Brand name: Vimpat
Drug class: Ion Channel Inhibition Agents

Medically reviewed by Drugs.com on Jun 10, 2024. Written by ASHP.

Introduction

Anticonvulsant; a functionalized amino acid.^{1 4 5 6 22 23 34}

Uses for Lacosamide

Seizure Disorders

Used orally as monotherapy or adjunctive therapy (i.e., in combination with other anticonvulsants) of partial-onset seizures in adults and pediatric patients ≥4 years of age.^{1 2 3 4 20 24 36 49 51 53 54 55 56}

Also available as an IV formulation for management of partial-onset seizures in adults when oral administration temporarily not feasible; IV use not evaluated in pediatric patients.^{1 20 24 36}

Neuropathic Pain

Has been used orally in the treatment of pain associated with diabetic peripheral neuropathy (DPN)^{† [off-label]}; additional controlled trials needed to confirm efficacy and safety.^{14 15 16 17 18 38 43}

Related/similar drugs

gabapentin, clonazepam, lamotrigine, lorazepam, pregabalin, topiramate, diazepam

Lacosamide Dosage and Administration

General

• Do not discontinue abruptly; withdraw gradually (e.g., over ≥1 week) to minimize potential for increased seizure frequency in patients with seizure disorders.¹ (See Discontinuance of Therapy under Cautions.)

• When converting from monotherapy with another anticonvulsant to lacosamide monotherapy, administer both anticonvulsant agents concomitantly until therapeutic dosage of lacosamide is achieved and has been administered for ≥3 days.¹ Withdraw concomitant anticonvulsant gradually over ≥6 weeks.¹

• Cardiac conduction abnormalities and arrhythmias reported with oral and IV use; obtain ECG prior to initiating therapy and after steady-state maintenance dosage is reached in patients who may be at risk.¹ Closely monitor patients receiving lacosamide by IV infusion.¹ (See Cardiac Effects under Cautions.)

• Closely monitor for notable changes in behavior that could indicate emergence or worsening of suicidal thoughts or behavior or depression.^{1 9 10 12} (See Suicidality Risk under Cautions.)

Administration

Administer orally (as tablets or oral solution).¹ May be administered by IV infusion in adults when oral administration temporarily not feasible.^{1 20 24 36 57}

Tablets and oral solution are bioequivalent.¹ The 30- and 60-minute IV infusions (but not the 15-minute IV infusion) are bioequivalent to the oral tablets.¹

Oral Administration

Administer orally (usually twice daily as tablets or oral solution) without regard to food.¹

Swallow tablets whole with liquid; do not divide.¹

Use a calibrated dosing device to measure and administer oral solution; household teaspoon or tablespoon not an adequate measuring device.¹

May administer oral solution through a nasogastric or gastrostomy tube.¹

IV Administration

Administer by IV infusion.¹ May administer without further dilution or mix with 5% dextrose injection, lactated Ringer’s injection, or 0.9% sodium chloride injection.^{1 24 36}

Vials are for single use only; discard any unused portions.¹

Rate of Administration

Administer over 30–60 minutes.¹ However, may administer as rapidly as over 15 minutes if necessary.^{1 24 36 40 41 57} Risk of adverse CNS effects may be increased with shorter durations of infusion.^{1 57}

Dosage

Pediatric Patients

Seizure Disorders

Partial Seizures in Children and Adolescents ≥4 Years of Age

Oral

Patients weighing ≥50 kg: Initially, 100 mg daily (given as 50 mg twice daily) as monotherapy or adjunctive therapy.¹ Based on clinical response and tolerability, may increase dosage by 100 mg daily (50 mg twice daily) no more frequently than once a week up to recommended maintenance dosage of 300–400 mg daily (150–200 mg twice daily) as monotherapy or 200–400 mg daily (100–200 mg twice daily) as adjunctive therapy.¹

Patients weighing 30 to <50 kg: Initially, 2 mg/kg daily (given as 1 mg/kg twice daily) as monotherapy or adjunctive therapy.¹ Based on clinical response and tolerability, may increase dosage by 2 mg/kg daily (1 mg/kg twice daily) no more frequently than once a week up to recommended maintenance dosage of 4–8 mg/kg daily (2–4 mg/kg twice daily) as monotherapy or adjunctive therapy.¹

