Cellular electrophysiology of WAY-123,398, a new class III antiarrhythmic agent: specificity of IK block and lack of reverse use dependence in cat ventricular myocytes

Abstract

The results indicate that WAY-123,398 is an effective and specific class III agent devoid of class I activity, and suggest that WAY-123,398 prolongs cardiac repolarisation by specifically blocking the delayed rectifier current (IK). The block was unchanged over a range of frequencies and duration of depolarisation, showing no evidence of "reverse use dependence" of block.

A HERG‐like K+ channel in rat F‐11 DRG cell line: pharmacological identification and biophysical characterization.

“…We show here that in the rat dorsal root ganglion (DRG) x mouse neuroblastoma hybrid F-Il clone (Platika, Boulos, Baizer & Fishman, 1985;Boland & Dingledine, 1990), IR was blocked by specific inhibitors of IK(r) such as E4031 (Sanguinetti et al 1990a) and by 398 (WAY,amido]benzenesulphonamide), another class III antiarrhythmic agent (Spinelli, Moubarak, Parsons & Colatsky, 1993). Moreover, unlike IK(r) in heart and IHERG in oocytes, our tumour cell current displayed a weak outward amplitude as compared with the inward.…”

Species Diversity and Peptide Toxins Blocking Selectivity of Ether-à-go-go-Related Gene Subfamily K+ Channels in the Central Nervous System

“…Appropriate quantities of the toxins from stocks in H 2 O were dissolved in the extracellular solution immediately before the experiments. When contaminating potassium currents were present, the specific ERG blocker WAY123,398 (Spinelli et al, 1993) was used at 2 M and the resulting traces were subtracted from control traces to obtain the WAY123,398-sensitive currents. The extracellular solutions were delivered through a nine-hole (0.6-mm) remote-controlled linear positioner with an average response time of 1 to 2 s that was placed near the cell under study.…”

Two Types of K+Channel Subunit, Erg1 and KCNQ2/3, Contribute to the M-Like Current in a Mammalian Neuronal Cell

“…We tested this pharmacologically, using the HERG channelblocking drug WAY 123,398 (Spinelli et al, 1993;Faravelli et al, 1996). As shown in Figure 1 A, 10 M WAY 123,398 blocked most of the long deactivation, leaving a residual fast component which was then eliminated by the M channel-blocking drug linopirdine (Aiken et al, 1995;Lamas et al, 1997).…”