| Indication | For the treatment of documented ventricular arrhythmias, such as sustained ventricular tachycardia, that, in the judgment of the physician, are life-threatening. |
| Pharmacodynamics | Tocainide is a primary amine analog of lidocaine with antiarrhythmic properties useful in the treatment of ventricular arrhythmias. Tocainide, like lidocaine, produces dose dependent decreases in sodium and potassium conductance, thereby decreasing the excitability of myocardial cells. In experimental animal models, the dose-related depression of sodium current is more pronounced in ischemic tissue than in normal tissue. Tocainide is a Class I antiarrhythmic compound with electrophysiologic properties in man similar to those of lidocaine, but dissimilar from quinidine, procainamide, and disopyramide. |
| Mechanism of action | Tocainide acts on sodium channels on the neuronal cell membrane, limiting the spread of seizure activity and reducing seizure propagation. Tocainide binds preferentially to the inactive state of the sodium channels.The antiarrhythmic actions are mediated through effects on sodium channels in Purkinje fibers. |
| Absorption | Following oral administration, the bioavailability approaches 100 percent, and is unaffected by food. |
| Volume of distribution | Not Available |
| Protein binding | Approximately 10 percent bound to plasma protein. |
| Metabolism | Negligible first pass hepatic degradation. No active metabolites have been found. |
| Route of elimination | Not Available |
| Half life | The average plasma half-life in patients is approximately 15 hours. May be prolonged up to 35 hours in patients with severe renal function impairment (creatinine clearance less than 30 mL per min per 1.73 square meters of body surface area. |
| Clearance | Not Available |
| Toxicity | The oral LD50 of tocainide was calculated to be about 800 mg/kg in mice, 1000 mg/kg in rats, and 230 mg/kg in guinea pigs; deaths were usually preceded by convulsions. |