Quinine sulfate 

Quinidine sulfate is an antiarrhythmic agent. Quinidine sulfate is a potent, orally active, selective cytochrome P450db inhibitor. Quinidine sulfate is also a K⁺ channel blocker with an IC₅₀ of 19.9 μM. Quinidine sulfate 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_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 sulfate also causes a 5 mV hyperpolarizing shift of the steady-state inactivation curve and increases the half-time for recovery from inactivation. Quinidine sulfate does not affect the onset of inactivation measured at -30 mV^[1].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

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 sulfate 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].

MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

422.50

C₂₀H₂₆N₂O₆S

549-56-4

Solid

White to off-white

O[C@H](C1=CC=NC2=C1C=C(OC)C=C2)[C@@]3([H])[N@](C[C@@H]4C=C)CC[C@H]4C3.O=S(O)(O)=O

Room temperature in continental US; may vary elsewhere.

4°C, protect from light, stored under nitrogen

*In solvent : -80°C, 6 months; -20°C, 1 month (protect from light, stored under nitrogen)

• [1]. Kehl SJ, et al. Quinidine-induced inhibition of the fast transient outward K+ current in rat melanotrophs. Br J Pharmacol. 1991 Jul;103(3):1807-13.  [Content Brief]

  [2]. Roden DM, et al. Class I antiarrhythmic agents: quinidine, procainamide and N-acetylprocainamide, disopyramide.  [Content Brief]

  [3]. Moody DE, et al. Quinidine inhibits in vivo metabolism of amphetamine in rats: impact upon correlation between GC/MS and immunoassay findings in rat urine. J Anal Toxicol. 1990 Sep-Oct;14(5):311-7.  [Content Brief]