Ibogaine is a psychoactive indole alkaloid from the root bark of the Central African shrub Tabernanthe iboga. A single large dose is reported to sharply reduce opioid withdrawal and craving, and is being studied for trauma, depression and brain injury. It also carries a documented risk of fatal cardiac arrhythmia and is not an approved medicine in any major jurisdiction.
This page is a high-level, neutral summary written for people trying to understand ibogaine properly: patients and families weighing treatment, veterans and clinicians, researchers, journalists and policymakers. Every section links to a deeper article on this site, and all claims are numbered to the source list at the bottom of the page.
How it worksOpioid dependencePTSD & traumaCardiac riskLegality by countryTreatment costClinical trials
Safety notice
Ibogaine prolongs the cardiac QT interval and has been associated with fatal arrhythmias, including in people with no known heart disease. Deaths have most often occurred without cardiac screening, without continuous ECG monitoring, or in combination with opioids and other drugs. Ibogaine is not approved as a medicine in any major jurisdiction. Read the cardiac risk overview. This page is encyclopedic information, not medical advice. It does not recommend ibogaine use or any provider. Decisions about treatment should be made with a qualified physician who has reviewed your full medical history and current medications.
Ibogaine is a naturally occurring psychoactive indole alkaloid found in the root bark of the Central African plant Tabernanthe iboga, and in related species of the family Apocynaceae. It has been used for centuries in the Bwiti initiatory tradition of Gabon and Cameroon, and since the 1960s has been investigated in the West for its reported ability to interrupt substance use disorders, particularly opioid dependence. More recent work has examined its potential in post-traumatic stress disorder, traumatic brain injury, and depression.
Ibogaine is also one of the more dangerous compounds in the psychedelic class. It prolongs the cardiac QT interval, and dozens of deaths have been temporally associated with its use. It is a Schedule I controlled substance in the United States and is controlled in much of Europe, while remaining unregulated in Mexico, Costa Rica and other jurisdictions where most treatment centers operate (see ibogaine legality by country).
Overview
Ibogaine belongs to the iboga family of monoterpene indole alkaloids and is the principal psychoactive constituent of Tabernanthe iboga root bark. In traditional use the bark is chewed or taken as a powdered extract; in contemporary clinical and quasi-clinical settings it is almost always given as purified ibogaine hydrochloride in a single large oral dose, commonly called a flood dose. Though micro-dosing and low/escalating dosing strategies have emerged.
The standardized dosage range commonly used to facilitate a flood dose is between 15-22 mg/Kg of body weight. It should be noted that doses in excess of 12 mg/Kg have been reported to have higher instances of cardiac abnormalities, and should be considered higher risk. Dosing should never exceed 24 mg/Kg in a 24-hour period. Threshold effects appear at 50-100mg, and low-dose taper strategies have used dosages ranging from 100mg to 600mg.
What distinguishes ibogaine from other psychedelics is the claim attached to it: that one administration can compress the acute phase of opioid withdrawal from days into hours and suppress craving for weeks or months afterwards. That claim rests largely on observational studies, retrospective case series and clinic records rather than randomized controlled trials, and it sits alongside a real risk of cardiac death.
Since 2024 the picture has begun to change. A Stanford-led open-label study of magnesium-ibogaine in military veterans with traumatic brain injury was published in Nature Medicine, state legislatures have begun funding drug-development pathways, and several registered studies are now underway. Ibogaine nevertheless remains unapproved everywhere as a medicine, and the honest summary of the evidence is that the signal is unusually strong for an unapproved compound while the controlled-trial evidence needed to act on it does not yet exist.
