great [2:<50 kg. b Pediatric Patients Ventricular Arrhythmias Oral Optimum pediatric dosage has not been established; however, dosage recommendations have been made based on clinical experience. b Initiate dose titration at the lower end of the recommended ranges; monitor plasma drug concentrations and therapeutic response carefully. b For children unable to swallow the capsules, a suspension may be extemporaneously prepared by mixing the contents of disopyramide phosphate conventional capsules in cherry syrup to produce suspensions that contain 1 10 mg of disopyramide per mL. b The extended-release capsules should not be used for the preparation of an extemporaneous suspension. b Give total daily dose in equally divided doses every 6 hours or at intervals according to individual requirements. b Total Daily Pediatric Dosage Based on Age and Weight Age Total Daily Pediatric Dosage> <1 year of age 10 30 mg/kg 1 4 years of age 10 20 mg/kg 4 12 years of age 10 15 mg/kg 12 18 years of age 6 15 mg/kg Adults Ventricular Arrhythmias Oral (Conventional Capsules) Usual dosage: 400 800 mg daily, given in divided doses. 112 Adults weighing 50 kg: Usually 150 mg every 6 hours. a b Adults weighing> <50 kg: Usually 100 mg every 6 hours. a b Oral (Extended-release Capsules) Usual dosage: 400 800 mg daily, given in divided doses. 112 Adults weighing 50 kg: Usually 300 mg every 12 hours. a b Adults weighing> <50 kg: Usually 200 mg every 12 hours. a b Rapid Control Oral (Conventional Capsules) Adults weighing 50 kg: Initially, 300 mg followed by 150 mg every 6 hours. b Adults weighing> <50 kg: Initially, 200 mg followed by 150 mg every 6 hours. b If there is no therapeutic response and if no toxic effects occur within 6 hours after the initial 300-mg dose, 200-mg doses may be given every 6 hours. b If there is no response to this dosage in 48 hours, discontinue disopyramide and initiate alternative therapy. b Alternatively, the patient may be hospitalized, closely evaluated, and continuously monitored while the dosage is increased to 250 or 300 mg every 6 hours. b Severe Refractory VT Oral (Conventional Capsules) Up to 400 mg every 6 hours may be required (resulting in plasma disopyramide concentrations up to 9 mcg/mL). a Patients should be hospitalized, closely evaluated, and continuously monitored. a Rapid Control In Patients with Cardiomyopathy or Possible Cardiac Decompensation Oral (Conventional Capsules) Do not administer an initial loading dose. b Do not exceed an initial dosage of 100 mg every 6 hours. b Carefully adjust dosage in these patients while closely monitoring for hypotension and/or CHF. b (See CHF and Hypotension under Cautions.) Switching from Another Class I Antiarrhythmic Agent Oral (Conventional Capsules or Extended-release Capsules) Administer the usual dosage of disopyramide (without an initial loading dose) 6 12 hours after the last dose of quinidine sulfate or 3 6 hours after the last dose of procainamide. b If withdrawal of quinidine or procainamide is likely to produce life-threatening arrhythmias, hospitalize and closely monitor patient. b Switching from Conventional to Extended-release Capsules Oral (Extended-release) Initiate usual maintenance schedule (e.g., 300 mg every 12 hours) of extended-release capsules 6 hours after the last dose of the conventional capsules. b Dosage Modification for Toxicity If increased anticholinergic adverse effects occur, monitor plasma concentrations of disopyramide and adjust dosage accordingly. a Dosage may be reduced by one-third and the same dosing interval maintained (e.g., 600 mg daily reduced to 400 mg daily). a Prescribing Limits Adults Ventricular Arrhythmias Patients with Cardiomyopathy or Possible Cardiac Decompensation Oral (Conventional Capsules) Maximum initial dosage: 100 mg every 6 hours. b Special Populations Hepatic Impairment Oral Usual dosage: 100 mg every 6 hours as conventional capsules or 200 mg every 12 hours as extended-release capsules. b Renal Impairment Oral Do not use extended-release capsules in patients with a Cl cr 40 mL/minute. b Patients with moderately impaired renal function (Cl cr> 40 mL/minute): Usually, 100 mg every 6 hours as conventional capsules or 200 mg every 12 hours as extended-release capsules. b In patients with severely impaired renal function (Cl cr 40 mL/minute), the usual dosage of conventional capsules is 100 mg (with or without an