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Anti-addiction drug ibogaine inhibits voltage-gated ionic currents: a study to assess the drug's cardiac ion channel profile.

Xaver Koenig, Michael Kovar, Lena Rubi, Ágnes K. Mike, Péter Lukács, Vaibhavkumar S Gawali, Hannes Todt, Karlheinz Hilber, Walter Sandtner

Toxicology and Applied Pharmacology December 1, 2013 DOI: 10.1016/j.taap.2013.05.012 (opens in new tab)

Study at a glance

AI-extracted from the abstract
Characteristics Experimental study Peer reviewed
Population Heterologously expressed human ion channels and guinea pig cardiomyocytes
Interventions Ibogaine 18-Methoxycoronaridine (18-MC)
Dose low micromolar concentrations, ≥ 10 μM
Topics Ibogaine Addiction
Keywords 18-mc 18-methoxycoronaridine Ap Anti-addiction drug Qt interval prolongation Voltage-gated ion channels Action potential Herg potassium channels Human ether-à-go-go-related gene Ibogaine pharmacology Cardiac ion channels Cardiac electrophysiology
Citations 46
Key findings Ibogaine inhibits hERG potassium channels at low micromolar concentrations and, at higher concentrations, also reduces sodium and calcium currents, with 18-MC showing diminished potency; despite hERG blockade, ibogaine did not prolong action potentials in guinea pig cardiomyocytes at low concentrations, but computer modeling suggests it may prolong the QT interval in humans.

Abstract

The plant alkaloid ibogaine has promising anti-addictive properties. Albeit not licensed as a therapeutic drug, and despite hints that ibogaine may perturb the heart rhythm, this alkaloid is used to treat drug addicts. We have recently reported that ibogaine inhibits human ERG (hERG) potassium channels at concentrations similar to the drugs affinity for several of its known brain targets. Thereby the drug may disturb the heart's electrophysiology. Here, to assess the drug's cardiac ion channel profile in more detail, we studied the effects of ibogaine and its congener 18-Methoxycoronaridine (18-MC) on various cardiac voltage-gated ion channels. We confirmed that heterologously expressed hERG currents are reduced by ibogaine in low micromolar concentrations. Moreover, at higher concentrations, the drug also reduced human Nav1.5 sodium and Cav1.2 calcium currents. Ion currents were as well reduced by 18-MC, yet with diminished potency. Unexpectedly, although blocking hERG channels, ibogaine did not prolong the action potential (AP) in guinea pig cardiomyocytes at low micromolar concentrations. Higher concentrations (≥ 10 μM) even shortened the AP. These findings can be explained by the drug's calcium channel inhibition, which counteracts the AP-prolonging effect generated by hERG blockade. Implementation of ibogaine's inhibitory effects on human ion channels in a computer model of a ventricular cardiomyocyte, on the other hand, suggested that ibogaine does prolong the AP in the human heart. We conclude that therapeutic concentrations of ibogaine have the propensity to prolong the QT interval of the electrocardiogram in humans. In some cases this may lead to cardiac arrhythmias.

Comparable studies

Other experimental studies on ibogaine for addiction, most cited first.

Study Year Design Participants
Noribogaine is a G-protein biased κ-opioid receptor agonist. 2015 Experimental study with binding experiments, functional assays, and computational simulations
Anti-addiction drug ibogaine inhibits hERG channels: a cardiac arrhythmia risk. Human cells 2014 Experimental study
Deconstructing the Iboga Alkaloid Skeleton: Potentiation of FGF2-induced Glial Cell Line-Derived Neurotrophic Factor Release by a Novel Compound. C6 glioma cells 2016 Laboratory study
Ibogaine signals addiction genes and methamphetamine alteration of long-term potentiation. Rat brain models 2002 Review with experimental data
Anti-addiction Drug Ibogaine Prolongs the Action Potential in Human Induced Pluripotent Stem Cell-Derived Cardiomyocytes. Human ventricular-like cardiomyocytes derived from induced pluripotent stem cells 2017 Experimental study

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