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Ibogaine is a naturally occurring indole alkaloid derived from the root bark of the West African rainforest shrub Tabernanthe iboga, used traditionally in Bwiti spiritual ceremonies and studied since the 1960s for a striking property: a single large dose can interrupt opioid withdrawal and reduce drug craving for extended periods. It is a genuine polypharmacological agent, engaging NMDA glutamate receptors, kappa- and mu-opioid receptors, sigma-2 sites, the serotonin transporter, and alpha3beta4 nicotinic receptors simultaneously, and it is metabolized by CYP2D6 to the long-lived active metabolite noribogaine that is thought to mediate much of its anti-addictive action. A prominent hypothesis is that ibogaine and noribogaine upregulate glial cell line-derived neurotrophic factor (GDNF) in the midbrain, resetting reward circuitry after chronic drug exposure. These effects are counterbalanced by a serious cardiac liability: ibogaine blocks the hERG potassium channel, prolongs the QT interval, and has been associated with fatal ventricular arrhythmias. It is not an approved medicine and remains investigational.
- A single dose can interrupt opioid withdrawal and reduce craving
- Long-lived metabolite noribogaine extends the anti-addictive effect for days
- Acts across NMDA, opioid, nicotinic, and serotonin systems at once
- Putative upregulation of GDNF may help reset reward circuitry
- QT prolongation and risk of fatal ventricular arrhythmia
- Reported fatalities, especially with cardiac or drug comorbidities
- Cerebellar ataxia and tremor at high doses
- Prolonged nausea, vomiting, and psychoactive effects
- CYP2D6 inhibition causing hazardous drug interactions
Mechanism
Ibogaine is best understood not through a single dominant target but as a multi-receptor modulator whose anti-addictive effects likely arise from synergy across several systems. It shows micromolar affinity for N-methyl-D-aspartate () receptors, kappa- and mu-opioid receptors, and sigma-2 binding sites, and it interacts with serotonergic, dopaminergic, and cholinergic signaling, acting as a transporter inhibitor and as an at alpha3beta4 receptors. In animal models it decreases self-administration of opioids, cocaine, nicotine, and alcohol, reduces the locomotor-stimulant effect of morphine, and lowers extracellular in the nucleus accumbens and striatum. A leading mechanistic account holds that ibogaine and its glial cell line-derived neurotrophic factor (GDNF) in the ventral tegmental area, activating a self-reinforcing neurotrophic pathway that durably dampens the motivation to consume drugs of abuse; ibogaine also alters expression of substance P, brain-derived neurotrophic factor, c-fos, and egr-1.
Ibogaine is rapidly metabolized in the body, principally by the cytochrome P450 enzyme CYP2D6, to noribogaine (10-hydroxyibogamine), which persists at clinically relevant concentrations for days after the parent drug has cleared and shows high brain uptake. Because a single ibogaine dose can produce prolonged effects on drug intake even though ibogaine itself is eliminated within hours, noribogaine is thought to mediate much of the sustained anti-withdrawal and anti-craving activity; oral noribogaine dose-dependently blocks naloxone-precipitated opioid withdrawal and reduces nicotine self-administration in rodents without producing conditioned place preference. Clinically, the large interindividual variability in CYP2D6 activity strongly influences ibogaine exposure and cardiac risk. The central safety concern is cardiotoxicity: ibogaine blocks hERG (ether-a-go-go-related gene) potassium channels that govern cardiac repolarization, delaying repolarization and prolonging the QT interval, which can progress to Torsades de Pointes, ventricular arrhythmia, and sudden cardiac arrest. These risks have driven efforts to develop safer analogues such as oxa-iboga compounds that retain efficacy in opioid-use-disorder models while avoiding the proarrhythmic liability in human cardiomyocytes.
receptor fingerprint
hERG potassium channelblocker
antagonist
Kappa-opioid receptoragonist
transporter (SERT)inhibitor
Alpha3beta4 receptorantagonist
Safetyrisks and cautions, not medical advice
Ibogaine carries a narrow therapeutic margin and a well-documented risk of serious harm, and it should never be taken outside rigorous medical supervision. Its central danger is cardiac: by blocking hERG potassium channels it prolongs the QT interval and can trigger potentially fatal ventricular arrhythmias including Torsades de Pointes, and these events have occurred at therapeutic doses in people without known pre-existing heart disease. Dozens of fatalities have been reported following ibogaine ingestion, frequently in the presence of cardiovascular or substance-use comorbidities or interacting medications, and CYP2D6 metabolizer status can markedly raise exposure in some individuals.