More detail: What is ibogaine · Iboga vs ibogaine · Ibogaine uses · Reported benefits
Key Facts
What it is
Indole alkaloid from Tabernanthe iboga root bark
Primary studied use
Interrupting opioid withdrawal and craving
Emerging studied uses
PTSD, traumatic brain injury, depression, other substance use
Typical dose form
Oral ibogaine hydrochloride, single 'flood' dose
Acute duration
24–72 hours; days of recovery afterwards
Main active metabolite
Noribogaine (long half-life, via CYP2D6)
Principal risk
QT prolongation and fatal cardiac arrhythmia
Approval status
Not approved as a medicine in any major jurisdiction
Evidence base
Observational studies and case series; randomized trials still lacking
Typical clinic cost
Roughly US$6,000–30,000+, rarely insured
Botanical Source and Tradition
Tabernanthe iboga is a perennial rainforest shrub of the family Apocynaceae, native to Gabon, Cameroon and the Republic of the Congo. It grows to roughly 1.5–2 meters and bears small white or pinkish flowers and orange fruit. Alkaloid content is highest in the root bark, which contains ibogaine along with ibogamine, tabernanthine and related compounds.
In Gabon the plant is central to Bwiti, an initiatory religious tradition in which large quantities of root bark are taken during multi-day ceremonies marking entry into adulthood or community membership. Iboga is recognized by the Gabonese state as national patrimony, and rising international demand has raised both conservation concerns and unresolved questions about benefit sharing with the communities that developed its use.
Ibogaine also occurs in Voacanga africana and Tabernaemontana species, which are now the main commercial feedstock for semi-synthesis. Total synthesis and semi-synthetic routes reduce pressure on wild iboga populations and allow better control of purity, which matters because alkaloid content in raw bark varies widely and makes accurate dosing difficult.
More detail: The iboga plant · Gabon · Iboga seeds and cultivation · Traditional ceremonies
Chemistry and Pharmacology
Ibogaine (12-methoxyibogamine) has the molecular formula C₂₀H₂₆N₂O and a molar mass of 310.44 g/mol. It is a monoterpene indole alkaloid combining an indole moiety with an isoquinuclidine ring system, poorly soluble in water as the free base and usually handled as the hydrochloride salt for oral administration.
After oral dosing, ibogaine undergoes extensive first-pass hepatic metabolism by CYP2D6 to noribogaine (12-hydroxyibogamine), an active metabolite with a substantially longer half-life than the parent compound. Noribogaine is thought to account for much of the sustained post-session effect. CYP2D6 is highly polymorphic, so poor metabolizers can reach far higher ibogaine concentrations than expected from dose alone — a plausible contributor to unpredictable toxicity.
More detail: Ibogaine hydrochloride · Half-life and pharmacokinetics · Ibogaine effects
How Ibogaine Is Thought to Work
No single receptor explains ibogaine's effects. It is a promiscuous compound acting across several systems at once, and the leading hypotheses combine acute receptor pharmacology with slower changes in growth-factor signaling.
Opioid receptors — kappa agonism and weak mu-receptor activity, plausibly relevant to withdrawal suppression.
NMDA receptors — non-competitive antagonism at glutamatergic NMDA receptors, a mechanism shared with other rapid-acting antidepressants.
Serotonin system — serotonin transporter inhibition and 5-HT₂A modulation, associated with the visionary, dreamlike phase of the experience.
Sigma-2 receptors — high affinity binding implicated in both neuroprotective and neurotoxic effects.
Nicotinic acetylcholine receptors — antagonism relevant to reported effects on nicotine and stimulant use.
GDNF signaling — ibogaine increases glial cell line-derived neurotrophic factor in the ventral tegmental area, which in rodents reduces alcohol self-administration and is a leading candidate for its durable effects.
hERG potassium channels — blockade of the cardiac hERG channel, the mechanism behind QT prolongation and arrhythmia risk.
Why the effect may outlast the drug
Two explanations are usually offered for why benefits are reported weeks after a single dose: long-lasting noribogaine exposure, and drug-induced neuroplasticity that reopens a window in which behavior and habit are more modifiable. The latter is supported by animal work on GDNF and by research on non-hallucinogenic analogs, but has not been demonstrated directly in humans.
