Potent Inhibition of Cytochrome P450IID6 (Debrisoquin 4‐Hydroxylase) by Flecainide In Vitro and In Vivo

@article{Haefeli1990PotentIO,
  title={Potent Inhibition of Cytochrome P450IID6 (Debrisoquin 4‐Hydroxylase) by Flecainide In Vitro and In Vivo},
  author={Walter Emil Haefeli and Mario J. Bargetzi and Ferenc Follath and Urs A. Meyer},
  journal={Journal of Cardiovascular Pharmacology},
  year={1990},
  volume={15},
  pages={776–779}
}
Flecainide acetate, a class Ic antiarrhythmic agent, is eliminated to a larger extent by renal excretion and to a minor extent by the liver. In patients with impaired renal function or with elevated urinary pH, however, its elimination is dominated by hepatic metabolism. Recent evidence suggests that the in vivo metabolism of flecainide is controlled by the genetic polymorphism of the debrisoquin/sparteine type; i.e., it is a substrate of cytochrome P4501ID6. We investigated the inhibitory… 

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It has high bioavailability after an oral dose with plasma half-life is about 20 hours with Peak serum concentrations can be seen 1 to 6 hours after ingestion of an oral dose. [1-2]. During oral