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| AM 92016 hydrochloridePotassium channel blocker |
Sample solution is provided at 25 µL, 10mM.
Nature.2017 Jan 19;541(7637):417-420.
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| Cas No. | 133229-11-5 | SDF | Download SDF |
| Chemical Name | N-(4-(3-((3,4-dichlorophenethyl)(methyl)amino)-2-hydroxypropoxy)phenyl)methanesulfonamide hydrochloride | ||
| Canonical SMILES | CN(CC(O)COC1=CC=C(NS(C)(=O)=O)C=C1)CCC2=CC(Cl)=C(Cl)C=C2.Cl | ||
| Formula | C19H24Cl2N2O4S.HCl | M.Wt | 483.84 |
| Solubility | <48.38mg l="" in="" dmso;=""><24.19mg l="" in="" h2o=""> | Storage | Store at RT |
| Physical Appearance | White solid | Shipping Condition | Evaluation sample solution : ship with blue ice.All other available size:ship with RT , or blue ice upon request |
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. | ||
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].
References:[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.
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