Quinidine

Itraconazole increases quinidine concentrations, potentially causing QT prolongation and Torsade de Pointes. Contraindicated during and 2 weeks after itraconazole treatment.

Ketoconazole increases quinidine plasma concentrations, potentially causing QT prolongation and life-threatening ventricular tachyarrhythmias including torsades de pointes.

Concomitant use is contraindicated due to increased risk of QT prolongation and torsades de pointes.

Co-administration may lead to torsade de pointes-type ventricular tachycardia due to QT prolongation. Avoid concomitant use.

Mifepristone increases quinidine exposure; concomitant use is contraindicated due to narrow therapeutic range.

Co-administration contraindicated due to potential for cardiac arrhythmias.

Additive QT interval prolongation effect anticipated, increasing risk of ventricular arrhythmias.

Concomitant use may result in increased plasma concentrations leading to QTc prolongation and torsades de pointes.

Inhibits CYP2D6 metabolic pathway, increasing propafenone steady-state concentrations more than 2-fold. Concomitant use should be avoided.

Completely inhibits CYP2D6 hydroxylation, increasing propafenone concentrations more than 2-fold; concomitant use should be avoided.

Class Ia antiarrhythmic; potential to prolong refractoriness. Discontinue for at least three half-lives prior to sotalol dosing.

CYP2D6 inhibitor that increases codeine plasma concentration but decreases morphine concentration, potentially causing reduced analgesic efficacy or opioid withdrawal symptoms. Discontinuation may cause increased morphine levels and potentially fatal respiratory depression.

Patients receiving quinidine should be observed carefully for development of cardiac arrhythmias.

Class I antiarrhythmic. Amiodarone inhibits quinidine metabolism. Reserve concomitant use; initiate at lower than usual dose and reduce previous dose by 30-50%.

Quinidine inhibits cytochrome P450 2D6, potentially causing toxic amitriptyline levels in normal metabolizers; may require lower amitriptyline doses.

CYP2D6 inhibitor that increases amphetamine exposure and risk of serotonin syndrome.

CYP2D6 inhibitor that increases amphetamine exposure and serotonin syndrome risk.

Strong CYP2D6 inhibitor increases aripiprazole exposure. Reduce aripiprazole dosage.

Strong CYP2D6 inhibitor that increases aripiprazole exposure. Avoid concomitant use because dosage cannot be modified.

CYP2D6 inhibitor that increases atomoxetine steady-state plasma concentrations in extensive metabolizers.

CYP2D6 inhibitor that increases atomoxetine steady-state plasma concentrations in extensive metabolizers.

CYP2D6 inhibitor may potentiate systemic beta-blockade with decreased heart rate and depression.

May prolong neuromuscular blockade action of cisatracurium besylate. Use peripheral nerve stimulator and monitor clinical signs.

Postmarketing reports of torsades de pointes occurring with concurrent use of clarithromycin and quinidine. CYP3A-based interaction increases serum concentrations.

Inhibits P450 2D6 and may increase clomipramine plasma levels, potentially causing toxicity.

Inhibits cytochrome P450 2D6, may increase desipramine plasma concentrations and risk of toxicity; dose adjustment may be necessary.

Strong CYP2D6 inhibitor that increases systemic exposure to active dihydro-metabolites of deutetrabenazine by approximately 3-fold. Maximum recommended dose should not exceed 36 mg per day.

CYP2D6 inhibitor increases dextroamphetamine exposure and serotonin syndrome risk. Use lower doses and monitor.

CYP2D6 inhibitor that increases amphetamine exposure and risk of serotonin syndrome. Initiate with lower doses and monitor for serotonin syndrome.

CYP2D6 inhibitor that increases dextroamphetamine exposure and risk of serotonin syndrome. Initiate with lower doses and monitor for serotonin syndrome symptoms.

Digoxin serum concentrations increased 54-83%. Reduce digoxin dose by 30-50% and monitor serum concentrations.

Concurrent use may cause excessive QRS widening and/or Q-T prolongation. Slight increases in disopyramide levels and decreases in quinidine levels observed.

Potent CYP2D6 inhibitor; expected to increase duloxetine concentrations.

Potent CYP2D6 inhibitor expected to increase duloxetine concentrations.

Potentiates arrhythmogenic effects of epinephrine.

Increases the arrhythmogenic potential of epinephrine; patients should be observed carefully for cardiac arrhythmias.

Class Ia anti-arrhythmic drug that may increase risk of QT prolongation and Torsades de Pointes due to additive effects on heart rate and QT interval.

Should be avoided due to risk of QT prolongation and torsades de pointes.

Inhibits cytochrome P450 2D6, reducing imipramine metabolism and increasing plasma concentrations. May cause abrupt toxicity in patients stable on imipramine doses.

Cardiac effects may be additive or antagonistic and toxic effects may be additive when administered with lidocaine.

P-glycoprotein inhibitor increases loperamide plasma concentrations 2- to 3-fold with potential for enhanced CNS adverse reactions.

Concomitant administration may produce electrocardiographic abnormalities and increase risk of convulsions. Delay mefloquine at least 12 hours after last dose if used for severe malaria treatment.

