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Austedo

Generic Name: Deutetrabenazine
Class: Vesicular Monoamine Transporter 2 (VMAT2) Inhibitors
Chemical Name: (3RS,11bRS)-9,10-Di([2H3]methoxy)-3-(2-methylpropyl)-1,3,4,6,7,11b-hexahydro-2H-benzo[a]quinolizin-2-one
Molecular Formula: C19H21D6NO3
CAS Number: 1392826-25-3

Medically reviewed on May 7, 2018

Warning

    Depression and Suicidality in Patients with Huntington's Disease
  • Deutetrabenazine increases the risk of depression and suicidal thoughts and behavior (suicidality) in patients with Huntington’s disease; balance this risk with clinical need for treatment of chorea.1

  • Closely monitor patients for the emergence or worsening of depression, suicidality, or unusual changes in behavior.1

  • Inform patients, caregivers, and families of risk of depression and suicidality and instruct them to promptly report any behaviors of concern to the treating clinician.1

  • Exercise particular caution when treating patients with a history of depression or prior suicide attempts or ideation, which are increased in frequency in Huntington's disease.1

  • Deutetrabenazine is contraindicated in patients with Huntington's disease who are suicidal or have untreated or inadequately treated depression.1 (See Depression and Suicidality in Patients with Huntington's Disease under Cautions.)

Introduction

A vesicular monoamine transporter 2 (VMAT2) inhibitor;1 5 8 deuterium-substituted derivative of tetrabenazine.2 5 8

Uses for Austedo

Huntington's Chorea

Treatment of chorea associated with Huntington's disease;1 2 designated an orphan drug by FDA for the treatment of Huntington's disease.3

Although no direct, comparative studies between deutetrabenazine and tetrabenazine have been conducted to date, the principal efficacy studies suggest that deutetrabenazine has a lower risk of moderate to severe adverse effects than tetrabenazine.9 In addition, deutetrabenazine usually is given twice daily compared with 3 times daily for most patients receiving tetrabenazine.5 9 These clinical differences appear to be related to the different pharmacokinetic profiles of deutetrabenazine and tetrabenazine (see Pharmacokinetics).5 9

Tardive Dyskinesia

Treatment of tardive dyskinesia.1 6 12

Tardive dyskinesia is a hyperkinetic movement disorder associated with prolonged use of antipsychotic agents or other antidopaminergic drugs (e.g., metoclopramide).28 100 101 102 104

There currently is no standard treatment for tardive dyskinesia; management generally has included discontinuance or dosage reduction of the precipitating drug when possible, switching from a conventional or first-generation antipsychotic to an atypical or second-generation antipsychotic, or switching to clozapine therapy.28 100 101 103 104

Tourette's Syndrome

Has been used for the symptomatic management of Tourette's syndrome (Gilles de la Tourette's syndrome);5 7 designated an orphan drug by FDA for the treatment of Tourette's syndrome in pediatric patients.3 (See Pediatric Use under Cautions.)

Austedo Dosage and Administration

General

  • Allow at least 14 days to elapse between discontinuance of an MAO inhibitor and initiation of deutetrabenazine; in addition, allow at least 20 days to elapse between discontinuance of reserpine and initiation of deutetrabenazine.1 (See Specific Drugs under Interactions.)

  • Observe patients with Huntington's disease closely for clinical worsening or emergence of depression, suicidal thoughts or behavior (suicidality), or unusual changes in behavior.1 (See Boxed Warning and also see Depression and Suicidality in Patients with Huntington's Disease under Cautions.)

  • In patients at risk for QT-interval prolongation, assess QT interval before and after increasing total deutetrabenazine dosage to >24 mg daily.1 (See Prolongation of QT Interval under Cautions.)

Restricted Distribution

  • Available only through a specialty pharmacy.10

  • Contact Shared Solutions at [Web] or at 800-887-8100 for specific availability information.10

Administration

Oral Administration

Administer orally with food.1 Swallow tablets whole; do not chew, crush, or break tablets.1

Total daily dosages <12 mg: Administer once daily.1

Total daily dosages ≥12 mg: Administer in 2 divided doses.1

Dosage

Individualize dosage based on symptom control (i.e., reduction of chorea or dyskinesia) and tolerability.1

If used with a potent CYP2D6 inhibitor, dosage adjustment may be required.1 (See Interactions.)

