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Cannabidiol

Class: Anticonvulsants, Miscellaneous
Chemical Name: 2-[(1R,6R)-3-methyl-6-prop-1-en-2-ylcyclohex-2-en-1-yl]-5-pentylbenzene-1,3-diol
Molecular Formula: C21H30O2
CAS Number: 13956-29-1
Brands: Epidiolex

Medically reviewed by Drugs.com on Oct 28, 2019. Written by ASHP.

Introduction

Anticonvulsant; a naturally occurring cannabinoid derived from the Cannabis sativa L. plant.

Uses for Cannabidiol

Seizure Disorders

Treatment of seizures associated with Lennox-Gastaut syndrome in adults and pediatric patients ≥2 years of age. Designated an orphan drug by FDA for use in this condition.

Treatment of seizures associated with Dravet syndrome in adults and pediatric patients ≥2 years of age. Designated an orphan drug by FDA for use in this condition.

Cannabidiol Dosage and Administration

General

  • Assess ALT, AST, and total bilirubin concentrations prior to initiating therapy. (See Hepatic Effects under Cautions.)

  • Avoid abrupt discontinuance; withdraw gradually to minimize potential for increased seizure frequency and status epilepticus. (See Discontinuance of Therapy under Cautions.)

  • Closely monitor for emergence or worsening of depression, suicidal thoughts or behavior (suicidality), or any unusual changes in mood or behavior. (See Suicidality Risk under Cautions.)

Restricted Distribution

  • Obtain cannabidiol through designated specialty pharmacies.

  • Contact the manufacturer at 833-426-4243 or consult the Epidiolex website ([Web]) for additional information.

Administration

Oral Administration

Administer orally (as an oral solution) twice daily.

Because food may affect exposure, some clinicians suggest that the drug be administered consistently in either the fed or fasting state. (See Food under Pharmacokinetics.)

Measure and administer prescribed dose using a calibrated measuring device (i.e., oral dosing syringe); a household teaspoon or tablespoon is not an adequate measuring device. For doses <1 mL, use a 1-mL oral syringe (e.g., provided by the pharmacy). For doses >5 mL, administer total dose in portions using the 5-mL oral syringe supplied by the manufacturer.

Administer directly into the patient’s mouth against the inside of the cheek.

Discard any unused portions of the oral solution 12 weeks after the container is first opened.

Dosage

Pediatric Patients

Seizure Disorders
Seizures Associated with Lennox-Gastaut Syndrome
Oral

Children and adolescents ≥2 years of age: Initially, 5 mg/kg daily (given as 2.5 mg/kg twice daily). Increase to maintenance dosage of 10 mg/kg daily (given as 5 mg/kg twice daily) after 1 week.

If further reduction of seizures is necessary and patient is tolerating a dosage of 10 mg/kg daily, may increase to maximum dosage of 20 mg/kg daily (given as 10 mg/kg twice daily).

Titrate dosage in weekly increments of 5 mg/kg daily (given as 2.5 mg/kg twice daily) as tolerated. If more rapid titration is necessary, may increase in increments of 5 mg/kg daily no more frequently than every other day.

In clinical studies, dosage of 20 mg/kg daily demonstrated slightly greater efficacy than dosage of 10 mg/kg daily, but was associated with a higher incidence of adverse effects.

Seizures Associated with Dravet Syndrome
Oral

Children and adolescents ≥2 years of age: Initially, 5 mg/kg daily (given as 2.5 mg/kg twice daily). Increase to maintenance dosage of 10 mg/kg daily (given as 5 mg/kg twice daily) after 1 week.

If further reduction of seizures is necessary and patient is tolerating a dosage of 10 mg/kg daily, may increase to maximum dosage of 20 mg/kg daily (given as 10 mg/kg twice daily).

Titrate dosage in weekly increments of 5 mg/kg daily (given as 2.5 mg/kg twice daily) as tolerated. If more rapid titration is necessary, may increase in increments of 5 mg/kg daily no more frequently than every other day.

In clinical studies, dosage of 20 mg/kg daily demonstrated slightly greater efficacy than dosage of 10 mg/kg daily, but was associated with a higher incidence of adverse effects.