initial 150-mg dose) given at the following approximate intervals depending on the patient s Cl cr : b Cl cr (mL/minute) Dosage Interval 30 40 every 8 h 15 30 every 12 h <15 every 24 h Geriatric Patients Select dosage with caution (generally starting at the low end of the dosing range) because of age-related decreases in hepatic, renal, and/or cardiac function, and concomitant disease and drug therapy. a If adverse anticholinergic effects occur, monitor plasma disopyramide concentrations and adjust dosage as needed. a (See Dosage Modification for Toxicity under Dosage and Administration.) Cautions for Disopyramide Phosphate Contraindications Preexisting 2nd or 3rd degree AV block (if an artificial pacemaker has not been inserted). b Cardiogenic shock. b Known hypersensitivity to disopyramide. b Warnings/Precautions Warnings Mortality In CAST study, excessive rate of mortality and nonfatal cardiac arrest reported in patients with asymptomatic, non-life-threatening ventricular arrhythmias and recent MI (> 6 days but <2 years previously) who were receiving encainide or flecainide compared with placebo. a Because of disopyramide s arrhythmogenic potential and the lack of evidence for improved survival for class I antiarrhythmic agents, 112 116 117 118 use disopyramide only for life-threatening arrhythmias. 112 Use in less severe arrhythmias currently is not recommended, and treatment of asymptomatic VPCs should be avoided. 112 Initiate therapy only in a hospital setting. 112 CHF and Hypotension May cause or worsen CHF or produce severe hypotension. a Hypotension occurs more commonly in patients with primary cardiomyopathy or inadequately compensated CHF. a Do not use in patients with uncompensated or marginally compensated CHF or hypotension unless the CHF or hypotension is secondary to cardiac arrhythmia. a In patients with a history of heart failure, cardiac function must be carefully maintained, including optimal digitalization. a If hypotension occurs or CHF worsens, discontinue disopyramide and, if necessary, resume therapy at a lower dosage only after establishing adequate cardiac compensation. a Increased risk of severe hypotension in patients with myocarditis or other cardiomyopathy. b Do not administer a loading dose to such patients; select initial dosage and make subsequent dosage adjustments under close supervision. b (See Patients with Cardiomyopathy or Possible Cardiac Decompensation under Dosage and Administration.) Arrhythmogenic Effects Possible worsening of existing arrhythmias or occurrence of new arrhythmias, including VT and VF associated with prolonged QT interval. a b Increased risk of such effects if used concomitantly with other drugs (i.e., quinidine) that prolong the QT interval. a b a b If a QT prolongation> 25% occurs and if ectopy continues, monitor patient closely. a Consider discontinuance of disopyramide. a Hypoglycemia Hypoglycemia reported rarely. a b Monitor blood glucose concentrations closely in patients with compromised glucoregulatory mechanisms in the absence of food (e.g., patients with CHF, chronic malnutrition, hepatic or renal disease, those using alcohol or receiving certain drugs [e.g., β-adrenergic blockers]). b Concurrent Use with Other Antiarrhythmics Reserve combined use for serious arrhythmias unresponsive to monotherapy; monitor closely. a Heart Block Reduce dosage if first-degree AV heart block occurs. b If the block persists, weigh the benefit of therapy against the potential risk of higher degrees of AV block. b If second- or third-degree AV block or unifascicular, bifascicular, or trifascicular block occurs, discontinue disopyramide therapy, unless the ventricular rate is adequately controlled by an artificial pacemaker. b Anticholinergic Effects Possible anticholinergic effects; do not use in patients with glaucoma, myasthenia gravis, or urinary retention without instituting adequate overriding measures (e.g., pilocarpine ophthalmic drops for glaucoma, catheter drainage or operative relief for urinary retention). a Possible increased risk of urinary retention in males with benign prostatic hypertrophy. a Measure intraocular pressure before initiating therapy in patients with a family history of glaucoma. a May precipitate myasthenic crisis; use with caution in patients with myasthenia gravis. a Use with caution in geriatric patients. (See Geriatric Use under Cautions.) a General