If treatment is interrupted for >1 week, retitrate dosage as with initial therapy.1 May resume treatment at the previous maintenance dosage (without titration) for treatment interruptions of <1 week.1

May discontinue treatment without tapering the dosage.1

Adults

Huntington's Chorea
Oral

Initially, 6 mg once daily.1 May increase daily dosage in 6-mg increments at weekly intervals up to the maximum recommended dosage of 48 mg daily.1

Administer daily dosages ≥12 mg in 2 divided doses.1

Tardive Dyskinesia
Oral

Initially, 6 mg twice daily.1 May increase daily dosage in 6-mg increments at weekly intervals up to the maximum recommended dosage of 48 mg daily.1

Administer daily dosages ≥12 mg in 2 divided doses.1

Transferring Patients from Tetrabenazine to Deutetrabenazine

In patients being switched from tetrabenazine: Discontinue tetrabenazine and initiate deutetrabenazine the following day.1 See Table 1 for recommended initial deutetrabenazine dosages based on current total daily dosage of tetrabenazine.1 After switching, adjust deutetrabenazine dosage at weekly intervals.1

Table 1. Initial Dosage Recommendations for Adults Being Transferred from Tetrabenazine to Deutetrabenazine Therapy.1

Current Tetrabenazine Daily Dosage

Initial Deutetrabenazine Dosage Regimen

12.5 mg

6 mg once daily

25 mg

6 mg twice daily

37.5 mg

9 mg twice daily

50 mg

12 mg twice daily

62.5 mg

15 mg twice daily

75 mg

18 mg twice daily

87.5 mg

21 mg twice daily

100 mg

24 mg twice daily

Prescribing Limits

Adults

Huntington's Chorea
Oral

Maximum 48 mg daily.1

Poor CYP2D6 metabolizer phenotype: Maximum 36 mg daily (maximum single dose 18 mg).1

Tardive Dyskinesia
Oral

Maximum 48 mg daily.1

Poor CYP2D6 metabolizer phenotype: Maximum 36 mg daily (maximum single dose 18 mg).1

Special Populations

Hepatic Impairment

Contraindicated in patients with hepatic impairment.1 (See Hepatic Impairment under Cautions.)

Renal Impairment

Not studied; manufacturer provides no specific dosage recommendations.1

Geriatric Patients

Select dosage with caution, usually beginning with the lower end of the dosage range, because of greater frequency of decreased hepatic, renal, and/or cardiac function and of concomitant disease or other drug therapy in geriatric patients.1

Poor CYP2D6 Metabolizers

Do not exceed 36 mg daily (maximum single dose 18 mg).1 (See Poor CYP2D6 Metabolizers under Cautions.)

Cautions for Austedo

Contraindications

  • Patients with Huntington's disease who are suicidal or have untreated or inadequately treated depression.1 (See Boxed Warning and also see Depression and Suicidality in Patients with Huntington's Disease under Cautions.)

  • Hepatic impairment.1 (See Hepatic Impairment under Cautions.)

  • Concomitant therapy with reserpine.1 (See Specific Drugs under Interactions.)

  • Concomitant therapy with an MAO inhibitor.1 (See Specific Drugs under Interactions.)

  • Concomitant therapy with tetrabenazine or valbenazine.1 (See Specific Drugs under Interactions.)

Warnings/Precautions

Warnings

Depression and Suicidality in Patients with Huntington's Disease

Increased risk for depression and suicidal ideation or behavior (suicidality) in patients with Huntington's disease.1 Deutetrabenazine may increase such risk.1 In the principal efficacy study, depression and suicidal ideation reported in 4 and 2% of deutetrabenazine-treated patients, respectively; no suicide attempts or completed suicides were reported.1

Balance potential risks of depression and suicidality with clinical need for treatment of chorea.1 Closely monitor patients for emergence or worsening of depression, suicidality, or unusual changes in behavior.1 Inform patients, caregivers, and families of these risks and instruct them to promptly report any behaviors of concern to the treating clinician.1 Immediately evaluate patients with Huntington's disease who express suicidal ideation.1 Consider drug discontinuance if depression or suicidality does not resolve.1

Exercise particular caution when treating patients with a history of depression or prior suicide attempts or ideation, which are increased in patients with Huntington's disease.1 (See Contraindications under Cautions.)