Adults

Seizure Disorders
Seizures Associated with Lennox-Gastaut Syndrome
Oral

Initially, 5 mg/kg daily (given as 2.5 mg/kg twice daily). Increase to maintenance dosage of 10 mg/kg daily (given as 5 mg/kg twice daily) after 1 week.

If further reduction of seizures is necessary and patient is tolerating a dosage of 10 mg/kg daily, may increase to maximum of 20 mg/kg daily (given as 10 mg/kg twice daily).

Titrate dosage in weekly increments of 5 mg/kg daily (given as 2.5 mg/kg twice daily) as tolerated. If more rapid titration is necessary, may increase in increments of 5 mg/kg daily no more frequently than every other day.

In clinical studies, dosage of 20 mg/kg daily demonstrated slightly greater efficacy than dosage of 10 mg/kg daily, but was associated with a higher incidence of adverse effects.

Seizures Associated with Dravet Syndrome
Oral

Initially, 5 mg/kg daily (given as 2.5 mg/kg twice daily). Increase to maintenance dosage of 10 mg/kg daily (given as 5 mg/kg twice daily) after 1 week.

If further reduction of seizures is necessary and patient is tolerating a dosage of 10 mg/kg daily, may increase to maximum of 20 mg/kg daily (given as 10 mg/kg twice daily).

Titrate dosage in weekly increments of 5 mg/kg daily (given as 2.5 mg/kg twice daily) as tolerated. If more rapid titration is necessary, may increase in increments of 5 mg/kg daily no more frequently than every other day.

In clinical studies, dosage of 20 mg/kg daily demonstrated slightly greater efficacy than dosage of 10 mg/kg daily, but was associated with a higher incidence of adverse effects.

Prescribing Limits

Pediatric Patients

Seizure Disorders
Seizures Associated with Lennox-Gastaut Syndrome
Oral

Maximum of 20 mg/kg daily.

Seizures Associated with Dravet Syndrome
Oral

Maximum of 20 mg/kg daily.

Adults

Seizure Disorders
Seizures Associated with Lennox-Gastaut Syndrome
Oral

Maximum of 20 mg/kg daily.

Seizures Associated with Dravet Syndrome
Oral

Maximum of 20 mg/kg daily.

Special Populations

Hepatic Impairment

Dosage reduction is recommended in patients with moderate or severe hepatic impairment; slower dosage titration may be necessary in such patients.

Moderate hepatic impairment (Child-Pugh class B): Initially 2.5 mg/kg daily (given as 1.25 mg/kg twice daily); increase to maintenance dosage of 5 mg/kg daily (given as 2.5 mg/kg twice daily). Maximum recommended dosage is 10 mg/kg daily (given as 5 mg/kg twice daily).

Severe hepatic impairment (Child-Pugh class C): Initially 1 mg/kg daily (given as 0.5 mg/kg twice daily); increase to 2 mg/kg daily (given as 1 mg/kg twice daily). Maximum recommended dosage is 4 mg/kg daily (given as 2 mg/kg twice daily).

Mild hepatic impairment (Child-Pugh class A): No dosage adjustment necessary. (See Hepatic Impairment under Cautions.)

Renal Impairment

Dosage adjustment not necessary. (See Renal Impairment under Cautions.)

Geriatric Patients

Select dosage cautiously, usually starting at the lower end of the dosage range.

Cautions for Cannabidiol

Contraindications

  • Hypersensitivity to cannabidiol or any excipient in the formulation, including sesame seed oil. (See Sensitivity Reactions under Cautions.)

Warnings/Precautions

Hepatic Effects

Elevations in serum aminotransferase concentrations (mainly ALT) reported; in some cases, hospitalization was required. Usually occurred in the first 2 months of therapy; however, some cases reported up to 18 months after initiation of treatment.

Risk factors include use of higher dosages of cannabidiol, concomitant use of valproate or clobazam, and elevated baseline aminotransferase concentrations. Majority of ALT elevations occurred in patients taking concomitant valproate; concomitant clobazam associated with hepatic enzyme elevations, but to a lesser extent.

Usually reversible following discontinuance or dosage reduction of cannabidiol and/or concomitant valproate.

