Quinine (hydrobromide)

Quinidine hydrobromide is an antiarrhythmic agent. Quinidine is a potent, orally active, selective cytochrome P450db inhibitor. Quinidine hydrobromide is also a K⁺ channel blocker with an IC₅₀ of 19.9 μM. Quinidine hydrobromide can be used for malaria research^[1][2][3]. In Vitro: Quinidine hydrobromide is an anti-arrythmic drug which affects ionic currents in heart muscle and which 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 hydrobromide causes 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 hydrobromide 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 hydrobromide does not affect the onset of inactivation measured at -30 mV^[1]. In Vivo: Quinidine hydrobromide is rapidly absorbed, with peak plasma concentrations 60-90 min after an oral dose. Other salts (gluconate, polygalacturonate) are more slowly absorbed, with lower peak concentrations^[2].
Quinidine hydrobromide 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 hydrobromide inhibits metabolism of amphetamine in rats. Quinidine hydrobromide 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].