Mechanism of action<unk>  works as an anti-arrhythmic agent and is used to treat cardiac arrhythmia. It induces rapid block of the batrachotoxin (BTX)-activated sodium channels of the heart muscle and acts as antagonist to long-gating closures. The block is voltage-dependent and can occur from both sides; either from the intracellular or the extracellular side. Blocking from the extracellular side is weaker than from the intracellular side because it occurs via the hydrophobic<unk> thway.<unk>  is present in charged form and probably requires a direct hydrophobic access to the binding site for blocking of the channel. Furthermore, blocking of the channel shows a decreased voltage sensitivity, which may result from the loss of voltage dependence of the blocking rate. Due to its charged and hydrophilic form,<unk>  has its effect from the internal side, where it causes blockage of voltage-dependent, open channels. With increasing concentration of<unk> , the frequency of long blockage becomes less without the duration of blockage being affected. The rate of fast blocking is determined by the membrane depolarization. Membrane depolarization leads to increased blocking and decreased unblocking of the channels.<unk>  slows the conduction velocity and increases the refractory period, such that the maximal rate of depolarization is reduced. Metabolism<unk>  is metabolized via different<unk> thways. The most common one is the acetylation of<unk>  to the less-toxic N-acetylprocainamide. The rate of acetylation is genetically determined. There are two phenotypes that result from the acetylation process, namely the slow and rapid acetylator.<unk>  can also be oxidized by the cytochrome P-450 to a reactive oxide metabolite. But it seems that acetylation of the nitrogen group of<unk>  decrease the amount of the chemical that would be available for the oxidative route. Other metabolites of<unk>  include desethyl-N-acetylprocainamide, desethylprocainamide, p-aminobenzoic acid, which are excreted via the urine. N-acetyl-4-aminobenzoic acid as well as N-acetyl-3-hydroxyprocainamide, N-acetylprocainamide-N-oxide and N-acetyl-4-aminohippuric acid are also metabolites of<unk> .
Procainamide
Tocainide
Flecainide
Acecainide
Setiptiline
Veratridine
Maprotiline
Verapamil