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• W2006214313 abstract "The long QT-related arrhythmia torsades de pointes (TdP) can arise with mutations in HERG and during treatment with drugs that block cardiac I Kr , the current encoded by HERG. Multiple test systems have been used to assess drug block of I Kr . This study evaluated the I Kr blocking potency of a series of antiarrhythmics associated with a range of clinical risks of TdP in two such systems: mouse AT-1 cells (in which I Kr is the major repolarizing current) and Ltk cells transiently transfected with HERG (n = 4–10 cells per drug). For each compound, the concentration required to produce 50% block of I Kr or HERG tail currents (IC 50 ) was determined. There was an excellent correlation (r = 0.98, p < 10 −5 ) between values obtained in the two systems. However, the relation between the liability of a drug to cause TdP appeared dissociated from I Kr blocking potency. Quinidine, dofetilide, ibutilide, procainamide, and disopyramide are all associated with TdP, but only the first three were potent blockers (IC 50 ≤ 1 μM), whereas procainamide and disopyramide were not (IC 50 > 50 μM). Conversely, verapamil and amiodarone, drugs not associated with TdP, were also blockers (IC 50 ≤ 1 μM). We conclude that I Kr blocking potency can be readily assessed in either AT-1 cells or systems in which HERG is heterologously expressed. However, not all drugs causing TdP are potent I Kr blockers, and I Kr block is not necessarily associated with TdP. Other properties of these drugs, therefore, contribute to their propensity to cause TdP." @default.
• W2006214313 created "2016-06-24" @default.
• W2006214313 creator A5058141203 @default.
• W2006214313 creator A5071594443 @default.
• W2006214313 creator A5088893226 @default.
• W2006214313 date "2001-11-01" @default.
• W2006214313 modified "2023-10-18" @default.
• W2006214313 title "Drug Block of I Kr : Model Systems and Relevance to Human Arrhythmias" @default.
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• W2006214313 doi "https://doi.org/10.1097/00005344-200111000-00010" @default.
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