Patients weighing 11 to <30 kg: Initially, 2 mg/kg daily (given as 1 mg/kg twice daily) as monotherapy or adjunctive therapy.¹ Based on clinical response and tolerability, may increase dosage by 2 mg/kg daily (1 mg/kg twice daily) no more frequently than once a week up to recommended maintenance dosage of 6–12 mg/kg daily (3–6 mg/kg twice daily) as monotherapy or adjunctive therapy.¹

Adults

Seizure Disorders

Partial Seizures in Adults ≥17 Years of Age

Oral

Initially, 200 mg daily (given as 100 mg twice daily) as monotherapy or 100 mg daily (given as 50 mg twice daily) as adjunctive therapy.¹

Based on clinical response and tolerability, may increase dosage by 100 mg daily (50 mg twice daily) no more frequently than once a week up to recommended maintenance dosage of 300–400 mg daily (150–200 mg twice daily) as monotherapy or 200–400 mg daily (100–200 mg twice daily) as adjunctive therapy.¹

Alternatively, may administer initial loading dose of 200 mg, followed 12 hours later by a dosage of 100 mg twice daily for 1 week; based on clinical response and tolerability, may increase dosage by 100 mg daily (50 mg twice daily) no more frequently than once a week up to recommended maintenance dosage of 300–400 mg daily (150–200 mg twice daily) as monotherapy or 200–400 mg daily (100–200 mg twice daily) as adjunctive therapy.¹ Steady-state concentrations produced by a single 200-mg loading dose are comparable to those produced by oral dosage of 100 mg twice daily.¹ Administer initial loading dose under medical supervision because of an increased risk of adverse CNS effects.¹

IV

When oral therapy is temporarily not feasible in adults, may administer by IV infusion at same dosages recommended for oral administration, including alternative loading dosage.¹ Clinical experience with IV dosing is limited to 5 consecutive days.^{1 24 36}

Neuropathic Pain† [off-label]

Pain Associated with Diabetic Peripheral Neuropathy† [off-label]

Oral

Initial dosage of 100 mg daily (given as 50 mg twice daily) usually has been used in clinical trials, with subsequent weekly increases to reach maintenance dosages of 400–600 mg daily (given as 200–300 mg twice daily) based on individual patient response and tolerability.^{14 15 16 17 18 38}

Prescribing Limits

Pediatric Patients

Seizure Disorders

Partial Seizures

Oral

Maximum recommended dosage is 400 mg daily.¹ In clinical studies, dosages >400 mg daily not more effective and associated with a substantially higher incidence of adverse effects.¹

Adults

Seizure Disorders

Partial Seizures

Oral/IV

Maximum recommended dosage is 400 mg daily.¹ In clinical studies, dosages >400 mg daily not more effective and associated with a substantially higher incidence of adverse effects.¹

Special Populations

Hepatic Impairment

Mild or moderate hepatic impairment: Titrate dosage with caution; reduce maximum dosage by 25%.¹ During dosage titration, closely monitor patients with coexisting hepatic and renal impairment.¹ (See Special Populations under Pharmacokinetics.)

Severe hepatic impairment: Use not recommended.¹ (See Special Populations under Pharmacokinetics.)

Patients with hepatic impairment who are taking potent inhibitors of CYP3A4 and/or CYP2C9: Dosage reduction of lacosamide may be required.¹

Renal Impairment

Mild to moderate renal impairment: Dosage adjustment not necessary.¹ (See Special Populations under Pharmacokinetics.)

Severe renal impairment (Cl_cr ≤30 mL/minute) or end-stage renal disease: Reduce maximum dosage by 25%.¹ In patients undergoing hemodialysis, consider dosage supplementation of up to 50% following hemodialysis.¹ (See Special Populations under Pharmacokinetics.)

Titrate dosage with caution in patients with any degree of renal impairment.¹

Patients with renal impairment who are taking potent inhibitors of CYP3A4 and/or CYP2C9: Dosage reduction of lacosamide may be required.¹

Geriatric Patients

Dosage adjustment based solely on age not necessary; however, manufacturer recommends cautious dosage titration.¹ (See Special Populations under Pharmacokinetics.)

