doses or with abrupt cessation seizures, delirium, and psychosis. Withdrawal from alprazolam is generally more severe than from longer-acting benzodiazepines and may require inpatient management.
• Dry mouth👤 no reports yet⚕️ no reports yetRate×
• Constipation👤 no reports yet⚕️ no reports yetRate×
• Falls👤 no reports yet⚕️ no reports yetRate×

  Substantially increased risk in elderly patients; the leading cause of benzodiazepine-related morbidity in older adults.

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Pharmacokinetics

Absorption

Oral bioavailability is approximately 80-90%. Peak plasma concentrations of the immediate-release formulation occur 1-2 hours after dosing; the extended-release formulation produces a slower, more sustained absorption profile with peak levels at 9-11 hours. Food modestly delays but does not reduce absorption.

Distribution

Plasma protein binding is approximately 80%, primarily to albumin. Volume of distribution approximately 0.84-1.42 L/kg. Alprazolam crosses the blood-brain barrier readily and the placenta freely; it is also excreted into breast milk.

Metabolism

Alprazolam is metabolized in the liver predominantly via CYP3A4 to two principal metabolites, alpha-hydroxyalprazolam and 4-hydroxyalprazolam, both of which have only weak activity at the GABA-A receptor and do not contribute meaningfully to clinical effect. A pharmacologically inactive benzophenone metabolite is also formed. Alprazolam itself has negligible CYP-inhibitory activity. The medicine's dependence on CYP3A4 metabolism creates clinically significant interactions with CYP3A4 inhibitors, with substantial increases in alprazolam exposure when given with ketoconazole, itraconazole, ritonavir, nefazodone, and other strong CYP3A4 inhibitors.

Elimination

Elimination is renal, almost entirely as metabolites; less than 20% of an oral dose is recovered unchanged in urine. Elimination half-life is 11-13 hours for the immediate-release formulation, 11-16 hours for the extended-release formulation. Half-life is prolonged in elderly patients, in obesity, in alcoholic cirrhosis, and in patients of Asian ancestry (mean half-life approximately 30% longer than in Caucasian patients).

Pharmacodynamics

Alprazolam is a high-potency positive allosteric modulator at the benzodiazepine binding site of the GABA-A receptor. The GABA-A receptor is a pentameric chloride channel; alprazolam binding enhances the channel's response to GABA, increasing chloride conductance and producing the inhibitory effects characteristic of the benzodiazepine class: anxiolysis, sedation, muscle relaxation, anticonvulsant activity, and anterograde amnesia. The fused triazole ring distinguishes alprazolam from the simple 1,4-benzodiazepines and is associated with antidepressant-like properties not seen with the older agents; the basis for this difference at the receptor level remains incompletely characterized.

Two pharmacodynamic features distinguish alprazolam clinically from longer-acting benzodiazepines. First, alprazolam produces a marked suppression of the hypothalamic-pituitary-adrenal axis, consistent with its anxiolytic potency but possibly relevant to the depressed mood that some long-term high-dose users describe. Second, limited imaging data suggest that alprazolam at clinical doses may produce a measurable increase in extracellular dopamine in the striatum more than lorazepam at equipotent doses; this dopaminergic action has been proposed as one possible contributor to alprazolam's reinforcing properties and higher abuse liability among benzodiazepines, though the imaging evidence is older and the magnitude of the effect uncertain.

Long-term benzodiazepine use produces adaptive changes at the GABA-A receptor that reduce its responsiveness to both endogenous GABA and exogenous benzodiazepines. This receptor downregulation is the molecular basis of tolerance and contributes to the rebound anxiety, insomnia, and dysphoria that characterize the withdrawal syndrome. The short elimination half-life of alprazolam relative to other benzodiazepines means that receptor exposure fluctuates substantially across the dosing interval, producing the inter-dose withdrawal symptoms that are a clinically distinctive feature of alprazolam dependence.

Interactions

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The clinically important interactions for prescribers:

• Opioids: life-threatening respiratory depression (FDA boxed warning, 2016). The single most consequential interaction. The FDA's August 2016 boxed warning, required on both benzodiazepines and opioids, addresses respiratory depression, coma, and death from combined use. If both are clinically necessary, use the lowest effective doses of both, monitor closely, counsel patients about respiratory risk, and offer take-home naloxone. Current public health guidance favors naloxone co-prescription for any patient receiving concurrent benzodiazepine and opioid therapy; patients should be instructed in its use, and a household member should be familiar with administration.
• Alcohol: synergistic CNS depression. Combined use produces severe sedation, ataxia, anterograde amnesia, and increased respiratory depression. Patients should be counseled to avoid alcohol during alprazolam treatment.
• Strong CYP3A4 inhibitors: substantial increases in alprazolam exposure. Contraindicated combinations include ketoconazole and itraconazole, which can increase alprazolam exposure several-fold. Other strong inhibitors requiring dose reduction or avoidance: ritonavir, nefazodone, clarithromycin, telithromycin. Moderate inhibitors (erythromycin, fluconazole, diltiazem, verapamil, grapefruit juice) require monitoring.
• Fluvoxamine, nefazodone, fluoxetine (via norfluoxetine): CYP3A4-mediated increases in alprazolam levels. Of the SSRIs, fluvoxamine and fluoxetine carry the most significant interaction; sertraline, citalopram, and escitalopram do not meaningfully affect alprazolam metabolism.
• Combined oral contraceptives: reduce alprazolam clearance and may increase plasma levels. Monitor for increased sedation, particularly when starting or stopping contraceptives in patients on chronic alprazolam.
• CYP3A4 inducers: reduce alprazolam effectiveness. St. John's wort, carbamazepine, rifampin, and phenytoin can substantially reduce alprazolam levels and effectiveness.
• Other CNS depressants (other benzodiazepines, barbiturates, sedating antihistamines, tricyclic antidepressants, gabapentinoids, muscle relaxants): additive sedation and respiratory depression. Avoid combinations where possible; if necessary, reduce doses.
• Tricyclic antidepressants (imipramine, desipramine): alprazolam co-administration increases imipramine levels by approximately 31% and desipramine by 20% via an incompletely characterized mechanism; clinical significance modest.
• Digoxin: alprazolam may increase digoxin serum levels, particularly in elderly patients, by an incompletely characterized mechanism. Consider digoxin level monitoring when starting alprazolam in patients on digoxin therapy.

  Pregnancy and lactation

Benzodiazepines including alprazolam cross the placenta freely and are excreted into breast milk. The historical pregnancy literature on the benzodiazepine class identified a signal for oral clefts (cleft lip and palate) with first-trimester exposure; the absolute risk is low, and the strength and specificity of the association remain debated. The alprazolam-specific pregnancy literature is smaller and less rigorously confounder-adjusted than the SSRI literature. Use of alprazolam in the third trimester may produce neonatal benzodiazepine withdrawal syndrome, "floppy infant syndrome," and respiratory depression at delivery. The abrupt discontinuation of alprazolam in long-term users carries substantial risks of its own: severe withdrawal syndrome with seizure risk, spontaneous abortion attributable to withdrawal stress, and severe rebound of the underlying anxiety condition. The clinical decision in pregnancy is genuinely complex, particularly for patients on alprazolam for panic disorder where untreated panic carries its own perinatal risks. For new pregnancies in women with anxiety disorders, SSRI treatment (typically sertraline) is generally preferred over benzodiazepine initiation. For women already maintained on alprazolam at the time of pregnancy, options include carefully supervised slow taper (over months, often with substitution to a longer-acting agent), continuation at the lowest effective dose with close monitoring, or substitution to an SSRI; the choice depends on clinical context and should be made in consultation with maternal-fetal medicine where available. Sertraline is generally preferred for breastfeeding women requiring anxiolytic pharmacotherapy; alprazolam is excreted into breast milk in low but pharmacologically active amounts.

Monitoring

Two boxed warnings apply to alprazolam. The 2016 boxed warning addresses respiratory depression, coma, and death from concomitant opioid use; see interactions and counseling. The 2020 class-wide boxed warning addresses the risks of abuse, misuse, addiction, physical dependence, and withdrawal reactions inherent to benzodiazepine treatment. Counsel patients about both risks at initiation and monitor across treatment. Patients on alprazolam for more than 3-4 weeks of daily use should be assumed to have developed clinically meaningful physiological dependence.

Screen for substance use disorder, alcohol use disorder, and respiratory disease before initiating. Particular caution in patients with obstructive sleep apnea, COPD, or other respiratory compromise; in patients with current or past opioid use; in patients with active mood disorders; and in patients with borderline personality disorder (paradoxical disinhibition and increased suicide risk are documented). Assess fall risk in elderly patients.

No routine laboratory monitoring required. Reassess clinical need, dose, and dependence status at each visit; document the indication and the plan for time-limited use where possible. Counsel about driving and other activities requiring vigilance, particularly early in treatment and after any dose change.

Overdose. Alprazolam overdose typically presents with progressive CNS depression: sedation, ataxia, dysarthria, confusion, and at higher doses respiratory depression and coma. Alprazolam alone is relatively safe in overdose by historical benzodiazepine standards, though it has been demonstrated to be more toxic than most other benzodiazepines in mixed overdose contexts. Most overdose mortality occurs in the context of polysubstance ingestion, particularly with opioids, alcohol, or other sedatives.