Other Warnings and Precautions

Clinical Worsening and Adverse Effects in Patients with Huntington's Disease

Huntington’s disease is a progressive disorder characterized by changes in mood, cognition, chorea, rigidity, and functional capacity over time.1 VMAT2 inhibitors, including deutetrabenazine, may cause worsening in mood, cognition, rigidity, and functional capacity.1

Periodically reevaluate need for continued deutetrabenazine therapy by assessing its effect on chorea and possible adverse effects (e.g., sedation or somnolence, depression and suicidality, parkinsonism, akathisia, restlessness, cognitive decline).1 Dosage reduction or drug discontinuance may help distinguish between drug-induced adverse effects and disease progression.1 Underlying chorea may improve over time, thereby possibly decreasing the need for deutetrabenazine.1

Prolongation of QT Interval

Small increase in corrected QT (QTc) interval observed; may be clinically important in patients who are poor CYP2D6 metabolizers or are concurrently receiving a potent CYP2D6 inhibitor.1 Dosage reduction may be necessary in such patients.1

Factors that may increase the risk of torsades de pointes and/or sudden death in association with drugs that prolong the QTc interval include bradycardia, hypokalemia or hypomagnesemia, concomitant use of other drugs that prolong the QTc interval, and presence of congenital long QT syndrome.1

Avoid use in patients with congenital long QT syndrome or history of cardiac arrhythmias.1

In patients concurrently receiving other drugs known to prolong the QT interval, monitor QTc interval before and after deutetrabenazine dosage increases to >24 mg daily or dosage increases of other drugs known to prolong the QT interval.1 (See Drugs that Prolong QT Interval under Interactions.)

Neuroleptic Malignant Syndrome

Neuroleptic malignant syndrome (NMS), a potentially fatal syndrome characterized by hyperpyrexia, muscle rigidity, altered mental status, and autonomic instability, has been reported with drugs that reduce dopaminergic transmission.1 Although not reported with deutetrabenazine, NMS has been reported with tetrabenazine (a closely related VMAT2 inhibitor).1 4

Immediately discontinue therapy and initiate supportive and symptomatic therapy if NMS occurs.1 Careful monitor for recurrence if therapy is reinstituted following recovery from NMS.1

Akathisia, Agitation, and Restlessness

Increased risk of akathisia, agitation, or restlessness in patients with Huntington's disease or tardive dyskinesia.1

Monitor for akathisia, restlessness, and agitation.1 If akathisia develops, reduce deutetrabenazine dosage; drug discontinuance may be necessary in some patients.1

Parkinsonism in Patients with Huntington's Disease

Parkinsonism may develop; may be difficult to distinguish between drug-induced effect and rigidity associated with progression of Huntington's disease.1 For some patients, drug-induced parkinsonism may result in more functional disability than untreated chorea.1

If parkinsonism develops, consider dosage reduction; some patients may require drug discontinuance.1

Sedation and Somnolence

Sedation or somnolence is a common dose-limiting adverse effect.1

May impair cognitive and/or physical abilities required to perform potentially hazardous tasks such as driving or operating machinery.1 (See Advice to Patients.)

Hyperprolactinemia

Elevated serum prolactin concentrations reported with tetrabenazine (a closely related VMAT2 inhibitor).1 4

If contemplating deutetrabenazine therapy in a patient with previously detected breast cancer, consider that approximately one-third of human breast cancers are prolactin dependent in vitro.1 In addition, chronic hyperprolactinemia has been associated with low estrogen concentrations and an increased risk of osteoporosis.1

Perform appropriate laboratory testing and consider drug discontinuance if symptomatic hyperprolactinemia (e.g., amenorrhea, galactorrhea, gynecomastia, impotence) suspected.1

Binding to Melanin-containing Tissues

Binds to melanin-containing tissues, possibly resulting in accumulation and toxicity with long-term use; clinical importance unknown.1 Ophthalmologic monitoring in clinical studies was inadequate to exclude possibility of injury after long-term drug exposure.1

Specific Populations

Pregnancy

Manufacturer states no adequate data available on developmental risk associated with deutetrabenazine in pregnant women.1 No clear adverse effects on embryofetal development observed in animal studies at supratherapeutic dosages.1 However, increased stillbirths, reduced pup survival, and delayed pup maturation observed when tetrabenazine (a closely related VMAT2 inhibitor) was administered to rats throughout pregnancy and lactation.1 4

