Comparative Pharmacology
Head-to-head clinical analysis: CIN QUIN versus DEXTROMETHORPHAN HYDROBROMIDE AND QUINIDINE SULFATE.
Peer-Reviewed Evidence
Head-to-head clinical analysis: CIN QUIN versus DEXTROMETHORPHAN HYDROBROMIDE AND QUINIDINE SULFATE.
CIN-QUIN vs DEXTROMETHORPHAN HYDROBROMIDE AND QUINIDINE SULFATE
Comparing the clinical profiles, pharmacokinetic behaviors, and safety indices of these two therapeutic agents.
Cin-Quin (quinidine) is a class Ia antiarrhythmic agent that blocks sodium channels, prolonging the effective refractory period and slowing conduction velocity. It also has anticholinergic and alpha-adrenergic blocking properties.
Dextromethorphan is an uncompetitive NMDA receptor antagonist and sigma-1 receptor agonist; quinidine is a CYP2D6 inhibitor that increases dextromethorphan bioavailability.
Quinine sulfate 648 mg (two 324 mg capsules) orally every 8 hours for 7 days, in combination with doxycycline, tetracycline, or clindamycin.
One capsule (dextromethorphan 20 mg/quinidine 10 mg) orally once daily, with a maximum dose of two capsules per day.
None Documented
None Documented
Terminal elimination half-life is approximately 4-5 hours in healthy volunteers; prolonged to 8-12 hours in severe malaria or hepatic impairment.
Dextromethorphan: 2-4 hours (extensive metabolizers); quinidine: 6-8 hours (inhibits CYP2D6, prolonging dextromethorphan half-life in poor metabolizers to >20 hours)
Primarily hepatic metabolism; renal excretion of unchanged drug <20%. Biliary/fecal excretion accounts for ~30% of total clearance.
Renal: quinidine 15-25% unchanged, dextromethorphan <1% unchanged; biliary/fecal: quinidine metabolites ~5%, dextromethorphan metabolites ~60-80% as dextrorphan conjugates
Category C
Category A/B
Antiarrhythmic (Class Ia)
Antiarrhythmic (Class Ia)