Vanoxerine dihydrochloride 是一种竞争性的、有效的、选择性的多巴胺再摄取抑制剂，能够与多巴胺转运体 (DAT) 上的靶点结合。

Vanoxerine dihydrochloride is a potent inhibitor that blocks dopamine uptake (IC50 : 1-51 nM)

In 9 SP dogs, 11 episodes each of sustained (>10 minutes) AF and AFL were induced. Electrophysiological studies were performed before and after infusion of vanoxerine, which effectively terminated AF and AFL in 19 of 22 episodes. Simultaneous multisite mapping during 3 AF and 3 AFL episodes demonstrated that termination of each arrhythmia occurred with termination of the driver (a reentrant circuit) following an increase in tachycardia CL. Except for conduction in an area of slow conduction in the driver's reentrant circuit, vanoxerine did not significantly affect intraatrial or atrioventricular conduction time, QRS duration, or QT/QTc intervals. Ventricular refractoriness prolonged minimally during ventricular pacing at 400 and 333 ms (176 +/- 16 ms to 182 +/- 16 ms; 173 +/- 11 ms to 178 +/- 18 ms, respectively). Vanoxerine minimally increased (mean 0.7 mA) atrial stimulus threshold for capture[1].Vanoxerine dihydrochloridealso blocks ligand binding to sigma receptors in rat brain (IC50 = 48 nM)[2].

67469-78-7

C28H34Cl2F2N2O

523.49

I893 dihydrochloride;伐诺司林二盐酸盐;GBR-12909 dihydrochloride

DMSO:9.4 mg/mL (17.96 mM)
Powder: -20°C for 3 years
In solvent: -80°C for 2 years