Lactation

Not known whether deutetrabenazine or its metabolites distribute into human milk.1 Effects of the drug or its metabolites on nursing infants and on milk production also are not known.1 Consider the developmental and health benefits of breast-feeding to the infant along with the mother's clinical need for deutetrabenazine and any potential adverse effects on the breast-fed infant from the drug or from the underlying maternal condition.1

Pediatric Use

Manufacturer states that safety and efficacy not established in pediatric patients.1

Has been used with some success and appeared to be well tolerated in a limited number of adolescents with Tourette's syndrome in a short-term, open-label study.7

Geriatric Use

Insufficient experience from clinical studies in patients ≥65 years of age to determine whether geriatric patients respond differently than younger adults.1 Other clinical experience has not identified differences in responses between geriatric and younger adult patients.1 Select dosage with caution.1 (See Geriatric Patients under Dosage and Administration.)

Hepatic Impairment

Pharmacokinetics not evaluated in patients with hepatic impairment; however, in a clinical study of tetrabenazine (a closely related VMAT2 inhibitor) in patients with hepatic impairment, substantially increased exposure of tetrabenazine and its active metabolites observed.1 4 (See Special Populations under Pharmacokinetics.) Clinical importance of increased exposure of tetrabenazine and its metabolites unknown.1 4 Because of the potential for serious adverse reactions, manufacturer states that deutetrabenazine is contraindicated in patients with hepatic impairment.1

Renal Impairment

Pharmacokinetics not evaluated in renal impairment.1

Poor CYP2D6 Metabolizers

Increased exposure of active metabolites deuterated α-dihydrotetrabenazine (deuterated α-HTBZ) and deuterated β-dihydrotetrabenazine (deuterated β-HTBZ) expected; limit daily dosage to ≤36 mg and single doses to ≤18 mg.1

Common Adverse Effects

Huntington's disease: Somnolence,1 2 diarrhea,1 2 dry mouth,1 2 fatigue,1 2 urinary tract infection,1 insomnia,1 anxiety,1 constipation,1 contusion.1

Tardive dyskinesia: Nasopharyngitis,1 12 insomnia,1 6 somnolence,6 fatigue,12 depression/dysthymic disorder,1 12 anxiety,12 diarrhea,12 dry mouth,12 akathisia/agitation/restlessness.1 6

Interactions for Austedo

Drug interaction studies evaluating the effect of deutetrabenazine or its active metabolites (deuterated α-HTBZ and deuterated β-HTBZ) on CYP isoenzymes or P-glycoprotein (P-gp) not conducted to date.1 Other metabolites of deutetrabenazine (M1 and M4) not expected to cause clinically important drug interactions.1

Deutetrabenazine's active metabolites (deuterated α-HTBZ and deuterated β-HTBZ) are substrates of CYP2D6.1

Tetrabenazine (a closely related VMAT2 inhibitor) and its α-HTBZ and β-HTBZ metabolites do not substantially inhibit CYP isoenzymes 1A2, 2B6, 2C8, 2C9, 2C19, 2D6, 2E1, or 3A, nor do they substantially induce CYP isoenzymes 1A2, 2B6, 2C8, 2C9, 2C19, or 3A4 in vitro.1 4 Neither tetrabenazine nor its α-HTBZ and β-HTBZ metabolites are likely to be substrates or inhibitors of the P-gp transport system.1 4

Drugs Affecting Hepatic Microsomal Enzymes

Potent CYP2D6 inhibitors: Potential pharmacokinetic interaction (increased exposure to deuterated α-HTBZ and deuterated β-HTBZ).1 During concurrent use, limit deutetrabenazine daily dosage to ≤36 mg and single doses to ≤18 mg.1 (See Specific Drugs under Interactions.)

Moderate or weak CYP2D6 inhibitors: Effects on pharmacokinetics of deutetrabenazine and its metabolites not evaluated.1

Drugs that Prolong QT Interval

Potential pharmacologic interaction (additive effect on QTc-interval prolongation).1 In patients receiving other drugs known to prolong the QTc interval, monitor QTc interval before and after deutetrabenazine dosage increases above 24 mg daily or dosage increases of other concurrently administered drugs known to prolong the QTc interval.1 (See Prolongation of QT Interval under Cautions.)

