AZD-1305
AZD-1305 is an antiarrhythmic agent and atrial selective sodium channel/potassium channel blocker, which can significantly prolongs action potential duration and reduces excitability, cause atrial selective ERP prolongation and acute termination of atrial fibrillation. AZD1305 can be used for atrial fibrillation research.
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- CAS. Nr.: 872045-91-5
- Formel: C22H31FN4O4
- Molecular Weight:434.50
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Speicherung:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biologische Aktivität
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Chemical Information
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Biologische Aktivität
AZD-1305 (1,3 μM) induces atrial selective PRR in isolated coronary-perfused preparations [1].
AZD-1305 (1,3 μM) produces a greater use-dependent reduction of maximum rate of rise of the action potential upstroke (Vmax) in atrial versus ventricular preparations[1].
AZD-1305 (1,3 μM) causes a greater increase in sodium channel–mediated parameters conduction velocity and diastolic threshold of excitation in atrial versus ventricular coronaryperfused preparations[1].
AZD-1305 (5 μM) induces greater tonic and steadystate inhibitions of atrial sodium channels than ventricular sodium channels in isolated coronary-perfused preparations[1].
AZD-1305 (1-10 μM) causes a significant decrease in Vmax, action potential amplitude, and takeoff potential in canine pulmonary vein sleeve preparations, and significantly increases action potential duration at 90% repolarization[2].
AZD-1305 (1-10 μM) significantly increases the basic cycle length at which 1:1 activation is maintained in canine pulmonary vein sleeve preparations, and pretreatment with amiodarone significantly potentiates the effect of AZD1305[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
AZD-1305 (steady state plasma concentrations of 1.2 and 4.5 μM, i.v.drip) increases conduction time and depress excitability in atria versus ventricles of Beagle dogs [1].
AZD-1305 (steady state plasma concentrations of 1-3 μM, i.v.drip) terminates persistent AF and prevents induction of AF in an ACh-mediated model of AF in Beagle dogs [1].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
| NCT Number | Sponsor | Condition | Start Date |
Phase
|
|---|---|---|---|---|
| NCT01329991 | Plexxikon| | 2011-05 | PHASE1 |
Chemical Information
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CAS. Nr. 872045-91-5
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Molecular Weight 434.50
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Formel C22H31FN4O4
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SMILES
O=C(OC(C)(C)C)NCCN1CC(O2)CN(CCOC3=CC=C(C#N)C=C3F)CC2C1
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Versand
Room temperature in continental US; may vary elsewhere.
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Speicherung
Please store the product under the recommended conditions in the Certificate of Analysis.
Reinheit & Dokumentation
Verweise
[1]. Charles Antzelevitch, et al. AZD1305 Exerts Atrial Predominant Electrophysiological Actions and Is Effective in Suppressing Atrial Fibrillation and Preventing Its Reinduction in the Dog. [J] Cardiovasc Pharmacol. 2010, Volume 56，Number 1. [Content Brief]
[2]. Serge Sicouri, et al. Electrophysiologic and antiarrhythmic effects of AZD1305 in canine pulmonary vein sleeves. THE JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS. 2010, Volume 334，Number 1. [Content Brief]
[3]. Alexander Burashnikov, et al. AZD1305 exerts atrial predominant electrophysiological actions and is effective in suppressing atrial fibrillation and preventing its reinduction in the dog. J Cardiovasc Pharmacol. 2010 Jul;56(1):80-90. [Content Brief]
Calculators
Konzentration (Stammlösung) × Volumen (Stammlösung) = Konzentration (Ziellösung) × Volumen (Ziellösung)
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