More detail: Mechanisms in detail · Effects on the brain · Anti-addictive properties
Opioid Dependence
Opioid dependence is the use case with the largest body of human data. Observational studies of clinic patients consistently report that objective and subjective withdrawal scores fall steeply within the first day after a flood dose, often to levels that would normally take a week or more of tapering to reach, and that craving remains reduced at follow-up in a substantial minority of participants.
A twelve-month follow-up of patients treated in New Zealand reported sustained reductions in opioid use for a subset of participants, with the largest gains in those who engaged with aftercare. A twelve-month United States and Mexico cohort reported similar patterns, with relapse concentrated in the first weeks after discharge. A Dutch open-label safety study confirmed the withdrawal effect while documenting QT prolongation in every participant.
The consistent caveat across this literature is that none of these studies were randomized or blinded, control groups were absent, participants were self-selected and highly motivated, and follow-up was frequently incomplete. Ibogaine is best described as a detoxification and craving-interruption intervention with promising uncontrolled data, not as an established treatment, and it is not a substitute for buprenorphine or methadone maintenance, which have decades of mortality-reduction evidence behind them.
More detail: Ibogaine for opioid addiction · Opioid withdrawal · Fentanyl dependence · Ibogaine vs methadone · Relapse prevention
Other Substance Use Disorders
Beyond opioids, ibogaine has been used and studied — with thinner evidence — for alcohol, stimulants including cocaine and methamphetamine, nicotine, and kratom dependence. A Brazilian retrospective study of patients treated in a supervised medical setting reported extended abstinence periods across several substance classes, with better outcomes after repeated sessions combined with psychotherapy.
Animal research supports a broad anti-addictive profile: ibogaine and its metabolites reduce self-administration of morphine, cocaine, alcohol and nicotine in rodents, and the alcohol effect appears to be mediated by GDNF in the ventral tegmental area. Whether these findings translate to durable human outcomes remains unresolved, and stimulant and alcohol use disorders lack even the observational depth available for opioids.
More detail: Alcohol use disorder · Stimulant addiction · Addiction treatment overview · Abstinence support
Trauma, PTSD and Brain Injury
The most rigorous ibogaine study published to date examined magnesium-ibogaine therapy in 30 US Special Operations Forces veterans with repeated blast exposure and traumatic brain injury. The study, run by Stanford researchers at a clinic in Mexico because of United States scheduling, reported large average improvements in disability, PTSD, depression and anxiety measures one month after a single dose, alongside improvements on cognitive testing. Magnesium was co-administered with the intent of reducing cardiac risk, and no serious cardiac adverse events were recorded.
The design limits how much weight the result can carry: it was open-label, with no control or placebo group, in a self-selected and highly motivated cohort that traveled abroad and expected benefit. An earlier survey of Special Operations veterans who had sought ibogaine and 5-MeO-DMT reported comparable self-rated improvements, with the same self-selection problem. Randomized, controlled work is the acknowledged next step, and several programs are now moving in that direction.
More detail: Ibogaine for PTSD · The Stanford study · Traumatic brain injury · Veterans and ibogaine · Magnesium protocol
Neuroplasticity and Neuroregeneration
A recurring hypothesis is that ibogaine's durable effects come less from the acute experience than from a period of heightened neuroplasticity afterwards. In rodents, ibogaine raises GDNF expression in dopaminergic midbrain regions, and blocking GDNF signaling abolishes its effect on alcohol intake — direct evidence that growth-factor signaling, not the psychedelic experience, carries at least part of the behavioral change.
This line of work produced tabernanthalog (TBG), an engineered iboga analog reported in Nature in 2021 to promote dendritic growth and reduce alcohol seeking and depression-like behavior in rodents without hallucinogenic or cardiotoxic effects. If non-hallucinogenic analogs hold up, they could separate the therapeutic mechanism from the two features that make ibogaine hard to deploy: a 24–72 hour incapacitating experience and cardiac risk. That work remains preclinical.