Strong CYP2D6 inhibitor that increases metoclopramide plasma concentrations and risk of extrapyramidal symptoms exacerbation. Dosage reduction recommended.

Strong CYP2D6 inhibitor increasing metoclopramide plasma concentrations with risk of exacerbation of extrapyramidal symptoms; dosage reduction recommended.

Strong CYP2D6 inhibitor that doubles metoprolol concentrations, decreasing cardioselectivity. Close monitoring required.

Strong CYP2D6 inhibitor that doubles metoprolol concentrations, decreasing cardioselectivity and requiring close monitoring.

Strong CYP2D6 inhibitor that doubles metoprolol plasma concentrations, decreasing cardioselectivity. Close monitoring required.

Strong CYP2D6 inhibitor that doubles metoprolol concentrations, decreasing cardioselectivity. Close monitoring required.

Strong CYP2D6 inhibitor that doubles metoprolol concentrations, decreasing cardioselectivity.

Metabolism of quinidine is inhibited by amiodarone. Initiate at lower dose and reduce dose by 30-50% when adding amiodarone.

Inhibits cytochrome P450 2D6, which may cause abrupt toxicity in patients stable on nortriptyline by increasing plasma concentrations.

Class Ia anti-arrhythmic; associated with Torsades de Pointes in bradycardia patients. Cardiologist advice recommended if ZEPOSIA treatment considered.

Quinidine inhibits cytochrome P450 2D6, potentially causing toxic amitriptyline concentrations; dose reduction may be necessary.

Class Ia anti-arrhythmic drug associated with Torsades de Pointes in bradycardic patients; cardiologist consultation advised.

CYP2D6 inhibitor that reduces metabolism of propranolol, leading to 2-3 fold increased blood concentration and greater beta-blockade.

Injection during recovery from neuromuscular blockade may cause recurrent paralysis when used with anticholinesterase agents.

May enhance rocuronium bromide activity and neuromuscular blockade.

Class Ia antiarrhythmic associated with Torsades de Pointes in bradycardia patients; seek cardiologist advice before using with siponimod.

May enhance the neuromuscular blocking action of succinylcholine.

Strong CYP2D6 inhibitor that markedly increases exposure to tetrabenazine metabolites. Dose reduction necessary; maximum daily dose 50 mg, maximum single dose 25 mg.

CYP2D6 inhibitor that potentiates systemic beta-blockade, resulting in decreased heart rate.

Potentiated systemic beta-blockade (decreased heart rate, depression) has been reported during combined treatment with this CYP2D6 inhibitor and timolol.

Potentiated systemic beta-blockade including decreased heart rate and depression has been reported during combined treatment.

Class IA antiarrhythmic that prolongs QT interval; should be avoided with toremifene citrate or requires close monitoring.

CYP2D6 inhibitor that increases tramadol plasma concentration and decreases M1 concentration, resulting in increased risk of seizures, serotonin syndrome, and opioid withdrawal symptoms.

CYP2D6 inhibitor may increase tramadol plasma concentration and decrease M1 concentration, resulting in increased risk of seizures, serotonin syndrome, and opioid withdrawal or toxicity.

CYP2D6 inhibitor that increases tramadol plasma concentration and decreases M1 concentration, risking seizures, serotonin syndrome, opioid withdrawal, and respiratory depression.

CYP2D6 inhibitor may increase tramadol plasma concentration and decrease M1 concentration, resulting in increased risk of seizures, serotonin syndrome, and opioid withdrawal or toxicity.

Quinidine inhibits P450 2D6, potentially causing abrupt toxicity in patients stable on trimipramine due to increased plasma concentrations.

Quinidine administration during recovery from vecuronium may cause recurrent paralysis.

Acetazolamide reduces urinary excretion of quinidine and may enhance its effect.

Acetazolamide reduces urinary excretion of quinidine and may enhance its effect.

Acetazolamide reduces urinary excretion of quinidine and may enhance its effect.

P-glycoprotein inhibitor that increases afatinib exposure. Reduce GILOTRIF dose by 10 mg per day if not tolerated.

Reduces renal clearance of amantadine by approximately 30%.

Reduces renal clearance of amantadine hydrochloride by approximately 30%.

Quinidine inhibits cytochrome P450 2D6 activity, which may increase amoxapine plasma concentrations and require dose adjustment.

Strong CYP2D6 inhibitor that increases aripiprazole exposure. Reduce aripiprazole dosage when used concomitantly.

May enhance the neuromuscular blocking action of atracurium.

CYP2D6 inhibitor expected to increase blood levels of carvedilol R(+) enantiomer, potentially increasing vasodilating effects and dizziness.

Potent CYP2D6 inhibitor expected to increase carvedilol R(+) enantiomer blood levels, potentially causing dizziness and vasodilation.

CYP2D6 or CYP3A4 inhibitor that can increase clozapine levels and lead to adverse reactions. Close monitoring and dose reduction may be necessary.

P-gp inhibitor that does not require dosage adjustment of dabigatran etexilate but increases exposure, especially with renal impairment.

CYP2D6 inhibitor; no dosing adjustments recommended for darifenacin when co-administered with quinidine.

