Way 123398 - CAS 138490-53-6
Catalog number: 138490-53-6
Category: Inhibitor
Please be kindly noted products are not for therapeutic use. We do not sell to patients.
Molecular Formula:
Molecular Weight:
Potassium Channel
Way 123398 is a class III antiarrhythmic agent. It is a Potassium channel antagonist originated by Wyeth. No preclinical development for Arrhythmias in USA was reported.
Way 123398; Way123398; Way-123398; N-methyl-N-(2-(methyl(1-methyl-1H-benzimidazol-2-yl)amino)ethyl)-4-((methylsulfonyl)amino)-Benzenesulfonamide
Soluble in DMSO
-20°C Freezer
Quality Standard:
In-house standard
Shelf Life:
2 month in rt, long time
Canonical SMILES:
Current Developer:
Originator Wyeth
1.Alpha 1-adrenergic receptor modulation of repolarization in canine Purkinje fibers.
Lee JH;Rosen MR J Cardiovasc Electrophysiol. 1994 Mar;5(3):232-40.
INTRODUCTION: ;Alpha 1-adrenergic receptor stimulation increases contractility and prolongs repolarization. These effects are modulated by alpha 1-adrenergic receptor-mediated inhibition of transsarcolemmal potassium currents.;METHODS AND RESULTS: ;We used standard microelectrode techniques to study the actions of 4-aminopyridine (4-AP), which blocks the transient outward current, I(to), and WAY-123,398, which blocks the delayed rectifier, Ik, on canine Purkinje fiber action potential prolongation induced by phenylephrine. At a basic cycle length of 1 second, phenylephrine (0.1 to 10 microM) dose-dependently prolonged action potential duration at 90% repolarization (APD90) from 331 +/- 10 msec to 400 +/- 12 msec (P < 0.05) at phenylephrine, 10 microM. Phenylephrine did not change phase 1 or plateau height. 4-AP (0.1 mM) decreased phase 1 magnitude, shifted plateau height to more positive potentials (from 0.1 +/- 1.8 mV to 14.3 +/- 1.1 mV [P < 0.05]), and shortened APD90 from 318 +/- 9 msec to 294 +/- 8 msec (P < 0.05). 4-AP did not block phenylephrine effects on APD90, which increased, at 10 microM phenylephrine, from 294 +/- 8 msec to 342 +/- 6 msec (P < 0.05). In contrast, WAY-123,398 (0.
2.A HERG-like K+ channel in rat F-11 DRG cell line: pharmacological identification and biophysical characterization.
Faravelli L;Arcangeli A;Olivotto M;Wanke E J Physiol. 1996 Oct 1;496 ( Pt 1):13-23.
1. The relationships between the K+ inward rectifier current present in neuroblastoma cells (IIR) and the current encoded by the human ether-á-go-go-related gene (HERG), IHERG, and the rapidly activating repolarizing cardiac current IK(r), were investigated in a rat dorsal root ganglion (DRG) x mouse neuroblastoma hybrid cell line (F-11) using pharmacological and biophysical treatments. 2. IIR shared the pharmacological features described for IK(r), including the sensitivity to the antiarrhythmic drugs E4301 and WAY-123,398, whilst responding to Cs+, Ba2+ and La3+ in a similar way to IHERG. 3. The voltage-dependent gating properties of IIR were similar to those of IK(r) and IHERG, although IIR outward currents were negligible in comparison. 4. In high K+ extracellular solutions devoid of divalent cations, IIR deactivation kinetics were removed resulting in long-lasting currents apparently activated in hyperpolarization, with a marked (2.7-fold) increase in conductance, as recorded from the instantaneous linear current-voltage relationship at -120 mV. Re-addition of Ca2+ restored the original closure of the channel whereas re-addition of Mg2+ reduced the peak current. 5. The IIR described here, the heart IK(r) and the IHERG could be successfully predicted by a unique kinetic model where the voltage dependencies of the activation/inactivation gates were properly voltage shifted.
3.[3H]dofetilide binding to HERG transfected membranes: a potential high throughput preclinical screen.
Finlayson K;Turnbull L;January CT;Sharkey J;Kelly JS Eur J Pharmacol. 2001 Oct 26;430(1):147-8.
The pharmacological characteristics of [3H]dofetilide binding were examined in membranes prepared from human embryonic kidney (HEK293) cells stably expressing human ether-á-go-go related gene (HERG) K+ channels. The classIII antiarrhythmic compounds dofetilide, clofilium, 4'-[[1-[2-(6-methyl-2-pyridyl)ethyl]-4-piperidyl]carbonyl]methanesulfonanilide (E-4031), N-methyl-N-[2-[methyl-(1-methyl-1H-benzimidazol-2-yl)amino]ethyl]-4-[(methylsulfonyl)amino]benzene-sulfonamide (WAY-123,398) and d-sotalol all inhibited [3H]dofetilide binding. In addition, the structurally unrelated compounds pimozide, terfenadine and haloperidol, all of which prolong the QT interval in man, also inhibited binding. These data indicate that a [3H]dofetilide binding assay using HERG membranes may help identify compounds that prolong the QT interval.
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