More detail: Neuroplasticity · Neuroregeneration · Brain effects of treatment · Alternatives and analogs
Risks, Cardiac Safety and Screening
Ibogaine blocks the cardiac hERG potassium channel, delaying ventricular repolarization and prolonging the QT interval. QT prolongation can progress to torsades de pointes, a polymorphic ventricular tachycardia that may be fatal. The effect is dose related, can persist for days because of noribogaine's long half-life, and is worsened by hypokalemia, hypomagnesemia, bradycardia, liver impairment and any co-administered QT-prolonging drug — a category that includes methadone, many antipsychotics, antidepressants and antibiotics.
A forensic review identified 19 deaths temporally associated with ibogaine between 1990 and 2008, most involving pre-existing cardiovascular disease or concurrent drug use.[1] Systematic reviews of adverse events reach similar conclusions: serious events are uncommon in screened, monitored settings and concentrate in unsupervised or poorly staffed ones. Commonly quoted fatality estimates of roughly 1 in 300 to 1 in 400 treatment episodes come from older subculture data and should be read as rough magnitude, not a precise rate.
Screening and monitoring considered essential before and during administration:
12-lead ECG with QTc measurement, and cardiology review where QTc is borderline or prolonged
Electrolyte panel with correction of potassium and magnesium before dosing
Liver function tests and a full metabolic panel
Medication reconciliation to exclude QT-prolonging and CYP2D6-interacting drugs
Opioid taper to a short-acting agent; methadone in particular is a common contraindication
Psychiatric assessment, excluding psychotic disorders and unstable mania
Continuous telemetry during the session and for at least 24 hours afterwards
On-site advanced cardiac life support, defibrillator and intravenous magnesium
Non-cardiac effects are near-universal and include nausea and vomiting, ataxia severe enough to prevent walking, tremor, and prolonged visual and auditory phenomena. Patients are typically incapacitated for the first day and fatigued for several days after. Post-session vulnerability also matters: reduced opioid tolerance after detoxification raises overdose risk sharply if a person returns to their previous dose.
More detail: Cardiac risk · Side effects · Medically supervised treatment · Administration protocols
Legal Status by Region
Ibogaine is not scheduled under the United Nations drug conventions, so national approaches differ sharply. Broadly, there are four categories: prohibited, prescription or medically regulated, unregulated, and uncertain or unaddressed in law.
RegionStatusNotesUnited StatesSchedule IIllegal outside approved research; state-funded research programs emergingCanadaUnapproved drugNot a controlled substance; access via special authorization onlyMexicoUnregulatedLargest concentration of treatment centers; no clinic licensing regime specific to ibogaineCosta RicaUnregulatedEstablished retreat and clinic sectorBrazilMedically regulatedUse permitted under medical supervision in defined settingsUnited KingdomControlledRestricted following review of psychoactive and cardiac riskFrance, Belgium, Sweden, DenmarkControlled substanceExplicit prohibitions adopted after adverse eventsNetherlands, GermanyUnapproved medicineNot explicitly scheduled; supply restricted via medicines lawSwitzerlandRestricted medical useLimited authorized use within research frameworksNew ZealandPrescription medicineLegal when prescribed and dispensed by qualified practitionersAustraliaProhibitedListed as a controlled substanceSouth AfricaRegulatedPermitted in defined medical and research contextsGabonLegal, culturally protectedIboga recognized as national patrimony; export restricted
Legal status changes frequently and enforcement varies within countries. In the United States, ibogaine has been Schedule I since 1970, and Texas appropriated funding in 2025 to support FDA drug development trials through a public-private partnership. Traveling abroad for treatment does not remove domestic legal exposure for importing or possessing ibogaine on return.
