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AVE 0118 hydrochloride
- Parent CAS: 498577-53-0
- Soluble in water and DMSO
- MF: C30H29N3O3.HCl
- MW: 516.03
Description
AVE 0118 hydrochloride is an atrium-selective potassium-channel blocker that inhibits Kv1.5 (IKur), Kv4.3 (Ito), Kir3.4 (IKAch) and IKr currents with IC50 values of 6.2 μM, 3.4 μM, 4.5 μM and 10 μM, respectively. It prolongs atrial effective refractory period while showing minimal impact on ventricular repolarization in reported studies.
Atrial-selective modulation of repolarizing potassium currents is an important strategy in atrial fibrillation research. AVE 0118 is useful for studying IKur/IKAch-dependent electrophysiology, atrial refractoriness and antiarrhythmic mechanisms with reduced ventricular liability.
Key Features
- Blocks Kv1.5, Kv4.3, Kir3.4 and IKr currents
- IC50: 6.2 μM at Kv1.5 (IKur)
- Atrium-selective antiarrhythmic profile
- Prolongs atrial effective refractory period
Applications
- Atrial electrophysiology research
- Atrial fibrillation model studies
- Potassium-channel pharmacology
- Antiarrhythmic mechanism assays
More Information
| Parent CAS No. | 498577-53-0 |
|---|---|
| Chemical Name | 2'-((2-(4-methoxyphenyl)acetamido)methyl)-N-(2-(pyridin-3-yl)ethyl)biphenyl-2-carboxamide hydrochloride |
| SMILES | C1(C2=CC=CC=C2CNC(CC2=CC=C(OC)C=C2)=O)=CC=CC=C1C(NCCC1=CC=CN=C1)=O.Cl |
| MFCD | N.A. |
| InChi | InChI=1S/C30H29N3O3.ClH/c1-36-25-14-12-22(13-15-25)19-29(34)33-21-24-8-2-3-9-26(24)27-10-4-5-11-28(27)30(35)32-18-16-23-7-6-17-31-20-23;/h2-15,17,20H,16,18-19,21H2,1H3,(H,32,35)(H,33,34);1H |
| InChiKey | VLHHQGXIOINJIC-UHFFFAOYSA-N |
| CID | 91826504 |
| Short Description | IKur channel blocker |
References
- H. Gögelein et al. Effects of the atrial antiarrhythmic drug AVE0118 on cardiac ion channels. Naun. Schmiedebergs Arch. Pharmacol. 2004, 370, 183-192.
- K.J. Wirth et al. Atrial effects of the novel K+-channel-blocker AVE0118 in anesthetized pigs. Cardiovascular Res. 2003, 60, 298-306.
- A. Burashnikov et al. Atrial-selective prolongation of refractory period with AVE0118 is due principally to inhibition of sodium channel activity. J. Cardiovasc. Pharmacol. 2012, 59, 539-546.
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