AM 92016 hydrochloride

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Background

AM 92016 hydrochloride is a specific inhibitor of delayed rectifier potassium current [1].
Potassium channel is an ion channel and acts to reset the resting potential and shapes the action potential. Delayed rectifier potassium channel (IK) is activated by the influx of Na+ and discharges K+, which repolarizes the membrane. IK restricts the duration of the nerve impulse.
AM 92016 hydrochloride is a specific iK inhibitor. In guinea-pig and rabbit ventricular cells, AM 92016 significantly increased action potential duration with 20% and 90% repolarization levels, respectively. Also, AM 92016 (1 μM) inhibited IK activated by step depolarizations in a time-dependent way [1]. In rabbit sino-atrial node cells, AM 92016 (50 nM) significantly inhibited IK with IC50 value of 40 nM in a concentration-dependent way [2]. In vascular smooth muscle cells (VSMC), AM92016 hydrochloride inhibited NO-induced ERK1/2 dephosphorylation [3].
In guinea-pigs, AM 92016 (1-5 mg/kg) significantly increased heart rate, left ventricular systolic pressure, systolic arterial blood pressure and the contractile index dp dtmax. AM 92016 exhibited proarrhythmic activity [4].

[1]. Connors SP, Gill EW, Terrar DA. Actions and mechanisms of action of novel analogues of sotalol on guinea-pig and rabbit ventricular cells. Br J Pharmacol, 1992, 106(4): 958-965.
[2]. Lei M, Brown HF. Inhibition by Compound II, a sotalol analogue, of delayed rectifier current (iK) in rabbit isolated sino-atrial node cells. Naunyn Schmiedebergs Arch Pharmacol, 1998, 357(3): 260-267.
[3]. Palen DI, Belmadani S, Lucchesi PA, et al. Role of SHP-1, Kv.1.2, and cGMP in nitric oxide-induced ERK1/2 MAP kinase dephosphorylation in rat vascular smooth muscle cells. Cardiovasc Res, 2005, 68(2): 268-277.
[4]. Hagerty MJ, Wainwright CL, Kane KA. The in-vivo cardiovascular effects of a putative class III anti-arrhythmic drug, AM 92016. J Pharm Pharmacol, 1996, 48(4): 417-421.