Overview
Alomone Labs Pilsicainide hydrochloride inhibits NaV1.7 channels expressed in HEK293 cells.A. Time course of current reversible inhibition by 100 μM Pilsicainide hydrochloride (#P-145). 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 100 μM Pilsicainide hydrochloride application.
Voltage-gated Na+ channels (VGSC, NaV) are critically important for electrogenesis and nerve impulse conduction. Certain Na+ 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.
Pilsicainide is a class IC anti-arrhythmic drug widely used in the treatment of supraventricular and ventricular tachyarrhythmias in Japan2. Results from voltage clamp experiments show that Pilsicainide is a pure Na+ channel blocker with little or no effect on other cardiac channels, probably with the exception of HERG channels3-5.
Measurements of Pilsicainide’s ability to block hNaV1.4 channels resulted in half-maximum inhibitory concentrations (IC50) of 189 ± 10 µM at 0.1 Hz, and 76 ± 7 µM at 10 Hz. Effects of Pilsicainide were similar on skeletal muscle hNaV1.4, brain hNaV1.1 and heart hNaV1.5 channels.
