Quinidine is an antiarrhythmic agent. Quinidine is a potent, orally active, selective cytochrome P450db inhibitor. Quinidine is also a blocker of K + channel with an IC 50 of 19.9 μM. Quinidine has potential to be used for malaria research [1] [2] [3].

Quinidine sulfate is an anti-arrythmic drug which affects ionic currents in heart muscle. Quinidine sulfate has also been shown to be a potent blocker of several classes of K + channel in a variety of cell types [1]. Bath application of quinidine sulfate results in a dose-dependent reduction of the peak amplitude of I k. The K d for blockade of I k at 0 mV is estimated to be 41 μM [1]. Quinidine sulfate elicits a dose-dependent increase of the rate of the decay of I k and this effect is enhanced by membrane depolarization. Quinidine also causes a 5 mV hyperpolarizing shift of the steady-state inactivation curve and increases the half-time for recovery from inactivation. Quinidine does not affect the onset of inactivation measured at -30 mV [1].

Quinidine sulfate is rapidly absorbed, with peak plasma concentrations 60-90 min after an oral dose, while other salts (gluconate, polygalacturonate) are more slowly absorbed, with lower peak concentrations [2]. Quinidine sulfate is approximately 70-90 % bound to plasma proteins. It undergoes hepatic oxidative metabolism to form an N-oxide, a 3-hydroxy form, an O-demethyl form and 2'-quinidinone [2]. Quinidine sulfate inhibits metabolism of amphetamine in rats. Quinidine pretreatment results in a significant decrease in the excretion of p-hydroxyamphetamine at 24 and 48 h to 7.2 and 24.1% of the vehicle-control levels, respectively, accompanied by a significant increase in amphetamine excretion between 24 and 48 h to 542% of the control [3].