Specific Drugs

Drug

Interaction

Comments

Alcohol

Potential additive effects on sedation and somnolence1

Antiarrhythmics (class Ia and III; e.g., amiodarone, procainamide, quinidine, sotalol)

Increased risk of QT-interval prolongation1

Assess QTc interval before and after dosage increases of deutetrabenazine above 24 mg daily or dosage increases of the antiarrhythmic1

Antipsychotic agents (e.g., chlorpromazine, haloperidol, thioridazine, ziprasidone) and other dopamine antagonists

Potential increased risk of parkinsonism, NMS, and akathisia1

Chlorpromazine, haloperidol, thioridazine, ziprasidone: Increased risk of QTc-interval prolongation1

Antipsychotics that increase risk of QTc-interval prolongation: Assess QTc interval before and after dosage increases of deutetrabenazine above 24 mg daily or dosage increases of the antipsychotic agent1

Bupropion

Possible decreased clearance and increased exposure of deutetrabenazine's active metabolites1

Limit deutetrabenazine daily dosage to ≤36 mg and single doses to ≤18 mg1

CNS depressants

Potential additive effects on sedation and somnolence1

Fluoxetine

Possible decreased clearance and increased exposure of deutetrabenazine's active metabolites1

Limit deutetrabenazine daily dosage to ≤36 mg and single doses to ≤18 mg1

MAO inhibitors

Possible antagonistic effects and increased toxicity1

Concomitant use contraindicated1

Allow at least 14 days to elapse between discontinuance of an MAO inhibitor and initiation of deutetrabenazine1

Moxifloxacin

Increased risk of QT-interval prolongation1

Assess QTc interval before and after dosage increases of deutetrabenazine above 24 mg daily or dosage increases of moxifloxacin1

Paroxetine

Increased peak plasma concentrations, AUCs, and half-lives of deutetrabenazine's active metabolites1

Limit deutetrabenazine daily dosage to ≤36 mg and single doses to ≤18 mg1

Quinidine

Possible decreased clearance and increased exposure of deutetrabenazine's active metabolites1

Increased risk of QT-interval prolongation1

Limit deutetrabenazine daily dosage to ≤36 mg and single doses to ≤18 mg1

Assess QTc interval before and after dosage increases of deutetrabenazine above 24 mg daily or dosage increases of quinidine1

Reserpine

Potential serotonin and norepinephrine depletion in the CNS1

Concomitant use contraindicated1

Wait for signs of chorea or dyskinesia to reemerge after discontinuing reserpine before initiating deutetrabenazine therapy1

Allow at least 20 days to elapse between discontinuance of reserpine and initiation of deutetrabenazine1

VMAT2 inhibitors (e.g., tetrabenazine, valbenazine)

Shared mechanism of action; potential for additive toxicity1

Concomitant use contraindicated1

Austedo Pharmacokinetics

Absorption

Bioavailability

Following oral administration, ≥80% absorbed.1

Deutetrabenazine is rapidly and extensively metabolized to the active metabolites deuterated α-HTBZ and deuterated β-HTBZ; plasma concentrations of the parent drug are generally undetectable.1 5

Peak plasma concentrations of active metabolites (deuterated α-HTBZ and deuterated β-HTBZ) reached within 3–4 hours.1

Food

Administration with food increases peak plasma concentrations of deuterated α-HTBZ and deuterated β-HTBZ by approximately 50%, but has no effect on AUC.1

Special Populations

Tetrabenazine, a closely related VMAT2 inhibitor: Mean peak plasma concentration up to 190-fold higher and exposure of tetrabenazine's active metabolites (α-HTBZ and β-HTBZ) up to 40% higher in patients with hepatic impairment compared with healthy individuals.1 4

Poor CYP2D6 metabolizers: Exposures to deuterated α-HTBZ and deuterated β-HTBZ expected to be increased approximately threefold.1

Distribution

Extent

Not known whether the drug or its metabolites are distributed into milk in humans.1

Distributes rapidly into the CNS, with highest and lowest concentrations occurring in the striatum and cortex, respectively.1

Elimination

Metabolism

Deutetrabenazine: Rapidly and extensively metabolized, mainly by carbonyl reductase, to deuterated α-HTBZ and deuterated β-HTBZ.1

Deuterated α-HTBZ and deuterated β-HTBZ: Metabolized primarily by CYP2D6 with minor contributions by CYP isoenzymes 1A2 and 3A4/5 to form several minor metabolites.1

Elimination Route

Eliminated in urine (75–86%) and feces (8–11%); <10% eliminated as unchanged deuterated α-HTBZ and deuterated β-HTBZ.1