Precautions Atrial Tachyarrhythmias Possible enhanced AV conduction; patients with atrial flutter or fibrillation should be digitalized prior to administration. b Conduction Abnormalities Use with caution in patients with sick sinus syndrome (including bradycardia-tachycardia syndrome), Wolff-Parkinson-White syndrome, or bundle-branch block, since effects of the drug in these conditions are unpredictable. b Potassium Imbalance Correct abnormalities in serum potassium concentration before initiating therapy. a May be ineffective in patients with hypokalemia and toxic effects may be enhanced in patients with hyperkalemia. a Specific Populations Pregnancy Category C. a Lactation Distributed into milk. 112 Discontinue nursing or the drug. 112 Pediatric Use Safety and efficacy not established. a However, disopyramide has been used in children. a b (See Pediatric Patients under Dosage and Administration.) Geriatric Use Insufficient experience in patients 65 years of age to determine whether geriatric patients respond differently than younger adults. a Select dosage with caution because of age-related decreases in hepatic, renal, and/or cardiac function and potential for concomitant disease and drug therapy. a (See Geriatric Patients under Dosage and Administration.) Substantially eliminated by kidneys; assess renal function periodically and adjust dosage accordingly. a (See Renal Impairment under Dosage and Administration.) Possible anticholinergic effects; not generally recommended for use in patients with glaucoma, urinary retention, or benign prostatic hypertrophy unless adequate overriding measures are taken. a (See Anticholinergic Effects under Warnings.) Hepatic Impairment Increased plasma half-life; dosage adjustment recommended. a (See Hepatic Impairment under Dosage and Administration.) Patients with cardiac dysfunction are more likely to have comorbid hepatic impairment. a Carefully monitor ECG for prolongation of PR interval, evidence of QRS widening, or other signs of toxicity. a Renal Impairment Increased plasma half-life; dosage adjustments necessary based on degree of renal impairment. a (See Renal Impairment under Dosage and Administration.) Carefully monitor ECG for prolongation of PR interval, evidence of QRS widening, or other signs of toxicity. a Not recommended for use in patients with severe renal insufficiency (Cl cr 40 mL/min). a Common Adverse Effects Anticholinergic effects (e.g., dry mouth, urinary hesitancy, constipation, blurred vision, dry nose/eyes/throat), urinary frequency/urgency, urinary retention, nausea, pain/bloating/gas, dizziness, general fatigue/muscle weakness, headache, malaise, aches/pains. a b Interactions for Disopyramide Phosphate Appears to be metabolized principally by CYP3A4. a Drugs Affecting Hepatic Microsomal Enzymes Inducers of hepatic microsomal enzymes: Potential pharmacokinetic interaction (decreased plasma disopyramide concentrations). a b When used concomitantly, closely monitor serum disopyramide concentrations to avoid subtherapeutic concentrations. b Inhibitors of CYP3A4: Potential pharmacokinetic interaction (increased plasma disopyramide concentrations). a Specific Drugs Drug Interaction Comments Antiarrhythmic agents (e.g., quinidine, procainamide, lidocaine, encainide, flecainide, propafenone, propranolol) Possible additive or antagonistic cardiac effects; toxic effects may be additive b Potential for severe negative inotropic effects or enhanced conduction prolongation, especially in cardiac decompensation a Concomitant use with quinidine may result in slight increases in plasma disopyramide concentrations and slight decreases in plasma quinidine concentrations 112 Reserve concomitant use for the management of life-threatening arrhythmias unresponsive to monotherapy; monitor closely b a Anticholinergic agents Possible additive effects b Diazepam No interaction noted in healthy individuals a Digoxin Concomitant use does not appear to increase serum digoxin concentrations 112 Macrolide antibiotics (e.g., erythromycin, clarithromycin) Increased plasma disopyramide concentrations and increased risk of serious toxicity (e.g., prolongation of the QT-interval, widening of the QRS complex, polymorphic ventricular tachycardia, ventricular fibrillation) 112 115 126 a b Close monitoring recommended 112 a Phenytoin Potential for increased metabolism of disopyramide b Monitor serum