Ibogaine
Ibogaine is a naturally occurring indole alkaloid from the West African shrub Tabernanthe iboga. It is an atypical, long-acting psychoactive with anti-addiction properties: observational and open-label studies report it can interrupt opioid withdrawal and reduce craving. It is also cardiotoxic, causing QT-interval prolongation and dangerous arrhythmias, and has been associated with multiple deaths.
01 Overview
Ibogaine has been investigated primarily for opioid and other substance-use disorders. Open-label studies and observational series report meaningful reductions in withdrawal severity and drug craving, sometimes after a single administration, and its main metabolite noribogaine is long-lived and pharmacologically active. This anti-addiction signal, along with associated psychedelic and oneirogenic (dream-like) effects lasting many hours, has driven ongoing research interest.
The central safety problem is cardiac. Ibogaine blocks the hERG potassium channel and prolongs the QT interval, which can trigger torsades de pointes and sudden cardiac death. Real deaths have been documented, frequently in unmonitored settings and often involving pre-existing cardiac risk, electrolyte disturbances, or concomitant drugs. This cardiac risk must be stated plainly: ibogaine can cause fatal arrhythmias. It is Schedule I in the United States, while a few countries permit supervised clinical or therapeutic use.
02 Mechanism
Complex, non-selective pharmacology: NMDA receptor antagonism, kappa- and mu-opioid receptor activity, serotonin transporter and nicotinic receptor interactions, and hERG potassium channel blockade (the basis of its QT prolongation). Its metabolite noribogaine contributes long-lasting effects.
03 Dosing
| Tier | Dose | Route | Notes |
|---|---|---|---|
| Threshold (stimulant-like) | 1–3 mg | Oral | Low mg/kg doses produce mild stimulant effects; far below flood-dose protocols. |
| Therapeutic (anti-addiction) | 10–20 mg | Oral | Weight-based anti-addiction protocols use roughly 10-20 mg/kg under cardiac monitoring; total doses reach the low grams. Not a self-administration setting. |
04 Effects
| Effect | Magnitude | Evidence | |
|---|---|---|---|
| Interruption of opioid withdrawal / craving reductionObservational and open-label studies report rapid reduction of opioid withdrawal and craving, sometimes after one administration. | Marked in open-label series | Observational | |
| Oneirogenic / psychedelic experienceDream-like waking visions and introspective states lasting many hours. | Prolonged, hours | Observational |
05 Side effects
| Effect | Severity | Frequency | Evidence | Countermeasures |
|---|---|---|---|---|
| Nausea and vomitingNausea and vomiting are frequently reported, adding aspiration and electrolyte-loss risk. | Mild | Common | Observational | |
| Ataxia and prolonged neurological effectsMarked ataxia, tremor, and impaired coordination during the long duration of effect. | Moderate | Very common | Observational | |
| QT prolongation and fatal arrhythmiaIbogaine reliably prolongs the QT interval and can cause torsades de pointes and sudden cardiac death. Multiple fatalities have been reported, especially without cardiac monitoring. | Life-threatening | QT prolongation common; deaths documented | Clinical |