An antiarrythmic agent that inhibits potassium channels
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Labeled Version(s)
26451Dofetilide-d4
Metabolite(s)
36294Dofetilide N-oxide
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Dofetilide

Item No. 15045

Technical Information
Formal Name
N-[4-[2-[methyl[2-[4-[(methylsulfonyl)amino]phenoxy]ethyl]amino]ethyl]phenyl]-methanesulfonamide
CAS Number
115256-11-6
Synonyms
  • Tikosyn
  • UK 68789
Molecular Formula
C19H27N3O5S2
Formula Weight
Purity
≥98%
Formulation
A crystalline solid
DMF: 30 mg/mlDMSO: 30 mg/mlDMSO:PBS (pH 7.2) (1:20): 0.4 mg/ml
λmax
232 nm
SMILES
CS(NC1=CC=C(OCCN(C)CCC2=CC=C(NS(C)(=O)=O)C=C2)C=C1)(=O)=O
InChi Code
InChI=1S/C19H27N3O5S2/c1-22(13-12-16-4-6-17(7-5-16)20-28(2,23)24)14-15-27-19-10-8-18(9-11-19)21-29(3,25)26/h4-11,20-21H,12-15H2,1-3H3
InChi Key
IXTMWRCNAAVVAI-UHFFFAOYSA-N
Shipping & Storage Information
Storage
-20°C
Shipping
Room temperature in continental US; may vary elsewhere
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    Product Description

    Dofetilide is a class III antiarrhythmic agent that prolongs cardiac action potential duration by selectively inhibiting the rapidly activating inward rectifying component of net delayed rectifier K+ current (IC50 = 31.5 nM in guinea pig cardiomyocytes).1 However, at 1 μM, dofetilide has pro-arrhythmic activity, inducing early afterdepolarizations (prolonged repolarization) in cell models and Torsade de Pointes in a rabbit screen for proarrhythmic properties when administered at a dose of 10 mg/kg.2 Formulations containing dofetilide have been used in the treatment of highly symptomatic atrial fibrillation and the conversion of flutter to normal sinus rhythm.3

    WARNING This product is not for human or veterinary use.

    References & Product Citations
    Product Description References

    1. Jurkiewicz, N.K., and Sanguinetti, M.C. Rate-dependent prolongation of cardiac action potentials by a methanesulfonanilide class III antiarrhythmic agent. Circ. Res. 72(1), 75-83 (1993).

    2. Nalos, L., Varkevisser, R., Jonsson, M.K., et alComparison of the IKr blockers moxifloxacin, dofetilide and E-4031 in five screening models of pro-arrhythmia reveals lack of specificity of isolated cardiomyocytes. Br. J. Pharmacol. 165(2), 467-478 (2012).

    3. Dunnink, A., van Opstal, J.M., Oosterhoff, P., et alVentricular remodelling is a prerequisite for the induction of dofetilide-induced torsade de pointes arrhythmias in the anaesthetized, complete atrio-ventricular-block dog. Europace 14(3), 431-436 (2012).