Monitor ALT, AST, and total bilirubin concentrations prior to initiating therapy; repeat monitoring at 1, 3, and 6 months after initiation of therapy, and periodically thereafter as clinically indicated. Also monitor ALT, AST, and total bilirubin concentrations within 1 month following any change in cannabidiol dosage or any addition or change to concomitant therapy with other potentially hepatotoxic drugs. Consider more frequent monitoring in patients receiving concomitant valproate or who have elevated liver enzymes at baseline.

If signs or symptoms suggestive of liver injury occur (e.g., unexplained nausea, vomiting, right upper quadrant pain, fatigue, anorexia, jaundice, and/or dark urine), promptly assess ALT, AST, and total bilirubin concentrations; interrupt or discontinue cannabidiol therapy as appropriate.

Discontinue therapy in patients with ALT or AST concentrations >3 times ULN and concurrent bilirubin concentrations >2 times ULN, and also in patients with sustained aminotransferase elevations >5 times ULN.

If used concomitantly with other potentially hepatotoxic drugs (e.g., valproate, clobazam), consider dosage adjustments. (See Interactions.)

Somnolence and Sedation

Somnolence and sedation may occur; effects are dose related, generally occur early in treatment, and may diminish with continued therapy. Risk is increased when used concomitantly with clobazam. (See Specific Drugs under Interactions.)

Monitor for somnolence and sedation, particularly when used concomitantly with other CNS depressants, including alcohol.

Suicidality Risk

Increased risk of suicidality (suicidal behavior or ideation) observed in an analysis of studies using various anticonvulsants in patients with epilepsy, psychiatric disorders, and other conditions; risk in patients receiving anticonvulsants (0.43%) was approximately twice that in patients receiving placebo (0.24%). Increased suicidality risk was observed as early as 1 week after initiation of anticonvulsant therapy; because most studies were ≤24 weeks' duration, risk of treatment beyond 24 weeks not known. Risk was higher for patients with epilepsy compared with those receiving anticonvulsants for other conditions.

Balance risk of suicidality with risk of untreated illness. Epilepsy and other illnesses treated with anticonvulsants are themselves associated with morbidity and mortality and an increased risk of suicidality.

Monitor all patients receiving anticonvulsants for suicidal thoughts and behavior. If suicidal thoughts or behavior emerges during anticonvulsant therapy, consider whether these symptoms may be related to the illness itself. (See Advice to Patients.)

Sensitivity Reactions

Hypersensitivity

Hypersensitivity reactions (e.g., pruritus, erythema, angioedema) requiring treatment with antihistamines reported.

If a hypersensitivity reaction occurs, discontinue cannabidiol oral solution and initiate appropriate therapy. Do not reinitiate therapy. (See Contraindications under Cautions.)

Discontinuance of Therapy

Abrupt withdrawal may increase seizure frequency and risk of status epilepticus. Withdraw gradually unless safety concerns require more rapid withdrawal. In clinical studies, dosage of cannabidiol was tapered over a period of 10 days.

Abuse Potential and Dependence

Cannabidiol is subject to control as a schedule V (C-V) drug.

Abuse-related adverse events not observed in phase 1 clinical studies. In an abuse potential study in recreational drug users, therapeutic and supratherapeutic doses of cannabidiol produced positive subjective responses (e.g., “drug liking,” “take drug again”) comparable to placebo. In animal studies, cannabinoid-like behavioral responses, including generalization to tetrahydrocannabinol (THC; the psychoactive component of Cannabis sativa ) and self-administration of the drug, not observed. No affinity for receptors associated with abuse potential identified in receptor binding studies.

Not likely to produce physical dependence; discontinuance after 28 days of administration did not produce withdrawal symptoms.

Laboratory Test Interferences.

May cause positive drug tests for cannabis.

Specific Populations

Pregnancy

No adequate data in humans; in animal studies, developmental toxicity and embryolethality observed at dose exposures similar to or higher than those achieved with recommended human dosages.

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

Lactation

Not known whether distributed into milk; effects on milk production or breast-fed infant also not known. Consider benefits of breast-feeding and importance of cannabidiol to the woman; also consider potential adverse effects on the breast-fed infant from the drug or underlying maternal condition.

Pediatric Use

Safety and efficacy for the treatment of seizures associated with Lennox-Gastaut syndrome or Dravet syndrome established in pediatric patients ≥2 years of age.

Safety and efficacy not established in patients <2 years of age.

Geriatric Use

No experience in patients ≥55 years of age to determine whether geriatric patients respond differently than younger adults.

