Comparative Pharmacology
Head-to-head clinical analysis: DEXTROMETHORPHAN HYDROBROMIDE AND QUINIDINE SULFATE versus QUINAGLUTE.
Peer-Reviewed Evidence
Head-to-head clinical analysis: DEXTROMETHORPHAN HYDROBROMIDE AND QUINIDINE SULFATE versus QUINAGLUTE.
DEXTROMETHORPHAN HYDROBROMIDE AND QUINIDINE SULFATE vs QUINAGLUTE
Comparing the clinical profiles, pharmacokinetic behaviors, and safety indices of these two therapeutic agents.
Dextromethorphan is an uncompetitive NMDA receptor antagonist and sigma-1 receptor agonist; quinidine is a CYP2D6 inhibitor that increases dextromethorphan bioavailability.
Class Ia antiarrhythmic agent; binds to sodium channels and inhibits the fast inward sodium current, slowing phase 0 depolarization and prolonging the action potential duration. Also exhibits anticholinergic and negative inotropic effects.
One capsule (dextromethorphan 20 mg/quinidine 10 mg) orally once daily, with a maximum dose of two capsules per day.
324-648 mg orally every 8-12 hours; extended-release formulation (quinidine gluconate).
None Documented
None Documented
Dextromethorphan: 2-4 hours (extensive metabolizers); quinidine: 6-8 hours (inhibits CYP2D6, prolonging dextromethorphan half-life in poor metabolizers to >20 hours)
Terminal elimination half-life is 5-7 hours in adults with normal renal function. In hepatic impairment, half-life may increase to 12-24 hours; in severe renal impairment (CrCl <10 mL/min), half-life may exceed 24 hours.
Renal: quinidine 15-25% unchanged, dextromethorphan <1% unchanged; biliary/fecal: quinidine metabolites ~5%, dextromethorphan metabolites ~60-80% as dextrorphan conjugates
Renal elimination of unchanged drug and metabolites accounts for approximately 60-70% of total clearance. Biliary/fecal excretion contributes about 20-30%. Acidic urine increases renal clearance.
Category A/B
Category C
Antiarrhythmic (Class Ia)
Antiarrhythmic (Class Ia)