disopyramide concentrations closely to avoid subtherapeutic concentrations b Verapamil Potential for additive negative inotropic effects b Concomitant use not recommended b Discontinue disopyramide 48 hours prior to initiating verapamil therapy; do not reinstitute disopyramide until 24 hours after verapamil has been discontinued b Disopyramide Phosphate Pharmacokinetics Absorption Bioavailability Rapidly absorbed (60 83%) after oral administration. b Bioavailability of disopyramide from the extended-release and conventional capsules appears similar. a Peak plasma concentrations attained in 2 2.5 or 4.9 hours after oral administration of conventional or extended-release capsules, respectively. a b Onset Onset of action usually is within 0.5 3 hours after oral administration of a single 300-mg dose (conventional capsules). a Duration Antiarrhythmic effect persists 1.5 8.5 hours after oral administration of conventional capsules. b Plasma Concentrations Plasma disopyramide concentrations of approximately 2 4 mcg/mL generally required to suppress ventricular arrhythmias; concentrations up to 9 mcg/mL have been required in a limited number of patients with severe refractory VT. a b Plasma concentrations >9 mcg/mL associated with toxic effects. b Distribution Extent Distributed throughout the extracellular body water; not extensively bound to tissues. b Equally distributed between plasma and erythrocytes. b Disopyramide crosses the placenta and is distributed into milk. a b Plasma Protein Binding Approximately 50 65%; decreases as the concentration of disopyramide and its metabolites increase. b Special Populations In patients with renal insufficiency, the volume of distribution is slightly decreased. b Patients with AMI (without CHF) may have lower peak plasma concentrations and smaller volumes of distribution compared with healthy individuals. b Elimination Metabolism Metabolized in the liver to an N -monodealkylated metabolite and other unidentified metabolites. b Plasma concentration of the N -monodealkylated metabolite is approximately 10% of the concentration of disopyramide. b The N -monodealkylated metabolite has less antiarrhythmic activity but greater anticholinergic activity than does disopyramide. b CYP3A4 involved in metabolism. a Elimination Route After oral administration, 50% of an oral dose excreted in urine as unchanged drug, 20% as the N -monodealkylated metabolite, and about 10% as unidentified metabolites; about 10% is excreted in feces as unchanged drug and metabolites. a b Urinary pH apparently does not affect the rate of renal excretion. b Half-life Conventional capsules: Elimination half-life 4 10 hours. a Extended-release capsules: Elimination half-life 6.9 16.4 hours. a Special Populations Plasma half-life prolonged in patients with hepatic or renal insufficiency. b In patients with Cl cr <40 mL/minute, plasma half-life ranged from 8 18 hours. b Disopyramide is removed by hemodialysis. b In patients with heart disease, including left ventricular dysfunction, the mean plasma half-life was slightly prolonged to 7.8 hours (range: 5 9.5 hours). a Stability Storage Oral Capsules (Conventional and Extended-release) 25 C (may be exposed to 15 30 C). a Suspension Oral suspensions of disopyramide phosphate prepared extemporaneously from conventional capsules of the drug and cherry syrup at concentrations ranging from 1 10 mg/mL reportedly are stable for 1 month when stored at 2 8 C. b Dispense in amber glass bottles. b Actions A class I (membrane-stabilizing) antiarrhythmic agent with actions similar to those of procainamide and quinidine. b Regarded as a myocardial depressant because it decreases myocardial excitability and conduction velocity, and may depress myocardial contractility. b Possesses anticholinergic properties, which may modify the direct myocardial effects of the drug. b Exact mechanism of antiarrhythmic action has not been established; is believed to combine with fast sodium channels in their inactive state and thereby inhibit recovery after repolarization in a time- and voltage-dependent manner that is associated with subsequent dissociation of the drug from the sodium channels. b Exhibits electrophysiologic effects characteristic of class IA antiarrhythmic agents (i.e., exhibits intermediate rates of attachment and dissociation transmembrane sodium channels). b Suppresses automaticity in the His-Purkinje