Hepatic Impairment

Increased systemic exposure in patients with moderate or severe hepatic impairment; dosage adjustments recommended. (See Hepatic Impairment under Dosage and Administration.)

Systemic exposure not affected by mild hepatic impairment.

Renal Impairment

Renal impairment (mild, moderate, or severe) does not have a clinically important effect on systemic exposure. (See Renal Impairment under Dosage and Administration.)

Common Adverse Effects

Somnolence, decreased appetite, diarrhea, elevated aminotransferase concentrations, fatigue/malaise/asthenia, rash, insomnia/sleep disorder/poor quality sleep, infection, irritability/agitation, lethargy, sedation, decreased weight, aggression/anger, vomiting, upper respiratory tract infection, status epilepticus, convulsion, pyrexia, anemia.

Adverse effects are similar among patients with Lennox-Gastaut syndrome and Dravet syndrome, and also in pediatric and adult patients.

Interactions for Cannabidiol

Metabolized by CYP3A4, CYP2C19, UGT1A7, UGT1A9, and UGT2B7.

May inhibit CYP2C8, CYP2C9, and CYP2C19; may induce or inhibit CYP1A2 and CYP2B6 at clinically relevant concentrations. Also inhibits UGT1A9 and UGT2B7, but does not inhibit UGT 1A1, 1A3, 1A4, 1A6, or 2B17.

Inactive metabolite (7-COOH-CBD) inhibits breast cancer resistance protein (BCRP) and bile salt export pump (BSEP) at clinically relevant concentrations. Cannabidiol and active metabolite (7-OH-CBD) not expected to affect BCRP, BSEP, P-glycoprotein (P-pg), organic anion transporters (OAT) 1 and OAT3, organic cation transporters (OCT) 1 and OCT2, multidrug and toxin extrusion transporters (MATE) 1 and MATE2K, or organic anion transport proteins (OATP) 1B1 and OATP1B3.

Drugs Affecting Hepatic Microsomal Enzymes

Moderate or potent CYP3A4 or CYP2C19 inhibitors: Possible increased plasma concentrations and adverse effects of cannabidiol. Consider dosage reduction of cannabidiol.

Potent CYP3A4 or CYP2C19 inducers: Possible decreased plasma concentrations and efficacy of cannabidiol. Consider dosage increase of cannabidiol based on clinical response and tolerability.

Drugs Metabolized by Hepatic Microsomal Enzymes

CYP1A2 or CYP2B6 substrates: Pharmacokinetic interactions possible; consider dosage adjustment of the CYP1A2 or CYP2B6 substrate as clinically appropriate.

CYP2C8 or CYP2C9 substrates: Possible increased plasma concentrations and adverse effects; consider dosage reduction of the CYP2C8 or CYP2C9 substrate as clinically appropriate (e.g., if adverse effects related to the substrate drug occur).

CYP2C19 substrates: Possible increased plasma concentrations of sensitive substrates; consider dosage reduction of the sensitive CYP2C19 substrate as clinically appropriate (e.g., if adverse effects related to the substrate drug occur).

CYP3A4 substrates: Pharmacokinetic interaction not expected.

Drugs Metabolized by Uridine Diphosphate-glucuronosyltransferase Enzymes

UGT1A9 or UGT2B7 substrates: Possible increased concentrations of the substrate; consider dosage reduction of the substrate as clinically appropriate (e.g., if adverse effects related to the substrate drug occur).

Specific Drugs

Drug

Interaction

Comments

Bupropion

Possible increased or decreased concentrations of bupropion (CYP2B6 substrate)

Consider dosage adjustment of bupropion as clinically appropriate

Caffeine

Possible increased or decreased concentrations of caffeine (CYP1A2 substrate)

Consider dosage adjustment of caffeine as clinically appropriate

Carbamazepine

Clinically important effects on carbamazepine concentrations not observed

Clobazam

Increased risk of hepatic enzyme elevations

Increased risk of somnolence and sedation

Increased peak plasma concentration and AUC of active cannabidiol metabolite; increased peak plasma concentration and AUC of N-desmethylclobazam

If hepatic enzyme elevations occur, consider dosage reduction or discontinuance of clobazam