Cautions for Lacosamide

Contraindications

• None.¹

Warnings/Precautions

Sensitivity Reactions

Multi-organ Hypersensitivity

Multi-organ hypersensitivity (also known as drug reaction with eosinophilia and systemic symptoms [DRESS]) reported with other anticonvulsants; can be fatal or life-threatening.¹ Clinical presentation is variable but typically includes fever, rash, lymphadenopathy, and/or facial swelling associated with other organ system involvement (e.g., eosinophilia, hepatitis, nephritis, hematologic abnormalities, myocarditis, myositis).¹

One case of symptomatic hepatitis and nephritis, consistent with a delayed multi-organ hypersensitivity reaction, reported in a healthy individual 10 days after discontinuing lacosamide; full recovery occurred within 1 month without specific treatment.¹ Additional potential cases included 2 patients with rash and elevated hepatic enzyme concentrations and one patient with myocarditis and hepatitis of uncertain etiology.¹

If manifestations of multi-organ hypersensitivity occur, evaluate patient immediately.¹ If an alternative cause cannot be identified, discontinue lacosamide.¹

Suicidality Risk

Increased risk of suicidality (suicidal ideation or behavior) observed in an analysis of studies using various anticonvulsants in patients with epilepsy, psychiatric disorders (e.g., bipolar disorder, depression, anxiety), and other conditions (e.g., migraine, neuropathic pain); risk in patients receiving anticonvulsants (0.43%) was approximately twice that in patients receiving placebo (0.24%).^{1 9 10 12} Increased suicidality risk was observed ≥1 week after initiation of anticonvulsant therapy and continued through 24 weeks.^{9 10} Risk was higher for patients with epilepsy compared with those receiving anticonvulsants for other conditions.^{1 9 10}

Closely monitor all patients currently receiving or beginning anticonvulsant therapy for changes in behavior that may indicate emergence or worsening of suicidal thoughts or behavior or depression.^{1 9 10 12}

Balance risk of suicidality with the risk of untreated illness.^{1 10} Epilepsy and other illnesses treated with anticonvulsants are themselves associated with morbidity and mortality and an increased risk of suicidality.^{1 12} If suicidal thoughts or behavior emerge during anticonvulsant therapy, consider whether these symptoms may be related to the illness itself.^{1 12} (See Advice to Patients.)

Dizziness and Ataxia

Dizziness and ataxia reported; in clinical studies, dizziness was the adverse effect most frequently leading to drug discontinuance.¹

Onset of dizziness and ataxia commonly observed during dosage titration.¹ Incidence was substantially increased at dosages >400 mg daily.¹ (See Advice to Patients.)

Cardiac Effects

Dose-dependent increases in PR interval and asymptomatic first-degree AV block observed in clinical studies.^{1 2 4 5 13 19 20 24 43} At steady state, the timing of maximum observed mean PR interval coincided with peak plasma lacosamide concentrations.¹

Profound bradycardia reported in a patient who received lacosamide 150 mg by IV infusion over 15 minutes.¹

Additional cases of cardiac arrhythmias (e.g., AV block, ventricular tachyarrhythmias, bradycardia) reported during postmarketing experience, mostly in patients with underlying proarrhythmic conditions or receiving concomitant drugs that affect cardiac conduction; rarely resulted in asystole, cardiac arrest, or death.¹

Use lacosamide with caution in patients with underlying proarrhythmic conditions such as known cardiac conduction abnormalities (e.g., marked first-degree AV block, second- or third-degree AV block, sick sinus syndrome without a pacemaker), cardiac sodium channelopathies (e.g., Brugada syndrome), or severe cardiovascular disease (e.g., myocardial ischemia, heart failure, structural heart disease) and in patients receiving concomitant drugs that affect cardiac conduction.^{1 23} When lacosamide is given with other drugs that prolong the PR interval, further PR prolongation is possible.^{1 23} (See Drugs that Affect Cardiac Conduction under Interactions.) Obtain an ECG before initiating lacosamide and after titration to steady state in such patients.¹ Closely monitor such patients who are receiving lacosamide by the IV route.¹

Atrial Fibrillation and Atrial Flutter

Lacosamide may predispose patients, particularly those with diabetic neuropathy and/or cardiovascular disease, to atrial arrhythmias (i.e., atrial fibrillation or flutter).¹ Atrial fibrillation or flutter reported in diabetic neuropathy studies; no cases reported in partial-onset seizure studies.¹ (See Advice to Patients.)