system. b Decreases the automaticity of ectopic atrial and ventricular pacemakers, shortens or does not change the sinus node recovery time, and decreases conduction velocity in the atria and ventricles. b Has little effect on conduction velocity through the AV node or the His-Purkinje system, but accessory pathway conduction velocity is decreased. b Generally prolongs the effective refractory period (ERP) of the atria and the ventricles. b Usually has little effect on the ERP of the AV node or the His-Purkinje system; however, the effect on the AV node is unpredictable in patients with preexisting conduction disturbances. b Generally causes little or no prolongation of the PR interval or the QRS complex, but the QT interval or QT interval corrected for rate (QT c ) may be prolonged. b Generally has little effect on resting sinus rate and has a direct negative inotropic effect on the heart. b Usually decreases cardiac output 10 15% in patients without compromised myocardial function. b It has not been established whether disopyramide has local anesthetic properties. b Advice to Patients Potential for toxicity (e.g., cardiovascular, anticholinergic). a Importance of women informing their clinician if they are or plan to become pregnant or plan to breast-feed. a Importance of informing clinicians of existing or contemplated concomitant therapy, including prescription and OTC drugs, as well as concomitant illnesses. a Importance of informing patients of other important precautionary information. a (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. * available from one or more manufacturer, distributor, and/or repackager by generic (nonproprietary) name Disopyramide Phosphate Routes Dosage Forms Strengths Brand Names Manufacturer Oral Capsules 100 mg (of disopyramide)* Disopyramide Phosphate Capsules Norpace Searle 150 mg (of disopyramide)* Disopyramide Phosphate Capsules Norpace Searle Capsules, extended-release 100 mg (of disopyramide)* Disopyramide Phosphate Extended-Release Capsules Ethex Norpace CR 150 mg (of disopyramide)* Disopyramide Phosphate Extended-release Capsules Ethex Norpace CR AHFS DI Essentials. Copyright 2017, Selected Revisions November 4, 2016. 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 51. Meinertz T, Langer KH, Kasper W et al. Disopyramide-induced intrahepatic cholestasis. Lancet . 1977; 2:828-9. [PubMed 71640] 52. Riccioni N, Bozzi L, Susini N et al. Disopyramide-induced intrahepatic cholestasis. Lancet . 1977; 2:1362-3. [PubMed 74773] 100. Haworth E, Burroughs AK. Disopyramide and warfarin interaction. Br Med J . 1977; 2:866-7. [PubMed 922330] 101. Ryll C, Davis LJ. Warfarin-disopyramide interaction? Drug Intell Clin Pharm . 1979; 13:260. 102. Sylven C, Anderson P. Evidence that disopyramide does not interact with warfarin. BMJ . 1983; 286:1181. [PubMed 6404381] 103. Mangini RJ, ed. Drug interaction facts. St. Louis: JB Lippincott Co; 1984(Jul):41. 104. Moore AR. Disopyramide and warfarin. Br Med J . 1977; 29:1158. 105. Edmonds ME, Hayler AM, Holt DW. Untitled. (A case of intra-hepatic cholestasis after disopyramide therapy.) Eur J Clin Pharmacol . 1980; 18:285-6. Letter. (IDIS 124932) 106. Bakris GL, Cross PD, Hammarsten JE. Disopyramide-associated liver dysfunction. Mayo Clin Proc . 1983; 58:265-7. [PubMed 6834895] 107. Craxi A, Gatto G, Maringhini A et al. Disopyramide and cholestasis. Ann Intern Med . 1980; 93(1 Part 1):150-1. [PubMed 7396302] 108. Doody PT. Disopyramide hepatotoxicity and disseminated intravascular coagulation. South Med J . 1982; 75:496-7. [PubMed 7071649] 109. Scheinman SJ, Poll DS, Wolfson S. Acute cardiac failure and hepatic ischemia induced by disopyramide phosphate. Yale J Biol Med . 1980; 53:361-6. [PubMed 7222741] 110. Antonelli D, Koltun B, Barzilay J. Acute hepatotoxic effect of disopyramide. Chest . 1984; 86:274. [PubMed 6744970] 111. Tonkin AM, Joel SE, Reynolds JL. Unusual hepatocellular and cardiovascular complications of disopyramide. Chest . 1980; 77:125. [PubMed 7351137] 112. Searle. Norpace and Norpace CR (disopyramide phosphate) prescribing information. Chicago, IL; 1997 Apr 4. 113. Epstein A, Barland P. The diagnostic value of antihistone antibodies in drug-induced lupus erythematosus. Arthritis Rheum . 1985; 28:158-62. [PubMed 3882094] 114. Wanner WR, Irvin WS. Disopyramide and antinuclear antibodies. Am Heart J . 