Deferasirox may induce CYP3A4 resulting in decreased quinidine concentration. Monitor for reduced effectiveness.

CYP2C19 inhibitor that decreases diazepam elimination, potentially increasing adverse reactions.

Class I antiarrhythmic agent may increase certain actions or side effects of dicyclomine hydrochloride.

Increased exposure of quinidine due to CYP3A4 inhibition; may require dose adjustment.

CYP2D6 inhibitor may potentiate systemic beta-blockade, causing decreased heart rate and depression.

Inhibits cytochrome P450 2D6, which may increase doxepin plasma concentrations. Concomitant use may require lower doses and monitoring of TCA plasma levels.

Potent CYP2D6 inhibitor expected to increase duloxetine concentrations.

Antagonizes pressor effect of ephedrine. Carefully monitor blood pressure.

Quinidine, a cytochrome P450IID6 inhibitor, might increase plasma flecainide concentrations, especially in extensive metabolizers on chronic therapy.

Glycerol phenylbutyrate may decrease systemic exposure. Monitor for decreased efficacy of this narrow therapeutic index drug.

Class 1A antiarrhythmic known to prolong QTc interval; caution advised when used with haloperidol decanoate due to risk of QT prolongation.

Class 1A antiarrhythmic that prolongs QTc interval and inhibits CYP2D6; caution advised due to risk of QT prolongation and increased haloperidol levels.

Inhibits cytochrome P450 2D6, increasing imipramine plasma concentrations. May require dose adjustment and TCA level monitoring.

Lanreotide may decrease metabolic clearance of quinidine; avoid concomitant use or consider dose reduction.

When administered with lidocaine, cardiac effects may be additive or antagonistic and toxic effects may be additive.

CYP2D6 inhibitor that inhibits donepezil metabolism in vitro; clinical effect not established.

Cationic drug eliminated by renal tubular secretion with potential for interaction with metformin by competing for common renal tubular transport systems.

Methylene blue inhibits CYP2D6 metabolism. Quinidine has narrow therapeutic index; clinical relevance unknown but concurrent use requires caution.

Strong CYP2D6 inhibitor that doubles metoprolol concentrations and decreases cardioselectivity; close monitoring required.

CYP3A4 substrate whose plasma levels may increase with concomitant metronidazole use. Monitor plasma concentrations.

P-glycoprotein inhibitor increasing plasma naldemedine concentrations; monitor for adverse reactions.

CYP2D6 inhibitor that may increase nebivolol levels; use caution when co-administered.

CYP2D6 inhibitor may increase nebivolol levels. Use caution when co-administered.

CYP3A substrate and inhibitor that increases nifedipine C max and AUC by 2.30 and 1.37 fold respectively, with increased heart rate up to 17.9 beats/minute. Heart rate monitoring and nifedipine dose adjustment recommended.

Quinidine 648 mg bid decreased nisoldipine AUC by 26% and immediate release nisoldipine increased quinidine concentrations by 20%. Clinical significance unknown; monitor ECG.

Octreotide used with quinidine (CYP3A4 substrate with narrow therapeutic index) should be used with caution and increased monitoring.

Octreotide may decrease metabolic clearance of quinidine through CYP3A4 suppression; use with caution due to low therapeutic index.

CYP2D6 inhibitor that increases oliceridine plasma concentration, resulting in increased or prolonged opioid effects. May require less frequent dosing and close monitoring for respiratory depression.

Sensitive CYP3A substrate with narrow therapeutic index. Dose may need reduction when coadministered with palbociclib.

Patiromer binds quinidine, potentially reducing systemic exposure and clinical efficacy. Separate dosing by at least 3 hours.

Rifapentine may increase metabolism and decrease activity. Dosage adjustment may be necessary.

Potent P-gp inhibitor that may increase rimegepant exposure. Avoid another dose within 48 hours when co-administered.

Stiripentol is an inhibitor and inducer of CYP3A4; consider dose adjustment of quinidine when administered concomitantly with DIACOMIT.

May enhance the neuromuscular blocking action of succinylcholine.

Sucralfate reduces the bioavailability of quinidine. Separate dosing administration is recommended.

Quinidine inhibits cytochrome P450 2D6, reducing trimipramine maleate metabolism and increasing plasma concentrations. Patient may become abruptly toxic.

BCRP and/or P-gp inhibitor that may increase ubrogepant exposure. Dose adjustment recommended.

Strong CYP2D6 inhibitor increases plasma concentrations of vortioxetine. Reduce TRINTELLIX dose by half when coadministered.

P-gp inhibitor that does not require dosage adjustment of PRADAXA.

CYP2D6 inhibitor; no dosing adjustments recommended.

Antiarrhythmic drug used concurrently with mexiletine in compassionate use program with sometimes improved ventricular ectopy control.

Weak CYP3A4 inhibitor; clinically significant increases in naloxegol concentrations are not expected and no dosage adjustments are necessary.

Prazosin has been administered without adverse drug interaction with quinidine in limited clinical experience.

Administered without adverse drug interaction in limited clinical experience.

Potential for drug-drug interaction due to possible competition for active tubular secretion via base-secreting system.