Syncope

Syncope or loss of consciousness reported in short-term diabetic neuropathy trials.¹ No increase in syncope observed in short-term, controlled trials in patients with partial-onset seizures; however, syncope reported in open-label studies in patients with preexisting cardiac risk factors.¹

Most cases of syncope occurred with dosages >400 mg daily.¹ The cause was not determined in most cases; however, several cases were associated with orthostatic changes in BP, atrial fibrillation/flutter (and associated tachycardia), or bradycardia.¹ (See Advice to Patients.)

Discontinuance of Therapy

Abrupt withdrawal of anticonvulsants may result in increased seizure frequency in patients with seizure disorders.¹ Withdraw lacosamide gradually (e.g., over ≥1 week).¹ (See General under Dosage and Administration.)

Phenylketonuria

Lacosamide oral solution contains aspartame, which is metabolized in the GI tract to provide 0.32 mg of phenylalanine per 20 mL of solution.^{1 44 45 46 47 48} Consider combined daily amount of phenylalanine from all sources, including from lacosamide oral solution, in patients with phenylketonuria.¹

Specific Populations

Pregnancy

North American Antiepileptic Drug (NAAED) Pregnancy Registry (for patients) at 888-233-2334 or [Web].¹

No adequate data in humans; in animal studies, developmental toxicity (i.e., increased embryofetal and perinatal mortality, growth deficit) observed at clinically relevant doses.¹

Developmental neurotoxicity observed in animals exposed to lacosamide during the period of postnatal development corresponding to the third trimester of human pregnancy.¹

Lactation

Lacosamide and/or its metabolites are distributed into milk in rats; not known if distributed into human milk.¹

Effects on nursing infant or milk production not known; consider known benefits of breast-feeding along with mother’s clinical need for lacosamide and any potential adverse effects on the infant from the drug or underlying maternal condition.¹

Pediatric Use

Safety and efficacy not established in pediatric patients <4 years of age.¹

Use of lacosamide tablets and oral solution in pediatric patients ≥4 years of age is supported by data from adult partial-onset seizure studies, pharmacokinetic studies, and safety data.¹ Safety of the injection not established in pediatric patients.¹

Has been shown in vitro to interfere with activity of collapsin response mediator protein-2 (CRMP-2), a protein involved in neuronal differentiation and control of axonal outgrowth; potential adverse effects on CNS development cannot be ruled out.¹ (See Actions.)

Decreased brain weights and long-term neurobehavioral changes (e.g., altered open field performance, deficits in learning and memory) observed in rats given lacosamide during neonatal and juvenile periods of postnatal development.¹

Geriatric Use

Insufficient experience in geriatric patients to determine whether they respond differently than younger patients.¹ (See Geriatric Patients under Dosage and Administration.)

Renal Impairment

Eliminated principally by renal excretion; drug exposure may be increased in patients with renal impairment.¹ Dosage adjustments may be necessary.¹ (See Renal Impairment under Dosage and Administration and see also Drugs Affecting or Metabolized by Hepatic Microsomal Enzymes under Interactions.)

Hepatic Impairment

Undergoes hepatic metabolism; drug exposure may be increased in patients with hepatic impairment.¹ Dosage adjustments may be necessary.¹ (See Hepatic Impairment under Dosage and Administration and see also Drugs Affecting or Metabolized by Hepatic Microsomal Enzymes under Interactions.)

Use not recommended in patients with severe hepatic impairment.^{1 21}

Common Adverse Effects

In studies with adjunctive lacosamide for partial-onset seizures: Dizziness,^{1 2 3 4 13 14 15 16 52} headache,^{1 4 13 14 15 16 52} diplopia,^{1 3 4 13 52} nausea,^{1 2 3 4 14 16 52} vomiting,^{1 2 3 4 13} fatigue,^{1 4 13 15 16} blurred vision,^{1 3 13} ataxia,^{1 2} somnolence,¹ tremor,^{1 3 15 16} nystagmus,^{1 2 3} memory impairment,¹ balance disorder,¹ vertigo,^{1 4} diarrhea.^{1 14}

In the monotherapy study for partial-onset seizures, adverse effects generally were similar to those observed in the adjunctive studies except for insomnia.¹

In studies with short-term IV lacosamide for partial-onset seizures, systemic adverse effects were similar to those observed with oral therapy; local adverse effects included injection site pain or discomfort, irritation, and erythema.^{1 8 24 36}

Drug Interactions

Metabolized by CYP3A4, 2C9, and 2C19.¹

Does not substantially induce CYP isoenzymes 1A2, 2B6, 2C9, 2C19, or 3A4 in vitro.^{1 19}