1981; 101:687-9. [PubMed 6971570] 115. Ragosta M, Weihl AC, Rosenfeld LE. Potentially fatal interaction between erythromycin and disopyramide. Am J Med . 1989; 86:465-6. [PubMed 2467560] 116. Teo KK, Yusuf S, Furberg CD. Effects of prophylactic antiarrhythmic drug therapy in acute myocardial infarction: an overview of results from randomized controlled trials. JAMA . 1993; 270:1589-95. [PubMed 8371471] 117. Pratt CM, Moye L. The Cardiac Arrhythmia Suppression Trial: implications for antiarrhythmic drug development. J Clin Pharmacol . 1990; 30:967-74. [PubMed 2122983] 118. Hine LK, Laird NM, Hewitt P et al. Meta-analysis of empirical long-term antiarrhythmic therapy after myocardial infarction. JAMA . 1989; 262:3037-40. [PubMed 2509746] 119. The Cardiac Arrhythmia Suppression Trial (CAST) investigators. Preliminary report: effect of encainide and flecainide on mortality in a randomized trial of arrhythmia suppression after myocardial infarction. N Engl J Med . 1989; 321:406-12. [PubMed 2473403] 120. Ruskin JN. The Cardiac Arrhythmia Suppression Trial (CAST). N Engl J Med . 1989; 321:386-8. [PubMed 2501683] 121. Vlay SC. Lessons from the past and reflections on the Cardiac Arrhythmia Suppression Trial. Am J Cardiol . 1990; 65:112-3. [PubMed 1688480] 122. Pratt CM, Brater DC, Harrell FE Jr et al. Clinical and regulatory implications of the Cardiac Arrhythmia Suppression Trial. Am J Cardiol . 1990; 65:103-5. [PubMed 1688479] 123. Morganroth J, Bigger JT Jr, Anderson JL. Treatment of ventricular arrhythmias by United States cardiologists: a survey before the Cardiac Arrhythmia Suppression Trial results were available. Am J Cardiol . 1990; 65:40-8. [PubMed 1688481] 124. Pratt C, Ward DE, Camm AJ. Lessons from the cardiac arrhythmia suppression trial. BMJ . 1989; 299:805-6. [PubMed 2510839] 125. Coyle JD, Schaal SF. An interim perspective on the removal of encainide and flecainide from the Cardiac Arrhythmia Suppression Trial. DICP . 1989; 23:478-9. [PubMed 2500783] 126. Paar D, Terjung B, Sauerbruch T. Life-threatening interaction between clarithromycin and disopyramide. Lancet . 1997; 349:326-7. [PubMed 9024381] 129. Fuster V, Ryden LE, Cannom DS et al. ACC/AHA/ESC 2006 guidelines for the management of patients with atrial fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients with Atrial Fibrillation). Circulation . 2006; 114:e257-354. [PubMed 16908781] 300. Page RL, Joglar JA, Caldwell MA et al. 2015 ACC/AHA/HRS Guideline for the Management of Adult Patients With Supraventricular Tachycardia: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol . 2016; 67:e27-e115. 301. January CT, Wann LS, Alpert JS et al. 2014 AHA/ACC/HRS guideline for the management of patients with atrial fibrillation: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol . 2014; 64:e1-76. [PubMed 24685669] a. Searle. Norpace and Norpace CR (disopyramide phosphate) prescribing information. Chicago, IL; 2001 Sept. b. AHFS drug information 2007. McEvoy GK, ed. Disopyramide Phosphate. Bethesda, MD: American Society of Health-System Pharmacists; 2007:1584-7. Next Interactions Print this page Add to My Med List More about disopyramide Side Effects During Pregnancy or Breastfeeding Dosage Information Drug Images Drug Interactions Support Group Pricing & Coupons En Español 5 Reviews Add your own review/rating Drug class: group I antiarrhythmics Consumer resources Disopyramide ... +3 more Professional resources Disopyramide (FDA) Disopyramide (Wolters Kluwer) Other brands: Norpace Related treatment guides Arrhythmia> ]} FEATURED: CAR-T Cell Therapy Overview Mechanism of Action KTE-C19 Studies KTE-C19 Cancer Targets Adverse Events Manufacturing Drug Status Rx Availability Prescription only C Pregnancy Category Risk cannot be ruled out N/A CSA Schedule Not a controlled drug Approval History Drug history at FDA Manufacturers Teva Pharmaceuticals USA, Inc. AvKare, Inc. Drug Class Group I antiarrhythmics Related Drugs Arrhythmia propranolol , amiodarone , verapamil , lidocaine , Inderal , Tikosyn , Pacerone , mexiletine , dofetilide , Calan , Cordarone , quinidine , Calan SR , Mexitil , procainamide , Verelan , disopyramide , Norpace , Nexterone , Isoptin SR , Procanbid , Cordarone IV , More... Disopyramide Rating 5 User Reviews 8.8 /10 5 User Reviews 8.8 Rate it! Disopyramide Images Disopyramide systemic 150 mg (ETHEX 002 ) View all images} } become older
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