If adverse effects of clobazam occur, consider reducing its dosage

Clonazepam

Clinically important effects on clonazepam concentrations not observed

CNS depressants

Increased risk of sedation and somnolence

Monitor for sedation and somnolence

Diazepam

Possible increased concentrations of diazepam (CYP2C19 substrate)

If adverse effects of diazepam occur, consider reducing its dosage as clinically appropriate

Diflunisal

Possible increased concentrations of diflunisal (UGT1A9 substrate)

If adverse effects of diflunisal occur, consider reducing its dosage as clinically appropriate

Efavirenz

Possible increased or decreased concentrations of efavirenz (CYP2B6 substrate)

Consider dosage adjustment of efavirenz as clinically appropriate

Eslicarbazepine

Substantially increased eslicarbazepine concentrations observed

Ethosuximide

Clinically important effects on ethosuximide concentrations not observed

Ezogabine

Clinically important effects on ezogabine concentrations not observed

Fenofibrate

Possible increased concentrations of fenofibrate (UGT1A9 substrate)

If adverse effects of fenofibrate occur, consider reducing its dosage as clinically appropriate

Gemfibrozil

Possible increased concentrations of gemfibrozil (UGT2B7 substrate)

If adverse effects of gemfibrozil occur, consider reducing its dosage as clinically appropriate

Lacosamide

Clinically important effects on lacosamide concentrations not observed

Lamotrigine

Possible increased concentrations of lamotrigine based on its pharmacokinetic disposition (UGT2B7 substrate); however, clinically important change in serum lamotrigine concentrations not observed in an open-label study

If adverse effects of lamotrigine occur, consider reducing its dosage as clinically appropriate

Levetiracetam

Clinically important effects on levetiracetam concentrations not observed

Lorazepam

Possible increased concentrations of lorazepam (UGT2B7 substrate)

If adverse effects of lorazepam occur, consider reducing its dosage as clinically appropriate

Midazolam

No affect on plasma concentrations of midazolam (sensitive CYP3A4 substrate)

Morphine

Possible increased concentrations of morphine (UGT2B7 substrate)

If adverse effects of morphine occur, consider reducing its dosage as clinically appropriate

Oxcarbazepine

Clinically important effects on oxcarbazepine concentrations not observed

Perampanel

Clinically important effects on perampanel concentrations not observed

Phenobarbital

Clinically important effects on phenobarbital concentrations not observed

Phenytoin

Possible increased concentrations and adverse effects of phenytoin based on its pharmacokinetic disposition (CYP2C9 substrate); however, clinically important change in serum phenytoin concentrations not observed in an open-label study

If adverse effects of phenytoin occur, consider reducing its dosage as clinically appropriate

Pregabalin

Clinically important effects on pregabalin concentrations not observed

Propofol

Possible increased concentrations of propofol (UGT1A9 substrate)

If adverse effects of propofol occur, consider reducing its dosage as clinically appropriate

Rufinamide

Substantially increased rufinamide concentrations observed

Stiripentol

Slightly increased stiripentol peak plasma concentration and AUC

Theophylline

Possible increased or decreased concentrations of theophylline (CYP1A2 substrate)

Consider dosage adjustment of theophylline as clinically appropriate

Topiramate

Substantially increased topiramate concentrations observed

Valproate

Increased risk of hepatic enzyme elevations

No effect on valproate systemic exposure

If hepatic enzyme elevations occur, consider dosage reduction or discontinuance of cannabidiol and/or valproate

Vigabatrin

Clinically important effects on vigabatrin concentrations not observed

Zonisamide

Substantially increased zonisamide concentrations observed

Cannabidiol Pharmacokinetics

Absorption

Bioavailability

Systemic exposure increases in a less than proportional manner over a dosage range of 5–20 mg/kg daily.

At steady state, peak plasma cannabidiol concentrations occur 2.5–5 hours following administration of the oral solution.

Low oral bioavailability; undergoes extensive first-pass metabolism.

Systemic exposure to the inactive metabolite 7-carboxy-cannabidiol (7-COOH-CBD) is approximately 40-fold higher than that of the parent drug.

Food

Administration with a high-fat, high-calorie meal increased AUC and peak plasma concentrations by fourfold and fivefold, respectively, and decreased total variability, compared with administration in the fasted state. (See Administration under Dosage and Administration.)

