Key result
Haloperidol potently blocked HERG channels with an IC50 of approximately 1 microM, binding preferentially to inactivated channels, which may explain its arrhythmogenic side effects.
Population
Xenopus oocytes expressing cloned cardiac K+ channels
Design
Preclinical
Authors
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Haloperidol warrants QT monitoring in patients; leaves open HERG as dominant mechanism in vivo.
Effect estimate: IC50 ~ 1 microM
Haloperidol blocks HERG potassium channels by binding to inactivated channels, providing a mechanistic explanation for its arrhythmogenic side effects such as QT prolongation.
Suessbrich et al. (1997) studied this question. Haloperidol was evaluated on Inhibition of HERG potassium channels (IC50 ~ 1 microM). Haloperidol potently blocked HERG channels with an IC50 of approximately 1 microM, binding preferentially to inactivated channels, which may explain its arrhythmogenic side effects.
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