Does not substantially inhibit CYP isoenzymes 1A1, 1A2, 2A6, 2B6, 2C8, 2C9, 2D6, 2E1, 3A4, or 3A5 at plasma concentrations observed in clinical studies.^{1 19} In vitro data suggest that lacosamide may inhibit CYP2C19 at therapeutic concentrations; however, in vivo data (with omeprazole) suggested minimal or no inhibition (see Specific Drugs under Interactions).^{1 19}

Does not inhibit and is not a substrate of the P-glycoprotein (P-gp) transport system.¹

Drugs Affecting or Metabolized by Hepatic Microsomal Enzymes

Potential for pharmacokinetic drug interactions generally appears to be low.^{1 4 19 26}

Increased exposure to lacosamide is possible in patients with renal or hepatic impairment receiving potent inhibitors of CYP3A4 and/or CYP2C9.¹

Drugs Affecting or Affected by P-gp

Pharmacokinetic interactions unlikely.¹

Drugs that Affect Cardiac Conduction

Potential pharmacodynamic interaction (additive proarrhythmic effects).^{1 23 39 42 43 59} (See Cardiac Effects under Cautions and also see Specific Drugs under Interactions.)

Protein-bound Drugs

Clinically relevant pharmacokinetic interactions unlikely.^{1 16}

Specific Drugs

Lacosamide Pharmacokinetics

Absorption

Pharmacokinetics of oral and IV lacosamide are generally dose-proportional over a range of 100–800 mg.^{1 19}

Bioavailability

Oral bioavailability is approximately 100%.¹ Peak plasma lacosamide concentrations attained within 0.5–4 hours after oral administration.^{1 8 22} Peak plasma concentrations of inactive O-desmethyl metabolite attained within 0.5–12 hours after oral administration.¹

Lacosamide 30- and 60-minute IV infusions (but not the 15-minute IV infusion) are bioequivalent to the oral tablet.¹ Peak plasma concentrations reached at end of infusion.¹

Food

Food does not affect rate or extent of absorption.¹

Special Populations

In individuals with mild or moderate renal impairment, AUC is increased by approximately 25%.^{1 41} In individuals with severe renal impairment, AUC is increased by approximately 60%.^{1 41} However, peak plasma concentrations were unaffected.^{1 41} A 4-hour hemodialysis session reduces AUC by approximately 50%.¹

Individuals with moderate hepatic impairment (Child-Pugh class B) exhibit approximately 50–60% higher AUC compared with healthy individuals.¹ Pharmacokinetics not specifically evaluated in individuals with severe hepatic impairment.¹

In geriatric individuals, AUC and peak plasma concentrations (normalized for dosage and body weight) were approximately 20% higher compared with younger individuals, possibly related to differences in body weight and renal clearance.¹

Distribution

Extent

Lacosamide and/or metabolites distribute into milk in rats; unknown if distributed into human milk.¹

Plasma Protein Binding

<15%.¹

Elimination

Metabolism

Metabolized by CYP2C19; effect of other CYP isoenzymes or non-CYP enzymes in the metabolism of lacosamide is unclear.¹

Elimination Route

Eliminated primarily by renal excretion and biotransformation.^{1 19} Following oral and IV administration of a 100-mg radiolabeled dose, approximately 95% of the dose was recovered in urine and <0.5% was recovered in feces; the principal compounds excreted were unchanged lacosamide (approximately 40%), O-desmethyl-lacosamide (approximately 30%; inactive metabolite), and a structurally unknown polar fraction (approximately 20%; possibly serine derivatives).¹

Half-life

Lacosamide: Approximately 12–13 hours.^{1 19 22}

O-desmethyl metabolite: 15–23 hours.¹

Stability

Storage

Oral

Oral Solution

20–25°C (may be exposed to 15–30°C); do not freeze.¹ Discard any unused solution remaining after 7 weeks of first opening bottle.¹

Tablets

20–25°C (may be exposed to 15–30°C).¹

Parenteral

Injection for IV Infusion

20–25°C (may be exposed to 15–30°C); do not freeze.¹

Following dilution, infusion solution is stable for 4 hours at room temperature.¹

Actions

• Exact mechanism(s) of anticonvulsant and antinociceptive action is unknown.^{1 2 4 5 7 8 14 15 16 19 21 22 25 26 27 41}