Special Populations

Hepatic impairment: Systemic exposure increased approximately 2.5- to 5.2-fold in patients with moderate (Child-Pugh class B) or severe (Child-Pugh class C) hepatic impairment. Systemic exposure not substantially affected by mild hepatic impairment (Child-Pugh class A).

Renal impairment: Systemic exposure not substantially affected by mild, moderate, or severe renal impairment.

Distribution

Extent

Distributes rapidly into CNS and adipose tissue. Not known whether distributed into milk.

Plasma Protein Binding

>94%.

Elimination

Metabolism

Extensively metabolized in the liver and gut, principally by CYP2C19, CYP3A4, UGT1A7, UGT1A9, and UGT2B7.

Elimination Route

Excreted primarily in feces, with minor renal clearance. Following administration of a radiolabeled dose of cannabidiol, approximately 84% of the radioactivity was recovered in feces and 8% in urine.

Half-life

56–61 hours.

Stability

Storage

Oral

Solution

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

Store container in an upright position and keep the cap tightly closed. Discard unused portions 12 weeks after container is first opened.

Actions

  • Exact mechanism of anticonvulsant action not fully elucidated; however, does not appear to be related to a direct effect on cannabinoid receptors.

  • A naturally occurring cannabinoid derived from the Cannabis sativa L. plant.

  • Exhibits anticonvulsant activity in several animal seizure models, including maximal electroshock seizures, audiogenic seizures, and chemically induced seizures. Also modulates various receptors and ion channels; however, further study is needed to determine clinical role of these effects.

  • Little to no affinity for cannabinoid receptors CB1 or CB2; unlike THC, does not possess psychoactive properties and has a low potential for abuse. (See Abuse Potential and Dependence under Cautions.)

Advice to Patients

  • Importance of advising patients and/or caregivers to read the patient information (medication guide) and the instructions for use.

  • Importance of instructing patients and/or caregivers regarding administration of cannabidiol oral solution. Importance of advising patients to discard any unused oral solution 12 weeks after the container is first opened. (See Administration under Dosage and Administration.)

  • Risk of hepatic injury; importance of informing patients and/or caregivers of the need for specific monitoring during therapy. Importance of informing clinician promptly of any signs or symptoms of liver injury (e.g., unexplained nausea, vomiting, abdominal pain, fatigue, anorexia, jaundice, dark urine).

  • Risk of somnolence and sedation, and impairment of judgment, thinking, or motor skills. Importance of advising patients not to drive or operate machinery until the effects of the drug are known.

  • Anticonvulsants, including cannabidiol, may increase the risk of suicidal thoughts or behavior. Importance of patients, caregivers, and family members being alert to and immediately reporting emergence or worsening of depression, any unusual changes in mood or behavior, or emergence of suicidal thoughts, behavior, or thoughts of self harm.

  • Importance of advising patients not to discontinue cannabidiol therapy without consulting with their clinician. Withdraw the drug gradually to minimize the risk of increased seizure frequency and status epilepticus.

  • Importance of informing patients that cannabidiol may cause positive cannabis drug screens.

  • Importance of informing clinicians of existing or contemplated concomitant therapy, including prescription (e.g., clobazam, valproate) and OTC drugs, vitamins, herbal supplements, and any cannabis-based products, as well as any concomitant illnesses (e.g., liver disease).

  • Importance of women informing clinicians if they are or plan to become pregnant or plan to breast-feed. Importance of clinicians informing women about the existence of and encouraging enrollment in the North American Antiepileptic Drug Pregnancy Registry. (See Pregnancy under Cautions.)

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

Preparations

Excipients in commercially available drug preparations may have clinically important effects in some individuals; consult specific product labeling for details.

Please refer to the ASHP Drug Shortages Resource Center for information on shortages of one or more of these preparations.

Cannabidiol oral solution is subject to control under the Federal Controlled Substances Act of 1970 as a schedule V (C-V) drug.

Distribution of cannabidiol is restricted. (See Restricted Distribution under Dosage and Administration.)

Cannabidiol

Routes

Dosage Forms

Strengths

Brand Names

Manufacturer

Oral

Solution

100 mg/mL

Epidiolex (C-V)

Greenwich Biosciences

AHFS DI Essentials™. © Copyright 2021, Selected Revisions October 28, 2019. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, Maryland 20814.

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