Anti-addiction drug ibogaine inhibits hERG channels: a cardiac arrhythmia risk.
Xaver Koenig, Michael Kovar, Stefan Boehm, Walter Sandtner, Karlheinz Hilber
Addiction Biology March 1, 2014 DOI: 10.1111/j.1369-1600.2012.00447.x (opens in new tab)
Study at a glance
AI-extracted from the abstract| Characteristics | Experimental study Peer reviewed |
|---|---|
| Population | Human cells |
| Intervention | Ibogaine |
| Dose | therapeutic concentrations |
| Topics | Ibogaine Addiction |
| Keywords | Anti-addiction drug Qt interval prolongation Herg potassium channels Indole alkaloid Ibogaine safety: ibogaine Safety profile Substance Cardiotoxicity: cardiac risk Life-threatening cardiac arrhythmias |
| Citations | 50 |
| Key findings | Therapeutic concentrations of ibogaine reduce currents through human ether-a-go-go-related gene potassium channels, providing a mechanism for potential life-threatening cardiac arrhythmias. |
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.