High doses can also produce cerebellar ataxia, tremor, prolonged psychoactive effects, nausea and vomiting, and, in animal studies, cerebellar neurodegeneration. Because it inhibits CYP2D6, ibogaine is prone to dangerous drug interactions, and combining it with opioids or other QT-prolonging agents is especially hazardous. It is not an approved therapy; any legitimate use requires cardiac screening, continuous monitoring, and emergency resuscitation capability. Not medical advice.
Subjective profileweighing the evidence above
Remarkable and dangerous in the same breath. A single dose really can interrupt opioid withdrawal for days, and it also prolongs the QT interval and has killed people at therapeutic doses with no known heart disease. Only defensible with cardiac monitoring under supervision; never at home, never alone.
Resources
This entry is here for reference.
Research
- 1996first citedIbogaine-like effects of noribogaine in rats
- 2026most recentFrom monotherapy to sequential models: An updated scoping review on ibogaine's role in treatmen…
- 1.How toxic is ibogaine?
- 2.The pharmacokinetics and pharmacodynamics of ibogaine in opioid use disorder patients
- 3.Main targets of ibogaine and noribogaine associated with its putative anti-addictive effects: A mechanistic overview
- 4.Oxa-Iboga alkaloids lack cardiac risk and disrupt opioid use in animal models
- 5.Ibogaine, an anti-addictive drug: pharmacology and time to go further in development. A narrative review
- 6.Noribogaine, but not 18-MC, exhibits similar actions as ibogaine on GDNF expression and ethanol self-administration
- 7.Ibogaine-like effects of noribogaine in rats
- 8.Noribogaine reduces nicotine self-administration in rats
- 9.Oral noribogaine shows high brain uptake and anti-withdrawal effects not associated with place preference in rodents
- 10.Medication development of ibogaine as a pharmacotherapy for drug dependence
- 11.Rare but relevant: Ibogaine and cardiovascular complications-prolonged QT interval and ventricular arrhythmias
- 12.From monotherapy to sequential models: An updated scoping review on ibogaine's role in treatment for psychiatric disorders
12 listed here; entry last updated August 2026
Reviews
My notesprivate to this device
FAQ
Why is ibogaine considered dangerous?
It blocks the heart's hERG potassium channel, prolonging the QT interval and creating a real risk of fatal ventricular arrhythmias such as Torsades de Pointes. These events have happened at therapeutic doses even in people with no known heart disease, and dozens of deaths have been reported. This is why any use demands cardiac screening and continuous monitoring.
What is noribogaine?
Noribogaine is the main metabolite produced when the liver enzyme CYP2D6 processes ibogaine. It lingers in the body for days, penetrates the brain well, and is believed to mediate much of ibogaine's sustained anti-withdrawal and anti-craving activity long after the parent drug is gone.
Is ibogaine an approved treatment for addiction?
No. Despite promising signals in observational reports and small studies, ibogaine is not an approved medicine anywhere in mainstream medical practice. Its narrow safety margin and cardiac toxicity mean researchers are also developing safer analogues, such as oxa-iboga compounds, that aim to keep the benefit without the arrhythmia risk.
Adverse effects
- QT prolongation and risk of fatal ventricular arrhythmia
- Reported fatalities, especially with cardiac or drug comorbidities
- Cerebellar ataxia and tremor at high doses
- Prolonged nausea, vomiting, and psychoactive effects
- CYP2D6 inhibition causing hazardous drug interactions