Anti-addiction drug ibogaine inhibits hERG channels: a cardiac arrhythmia risk

Authors

  • Xaver Koenig,

    1. Center for Physiology and Pharmacology, Department of Neurophysiology and Pharmacology, Medical University of Vienna, Vienna, Austria
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    • These authors contributed equally.

  • Michael Kovar,

    1. Center for Physiology and Pharmacology, Department of Neurophysiology and Pharmacology, Medical University of Vienna, Vienna, Austria
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    • These authors contributed equally.

  • Stefan Boehm,

    1. Center for Physiology and Pharmacology, Department of Neurophysiology and Pharmacology, Medical University of Vienna, Vienna, Austria
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  • Walter Sandtner,

    1. Center for Physiology and Pharmacology, Institute of Pharmacology, Medical University of Vienna, Vienna, Austria
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  • Karlheinz Hilber

    Corresponding author
    1. Center for Physiology and Pharmacology, Department of Neurophysiology and Pharmacology, Medical University of Vienna, Vienna, Austria
    • Karlheinz Hilber, Center for Physiology and Pharmacology, Department of Neurophysiology and Pharmacology, Medical University of Vienna, Schwarzspanierstrasse 17, 1090 Vienna, Austria. E-mail: karlheinz.hilber@meduniwien.ac.at

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ABSTRACT

Ibogaine, an alkaloid derived from the African shrub Tabernanthe iboga, has shown promising anti-addictive properties in animals. Anecdotal evidence suggests that ibogaine is also anti-addictive in humans. Thus, it alleviates drug craving and impedes relapse of drug use. Although not licensed as therapeutic drug, and despite evidence that ibogaine may disturb the rhythm of the heart, this alkaloid is currently used as an anti-addiction drug in alternative medicine. Here, we report that therapeutic concentrations of ibogaine reduce currents through human ether-a-go-go-related gene potassium channels. Thereby, we provide a mechanism by which ibogaine may generate life-threatening cardiac arrhythmias.

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