Ibogaine: Compound Guide

Heart risk first. Ibogaine can delay the heart's electrical recovery (called QT prolongation) and has been linked to dangerous rhythms, cardiac arrest and deaths. A toxicology review counted 27 fatalities reported after ibogaine ingestion. [1] If someone has taken ibogaine and has fainting, chest pain, a racing or irregular heartbeat, seizures or trouble breathing, call 911 (US) or your local emergency number. In the US, Poison Help is 1-800-222-1222. See poisoning: what to do first. This page is information only. It gives no amounts, preparation steps or advice to take ibogaine.

Evidence labels used here: approved medicine (a regulator has approved it for a stated use), promising but limited, insufficient evidence, preclinical (cells or animals only), evidence of harm. Where we looked and found nothing usable, we write "Proper evidence not found."

What ibogaine is, and what it is not

Ibogaine is a single chemical, an indole alkaloid, found in the root bark of the West and Central African shrub Tabernanthe iboga (accepted name checked in GBIF). [1][2] Several things share the name "iboga" and are easy to confuse:

• The iboga plant. Its root bark holds several alkaloids, of which ibogaine is the best known. [3] See the plant profile: Iboga (Tabernanthe iboga).
• Ibogaine. The isolated compound. A Chacruna article describes ibogaine hydrochloride that is semi-synthesized from another plant, Voacanga africana, rather than taken from iboga. [4]
• Noribogaine. The main product the body makes from ibogaine, mostly through the CYP2D6 enzyme. It stays in the body for days, long after ibogaine itself is cleared. [1]
• Bwiti. A religious tradition of Gabon, Equatorial Guinea and southern Cameroon that uses iboga. [3] The compound is not the tradition. See Iboga and Bwiti traditions.

NIDA places ibogaine among drugs that work differently from classic psychedelics such as psilocybin and LSD, noting that it affects a variety of brain receptors. [5] A review describes micromolar affinity for NMDA, kappa and mu opioid, and sigma-2 receptor sites, plus interactions with serotonin and dopamine systems, so its profile is broader than the serotonin 5-HT2A pattern NIDA describes for classic psychedelics. [1][5]

Regulatory status (not legal advice; laws change)

• United States, federal: ibogaine is named in the Schedule I list in 21 CFR 1308.11 (read 2026-10-22). [6]
• United Kingdom: a poisons-service case series states that ibogaine is not licensed there. [7] We did not find ibogaine named in Schedule 2 of the Misuse of Drugs Act 1971 (read 2026-10-22); other UK controls were not checked. [8]
• Other countries and US states: not verified. See legal status by country.
• Approved medicine: we found no regulator approval of ibogaine for any use in the sources we read.

What research shows

• Opioid use disorder: insufficient evidence. A 2026 review of 24 studies and 38 case reports found that most positive efficacy data came from uncontrolled, open-label or retrospective studies with high risk of bias, and that no double-blind randomized trial has shown ibogaine or noribogaine treats opioid use disorder. [9] Observational reports of 44 people in two treatment studies describe intense experiences; they do not prove benefit. [10]
• Cocaine use disorder: insufficient evidence. The same review found one small randomized trial with significant effects. [9]
• Veterans with brain injury: insufficient evidence. An observational open-label study (MISTIC) treated 30 male special operations veterans with ibogaine together with magnesium and other treatments. Disability, PTSD, depression and anxiety scores improved at one month and no unexpected or serious adverse events occurred. There was no control group, and the authors say controlled trials are needed. Two authors report a patent application related to the protocol. [11]
• Neurotoxicity: preclinical. Rat studies showed damage to cerebellar cells at higher doses; relevance to people is unclear. [1]

Risks and who is most vulnerable

• Cardiac. Blocking the heart's hERG potassium channels delays repolarization, which can lead to QT prolongation, arrhythmia and sudden cardiac arrest. Eight case reports suggested ibogaine itself caused ventricular tachyarrhythmias. [1] One case describes a 61-year-old man whose QT interval took 7 days to return to normal because ibogaine clears slowly. [12]
• Poison-service data. Over ten years the UK National Poisons Information Service logged seven patients; all had symptoms and six showed heart toxicity, including cardiac arrest and torsades de pointes. [7]
• Deaths. A forensic review of 19 deaths found advanced existing illness, mostly cardiovascular, or other substances contributed in 12 of 14 cases with enough data. It also named seizures linked to alcohol or benzodiazepine withdrawal and uninformed use of plant-based forms. [13]
• Medicines. Differences in CYP2D6 can change ibogaine levels, which matters with medicines that use the same enzyme. [1] See how interactions work. Do not stop or change any medicine without the prescriber.
• Setting. A systematic review of 12 clinical sources concluded that trained staff and equipment for medical, psychiatric and cardiac monitoring are essential for safety. [14]
• Pregnancy, children, older adults: Proper evidence not found (we checked the toxicology and clinical reviews above).

Quality and labeling

Plant-based forms vary in what they contain, and reviewers flag uninformed use of them as a risk. [13] We found no regulator-published testing of ibogaine products, so purity or strength claims are a marketing claim.

Where to get support

If you are struggling with substance use, talk with a licensed clinician: substance use support and urgent help. In the US, the 988 Suicide & Crisis Lifeline is available in a mental health crisis. For the cultural and conservation side, see Indigenous traditions, ethics and conservation.