Quinidine is an antiarrhythmic agent. Quinidine is a potent, orally active, selectivecytochrome P450dbinhibitor. Quinidine is also aK⁺channelblocker with anIC₅₀of 19.9 μM. Quinidine can be used for malaria research^[1][2][3].

Quinidine sulfate 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 sulfate causes a dose-dependent reduction of the peak amplitude of I_k. The K_dfor blockade of I_kat 0 mV is estimated to be 41 μM^[1].
Quinidine sulfate elicits a dose-dependent increase of the rate of the decay of I_kand 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. 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].

422.50

C₂₀H₂₆N₂O₆S

549-56-4

奎宁硫酸盐

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