• In vitro electrophysiologic studies have shown that lacosamide selectively enhances slow inactivation of voltage-gated sodium channels, which results in stabilization of hyperexcitable neuronal membranes and inhibition of repetitive neuronal firing.^{1 2 4 5 7 8 16 19 22 25 27}

• In some preclinical tests, lacosamide was found to bind to collapsin response mediator protein-2 (CRMP-2), a phosphoprotein that is mainly expressed in the nervous system and involved in neuronal differentiation, polarization, gene expression, and control of axonal outgrowth.^{1 7 8 13 16 25 27 28 30} It was suggested that this binding may contribute to the anticonvulsant and antinociceptive activity of the drug.^{1 7 8 13 16 25 27 28 30} However, binding was not confirmed in subsequent tests.⁴¹

• Does not exhibit binding affinity for GABA, N-methyl-D-aspartic acid (NMDA), adenosine, muscarinic, serotonin, histamine, dopamine, or other receptors.^{14 20 26} Does not affect reuptake or metabolism of norepinephrine, dopamine, serotonin, or GABA.^{6 7 20 26} Does not affect voltage-activated calcium channels (L-, N-, P/Q-, or T-type) or voltage-activated potassium channels and does not modulate delayed-rectifier or A-type potassium currents.^{6 20 22 26}

Advice to Patients

• Importance of advising patients or their caregivers to read the patient information (medication guide).¹

• Risk of suicidality (anticonvulsants, including lacosamide, may increase risk of suicidal thoughts or actions in about 1 in 500 people).^{1 10 12} Importance of patients, family, and caregivers being alert to day-to-day changes in mood, behavior, and actions and immediately informing clinician of any new or worrisome behaviors (e.g., talking or thinking about wanting to hurt oneself or end one’s life, withdrawing from friends and family, becoming depressed or experiencing worsening of existing depression, becoming preoccupied with death and dying, giving away prized possessions).^{1 10}

• Importance of taking lacosamide only as prescribed.¹

• Risk of dizziness, drowsiness, blurred vision, or problems with coordination and balance.^{1 6 35} Importance of advising patients not to drive, operate complex machinery, or engage in other hazardous activities until they have become accustomed to any such effects.^{1 35}

• Risk of dizziness, lightheadedness, fainting, or irregular heart beat, particularly in patients with underlying cardiovascular disease or cardiac conduction abnormalities and in those taking other drugs that affect the heart.^{1 35} These symptoms are more likely to occur when rising quickly from a recumbent position.³⁵ Cardiac arrest has been reported rarely.¹ Importance of advising patients who develop syncope to lie down with their legs raised until they feel better and to contact their clinician promptly.^{1 35}

• Risk of serious hypersensitivity reactions affecting multiple organs (e.g., liver, kidney); lacosamide should be discontinued if serious hypersensitivity reactions are suspected.¹ Importance of informing patients to contact their clinician promptly if symptoms suggestive of liver damage occur (e.g., fatigue, jaundice, dark urine).¹

• Importance of women informing clinicians if they are or plan to become pregnant or plan to breast-feed.^{1 35} Importance of clinicians informing women about the existence of and encouraging enrollment in pregnancy registries (see Pregnancy under Cautions).¹

• Importance of informing patients not to stop taking lacosamide without first talking to their clinician since stopping the drug suddenly can cause serious problems, including seizures.^{1 35}

• Importance of informing clinicians of existing or contemplated concomitant therapy, including prescription and OTC drugs and dietary or herbal supplements, as well as any concomitant illness (e.g., heart disease, kidney disease, liver disease, depression, bipolar disorder) or family history of suicidality or bipolar disorder.^{1 35}

• Importance of informing patients of other important precautionary information.¹ (See Cautions.)

Additional Information

The American Society of Health-System Pharmacists, Inc. represents that the information provided in the accompanying monograph was formulated with a reasonable standard of care, and in conformity with professional standards in the field. Readers are advised that decisions regarding use of drugs are complex medical decisions requiring the independent, informed decision of an appropriate health care professional, and that the information contained in the monograph is provided for informational purposes only. The manufacturer’s labeling should be consulted for more detailed information. The American Society of Health-System Pharmacists, Inc. does not endorse or recommend the use of any drug. The information contained in the monograph is not a substitute for medical care.

Preparations

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