- Alomone Labs Lorcainide HCl inhibits NaV1.7 channels expressed in HEK293 cells.A: Time course of current reversible inhibition by 50 μM Lorcainide HCl (#L-135). Currents were elicited by a voltage ramp from a holding potential of -100 mV to 60 mV (30 ms) delivered every 10 seconds. B: Example traces of current response to voltage ramp stimulation before and during 50 μM Lorcainide HCl application.
Voltage-gated sodium channels (VGSC, NaV) are critically important for electrogenesis and nerve impulse conduction. Certain sodium channel isoforms are predominantly expressed in peripheral sensory neurons associated with pain sensation, and the expression and functional properties of NaV in peripheral sensory neurons can be dynamically regulated following axonal injury or peripheral inflammation1.
Lorcainide is an acetanilide derivative which blocks NaV channels. It possesses both local anesthetic and antiarrhythmic2,3 properties and in experimental animals it elevates the ventricular fibrillation threshold and protects against ouabain-induced arrhythmias4,5. Clinically, it is gaining an important place in the therapy of recurrent premature ventricular contractions6, recurrent ventricular tachycardia and repetitive atrial tachycardias7-9.
Compounds with antiarrhythmic activity show great variation in their chemical structure and have been classified according to: (1) their anatomical site of action; (2) their clinical range of activity; and (3) their electrophysiological action on isolated cardiac fibers. Like other class 1 antiarrhythmic drugs, the primary electrophysiological effect of Lorcainide is the reduction of the rate of rise of action potential during phase 04. Because of the slow recovery kinetics of the sodium ion channel, it has been classified as a class 1 antiarrhythmic agent10-12.
The effective concentrations for Lorcainide in humans are between 0.2 and 0.5 mg·litre-1 13 and 10 μM or 100 μM of Lorcainide may also protect central neuronal axons from hypoxic injury14.