Comparative Pharmacology
Head-to-head clinical analysis: DEXTROMETHORPHAN HYDROBROMIDE AND QUINIDINE SULFATE versus QUINACT.
Peer-Reviewed Evidence
Head-to-head clinical analysis: DEXTROMETHORPHAN HYDROBROMIDE AND QUINIDINE SULFATE versus QUINACT.
DEXTROMETHORPHAN HYDROBROMIDE AND QUINIDINE SULFATE vs QUINACT
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.
Quinacrine is a 9-aminoacridine derivative that intercalates into DNA, inhibiting DNA replication and transcription, and also has antimalarial, anti-inflammatory, and antihelminthic properties. It inhibits phospholipase A2 and suppresses immune responses.
One capsule (dextromethorphan 20 mg/quinidine 10 mg) orally once daily, with a maximum dose of two capsules per day.
100 mg orally three times daily.
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: 12-15 hours (prolonged in renal impairment; CrCl <30 mL/min: 24-40 hours)
Renal: quinidine 15-25% unchanged, dextromethorphan <1% unchanged; biliary/fecal: quinidine metabolites ~5%, dextromethorphan metabolites ~60-80% as dextrorphan conjugates
Renal: 70% unchanged; biliary/fecal: 20% as metabolites; 10% other
Category A/B
Category C
Antiarrhythmic (Class Ia)
Antiarrhythmic (Class Ia)