Management is primarily supportive: airway protection, ventilatory support as needed, monitoring of vital signs and consciousness. Activated charcoal may be considered within one hour of ingestion if the airway is protected.

Flumazenil, a benzodiazepine receptor antagonist, can reverse alprazolam effects but is used cautiously and is generally avoided in patients with chronic benzodiazepine use (where it can precipitate acute withdrawal seizures), in patients with mixed overdoses involving pro-convulsant agents such as tricyclic antidepressants, in patients with seizure disorder, and in patients with elevated intracranial pressure. The risk-benefit balance for flumazenil in benzodiazepine overdose generally favors supportive care over reversal, with flumazenil reserved for specific clinical situations (typically iatrogenic benzodiazepine oversedation in benzodiazepine-naive patients).

Patient counseling

Two boxed warnings apply to alprazolam. Counsel patients at initiation about both.

Opioid combination warning (2016 boxed warning): counsel patients explicitly never to combine alprazolam with prescription opioids, illicit opioids, or alcohol because of life-threatening respiratory depression risk. Patients should not borrow opioid medications from family members and should not use alprazolam recreationally with substances of unknown composition. For any patient receiving concurrent benzodiazepine and opioid therapy, offer take-home naloxone and instruct the patient and a household member in its administration.

Dependence and withdrawal warning (2020 boxed warning): counsel patients before initiation about the risks of dependence and withdrawal with regular use. Alprazolam works rapidly to relieve acute anxiety, but the same features that make it effective in the short term (high potency, rapid onset, short half-life) also drive its dependence liability. Patients should expect that taking alprazolam regularly for more than a few weeks will produce physical dependence, that stopping abruptly after dependence has developed can produce severe withdrawal including seizures, and that the only safe way to come off the medicine is a slow medically-supervised taper.

Alcohol: avoid alcohol during alprazolam treatment; the combination can produce severe sedation, behavioral disinhibition, and intoxication that exceeds either substance alone.

Driving and operating machinery: do not drive or operate machinery early in treatment, after any dose increase, or when combining alprazolam with other CNS depressants. Even at stable doses, alprazolam produces measurable impairment in attention, memory, and psychomotor speed that the patient may not subjectively perceive.

Discontinuation: do not stop alprazolam abruptly after more than 3-4 weeks of regular use. Taper slowly under medical supervision following the hyperbolic-taper principles outlined in the dosing section. Symptoms of withdrawal include rebound anxiety, insomnia, irritability, tremor, sweating, and at higher doses or with abrupt cessation, seizures and delirium.

Pregnancy: if pregnancy is planned or discovered, contact the prescriber immediately to discuss options. Do not stop alprazolam abruptly because of pregnancy concerns; the withdrawal stress carries its own risk to the pregnancy.

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See also

Diazepam, Clonazepam, Lorazepam, Sertraline, Triazolam

References

Summary

Classes

Benzodiazepine, Triazolobenzodiazepine, Anxiolytic

Common uses

• Anxiety★★★★★★★★★★★★★★★—×
• Anxiety disorders broadly★★★★★★★★★★★★★★★—×
• Generalized Anxiety Disorder★★★★★★★★★★★★★★★—×
• Panic disorder★★★★★★★★★★★★★★★—×

Pharmacy

Starting dose

0.25 mg

Preparations

0.25 mg, 0.5 mg, 1 mg, 2 mg tablets (immediate-release and orally disintegrating); 0.5 mg, 1 mg, 2 mg, 3 mg extended-release tablets; 1 mg/mL oral concentrate

US FDA Max

10 mg/d

Pill ID

• 0.25 mg: white oval scored tablet
• 0.5 mg: peach/orange oval scored tablet
• 1 mg: blue oval scored tablet
• 2 mg: white rectangular bar with three score lines (the "Xanax bar")
• XR forms: film-coated, varying shapes and colors by strength and manufacturer
• Oral concentrate: 1 mg/mL, alcohol-free solution

Pharmacology

Routes

Oral

Onset

30-60 min (immediate-release); 1-2 h (extended-release)

Duration

6 h (immediate-release); ~11 h (extended-release)

Half-life

11-13 h (immediate-release); 11-16 h (extended-release)

Bioavailability

80-90% oral

Pregnancy

Category D

Legal status

Schedule IV (US)

Purported mechanism

GABA-A positive allosteric modulator Alprazolam binds at an allosteric site on the GABA-A receptor and enhances the effects of GABA.▲0▼