Half-life

Deuterated α-HTBZ and deuterated β-HTBZ (combined): 9–10 hours.1

Stability

Storage

Oral

Tablets

25°C (may be exposed to 15–30°C).1 Protect from light and moisture.1

Actions

  • Deuterium-substituted analog of tetrabenazine; deuterium, a nontoxic, naturally occurring isotope of hydrogen with a higher relative mass, forms a stronger bond with carbon molecules that hinders metabolism by CYP isoenzymes.2 5 8 Deutetrabenazine's active metabolites have a longer half-life, higher AUC, and lower peak plasma concentrations than those of an equivalent dose of tetrabenazine.5 8

  • Precise mechanism by which deutetrabenazine exerts its effects in tardive dyskinesia and chorea associated with Huntington's disease not established, but appears to be related to drug's ability to reversibly and selectively inhibit VMAT2 in CNS, thereby decreasing uptake of monoamines (e.g., dopamine, norepinephrine, serotonin, histamine) into synaptic vesicles and depleting monoamine stores from nerve terminals.1 4 5 8 59

  • Preferentially affects dopaminergic neurotransmission in the CNS over adrenergic, serotonergic, and histaminergic neurotransmission at clinically relevant plasma concentrations.5 8 11

Advice to Patients

  • Importance of advising patients and their caregivers to read the manufacturer's patient information (medication guide).1

  • Importance of informing patients that deutetrabenazine should be taken with food and that tablets should be swallowed whole and not chewed, crushed, or broken.1

  • Risk of depression, worsening of depression, and suicidality in patients with Huntington's disease; importance of immediately notifying clinicians of emergence of suicidality, emergence or worsening of depression, suicidality, or unusual changes in behavior in such patients.1

  • Risk of QTc-interval prolongation.1 Importance of patients immediately notifying clinicians if they feel faint, lose consciousness, or experience heart palpitations.1 Importance of patients advising clinicians that they are taking deutetrabenazine before any new drug is taken.1

  • Risk of sedation and somnolence.1 Importance of advising patients to exercise caution or avoid engaging in activities requiring mental alertness and coordination such as operating a motor vehicle or other dangerous machinery until they are on a maintenance dosage of deutetrabenazine and the effects of the drug on the individual are known.1

  • Importance of informing patients that concomitant use of alcohol or other CNS depressants may worsen the sedative effects of deutetrabenazine.1

  • Importance of informing clinicians of existing or contemplated concomitant therapy, including prescription and OTC drugs or herbal supplements (see Interactions), as well as any concomitant illnesses (e.g., depression or other psychiatric disorders, liver disease, arrhythmias).1

  • Importance of women informing clinicians if they are or plan to become pregnant or plan to breast-feed.1

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

Distribution of deutetrabenazine is restricted.10 (See Restricted Distribution under Dosage and Administration.)

Deutetrabenazine

Routes

Dosage Forms

Strengths

Brand Names

Manufacturer

Oral

Tablets, coated

6 mg

Austedo

Teva

9 mg

Austedo

Teva

12 mg

Austedo

Teva

AHFS DI Essentials. © Copyright 2018, Selected Revisions May 7, 2018. American Society of Health-System Pharmacists, Inc., 4500 East-West Highway, Suite 900, Bethesda, Maryland 20814.

† Use is not currently included in the labeling approved by the US Food and Drug Administration.

References

1. Teva Pharmaceuticals USA, Inc. Austedo (deutetrabenazine) tablets prescribing information. North Wales, PA; 2017 Aug. http://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?setid=7ea3c60a-45c7-44cc-afc2-d87fa53993c0

2. Huntington Study Group, Frank S, Testa CM et al. Effect of Deutetrabenazine on Chorea Among Patients With Huntington Disease: A Randomized Clinical Trial. JAMA. 2016; 316:40-50. http://www.ncbi.nlm.nih.gov/pubmed/27380342?dopt=AbstractPlus

3. US Food and Drug Administration. Search orphan drug designations and approvals. From FDA website. Accessed 2017 Apr 26. https://www.accessdata.fda.gov/scripts/opdlisting/oopd/index.cfm

4. Lundbeck Inc. Xenazine (tetrabenazine) tablets prescribing information. Deerfield, IL; 2015 Jun.

5. Paton DM. Deutetrabenazine: Treatment of hyperkinetic aspects of Huntington's disease, tardive dyskinesia and Tourette syndrome. Drugs Today (Barc). 2017; 53:89-102. http://www.ncbi.nlm.nih.gov/pubmed/28387387?dopt=AbstractPlus

