Quinidine is a potent, orally active, selective inhibitor of cytochrome P450db. Quinidine hydrobromide is a K + channel blocker (IC 50= 19.9 μM). Quinidine hydrobromide shows antiarrhythmic activity. Quinidine hydrobromide can be used for malaria research.

Quinidine hydrobromide, an anti-arrhythmic agent, modulates ionic currents in heart muscle and acts as a potent K+ channel blocker across various cell types. When applied, it dose-dependently lowers the peak amplitude of I_k with a K_d of 41 μM for I_k blockade at 0 mV. Additionally, it increases the decay rate of I_k in a dose-dependent manner, an effect that intensifies with membrane depolarization. Quinidine induces a 5 mV hyperpolarizing shift in the steady-state inactivation curve and prolongs the half-time for recovery from inactivation, without influencing the onset of inactivation at -30 mV.

Quinidine hydrobromide is swiftly absorbed into the bloodstream, achieving peak plasma levels between 60 and 90 minutes after ingestion. In contrast, its other salts (gluconate, polygalacturonate) absorb more gradually, resulting in lower peak levels [2]. This compound binds to plasma proteins at a rate of approximately 70-90% and is metabolized in the liver through oxidative pathways, producing several metabolites including an N-oxide, a 3-hydroxy form, an O-demethyl form, and 2'-quinidinone [2]. Additionally, quinidine hydrobromide impedes the metabolism of amphetamine in rats, leading to a marked reduction in p-hydroxyamphetamine excretion 24 and 48 hours post-administration, to 7.2 and 24.1% of control levels, respectively. This is coupled with a significant uptick in amphetamine excretion over the same period, reaching 542% of control levels [3].