6. Fernandez HH, Factor SA, Hauser RA et al. Randomized controlled trial of deutetrabenazine for tardive dyskinesia: The ARM-TD study. Neurology. 2017; 88:1-8. http://www.ncbi.nlm.nih.gov/pubmed/28446646?dopt=AbstractPlus

7. Jankovic J, Jimenez-Shahed J, Budman C et al. Deutetrabenazine in Tics Associated with Tourette Syndrome. Tremor Other Hyperkinet Mov (N Y). 2016; 6:422. http://www.ncbi.nlm.nih.gov/pubmed/27917309?dopt=AbstractPlus

8. Jankovic J. Dopamine depleters in the treatment of hyperkinetic movement disorders. Expert Opin Pharmacother. 2016; 17:2461-2470. http://www.ncbi.nlm.nih.gov/pubmed/27819145?dopt=AbstractPlus

9. Claassen DO, Carroll B, De Boer LM et al. Indirect tolerability comparison of Deutetrabenazine and Tetrabenazine for Huntington disease. J Clin Mov Disord. 2017; 4:3. http://www.ncbi.nlm.nih.gov/pubmed/28265459?dopt=AbstractPlus

10. Teva Neuroscience, Inc. Getting started with Austedo (deutetrabenazine) tablets. From Austedo website. Accessed 2017 Jun 8. http://www.austedo.com/hcp/getting-started

11. Prestwick Pharmaceuticals. Peripheral and central nervous system advisory committee briefing document on tetrabenazine. December 6, 2007. From FDA website. http://www.fda.gov/ohrms/dockets/ac/07/briefing/2007-4328b1-02-Prestwick.pdf

12. Anderson KE, Stamler D, Davis MD et al. Deutetrabenazine for treatment of involuntary movements in patients with tardive dyskinesia (AIM-TD): a double-blind, randomised, placebo-controlled, phase 3 trial. Lancet Psychiatry. 2017; 4:595-604. http://www.ncbi.nlm.nih.gov/pubmed/28668671?dopt=AbstractPlus

13. Neurocrine Biosciences, Inc. Ingrezza (valbenazine) capsules prescribing information. San Diego, CA; 2017 Apr.

28. American Psychiatric Association. Practice guideline for the treatment of patients with schizophrenia, second edition. Am J Psychiatry. 2004; 161(2 Suppl):1-56.

59. Kaur N, Kumar P, Jamwal S et al. Tetrabenazine: Spotlight on Drug Review. Ann Neurosci. 2016; 23:176-185. http://www.ncbi.nlm.nih.gov/pubmed/27721587?dopt=AbstractPlus

100. Waln O, Jankovic J. An update on tardive dyskinesia: from phenomenology to treatment. Tremor Other Hyperkinet Mov (N Y). 2013; 3 http://www.ncbi.nlm.nih.gov/pubmed/23858394?dopt=AbstractPlus

101. Rakesh G, Muzyk A, Szabo ST et al. Tardive dyskinesia: 21st century may bring new treatments to a forgotten disorder. Ann Clin Psychiatry. 2017; 29:108-19. http://www.ncbi.nlm.nih.gov/pubmed/28207919?dopt=AbstractPlus

102. Margolese HC, Chouinard G, Kolivakis TT et al. Tardive dyskinesia in the era of typical and atypical antipsychotics. Part 1: pathophysiology and mechanisms of induction. Can J Psychiatry. 2005; 50:541-7. http://www.ncbi.nlm.nih.gov/pubmed/16262110?dopt=AbstractPlus

103. Margolese HC, Chouinard G, Kolivakis TT et al. Tardive dyskinesia in the era of typical and atypical antipsychotics. Part 2: Incidence and management strategies in patients with schizophrenia. Can J Psychiatry. 2005; 50:703-14. http://www.ncbi.nlm.nih.gov/pubmed/16363464?dopt=AbstractPlus

104. Lerner PP, Miodownik C, Lerner V. Tardive dyskinesia (syndrome): Current concept and modern approaches to its management. Psychiatry Clin Neurosci. 2015; 69:321-34. http://www.ncbi.nlm.nih.gov/pubmed/25556809?dopt=AbstractPlus

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