More detail: Legality by country · US legal status · Drug classification · Europe
Treatment Settings and What to Expect
Because of its legal status, most ibogaine administration happens in private clinics and retreats in Mexico, Costa Rica, the Bahamas, Thailand and parts of Africa and Europe. Standards vary enormously, from hospital-adjacent facilities with anesthesiologists and telemetry to unlicensed retreats with no medical staff at all. The Global Ibogaine Therapy Alliance published clinical guidelines intended to standardize screening, dosing and monitoring, but adherence is voluntary and unverified.
A typical medically supervised program runs roughly as follows:
Pre-arrival screening — medical history, ECG, bloodwork, medication review and a taper plan from long-acting opioids to a short-acting agent.
Arrival and stabilization, usually one to two days: repeat ECG, electrolyte correction, hydration, and a test dose in some protocols.
Dosing day — a single oral flood dose under continuous cardiac monitoring, with staff present throughout. Onset is one to three hours.
Acute phase, 4–8 hours: intense dreamlike visual and autobiographical imagery, nausea, and inability to walk unassisted.
Reflective phase, 8–24 hours: reduced imagery, sustained introspection, insomnia and continued monitoring.
Residual phase, 24–72 hours and beyond: fatigue, ataxia and sleep disruption that can persist for days to weeks.
Integration and aftercare — therapy, peer support and relapse-prevention planning, which observational data associate with markedly better outcomes.
Questions worth asking a provider
Who performs the pre-treatment ECG and who reads it? Is telemetry continuous and staffed overnight? Is a physician on site during and after dosing, and what emergency equipment is available? What is the protocol if QTc prolongs? How is the ibogaine sourced and assayed for purity? What aftercare is included, and what are the documented outcomes and adverse events for this facility?
More detail: Ibogaine treatment overview · What it feels like · Duration of effects · Evaluating treatment centers · How to get treatment safely
Cost and Access
Ibogaine treatment is a private, out-of-pocket expense. Published clinic pricing generally falls between about US$6,000 and US
Price is a weak proxy for quality. What tends to drive legitimate cost is medical staffing — an on-site physician, overnight nursing, telemetry and emergency equipment — along with program length and the depth of aftercare. Very low prices often indicate absent monitoring, while high prices do not guarantee it.
More detail: Treatment cost in detail · Ibogaine clinics · Where treatment is available · Psychedelic tourism risks
Current Research and Policy Momentum
The research landscape has shifted faster since 2023 than in the previous three decades. The Nature Medicine magnesium-ibogaine study gave the field its first high-profile prospective dataset in a serious clinical population; registered studies of ibogaine and noribogaine have expanded; and work on non-hallucinogenic analogs has attracted substantial pharmaceutical investment.
Policy has moved alongside the science, largely driven by veteran advocacy. Texas enacted legislation in 2025 establishing a funded consortium to pursue FDA-directed ibogaine trials, Arizona appropriated funds for ibogaine research into brain injury, and comparable proposals have appeared in other states (see Texas SB 2308, Arizona's research funding and the IBOGAINE Act).[2] Public advocacy from figures including Rick Perry, Bryan Hubbard, Joe Rogan and Conor McGregor has kept the issue visible, and sustained reporting in outlets including The New York Times has documented both the demand and the harm.
What is still missing is the thing that would settle the question: adequately powered randomized controlled trials with cardiac safety endpoints, standardized dosing and long-term follow-up. Until those exist, ibogaine remains a compound with a striking but unproven signal, a real fatality risk, and a treatment economy operating largely outside medical regulation.
More detail: Clinical trials · Current and planned research · Systematic reviews · Federal policy developments · Latest news
History
Iboga use in Central Africa predates European contact. French and Belgian explorers documented Bwiti practice in the 19th century, and ibogaine was isolated and named by Dybowski and Landrin in 1901. It was marketed in France from the 1930s as Lambarène, a stimulant tonic, and withdrawn in the 1960s.
Western interest in its anti-addictive properties began in 1962 when Howard Lotsof, then a young heroin user, took ibogaine recreationally and found his withdrawal symptoms absent. Lotsof filed patents for its use against opioid, cocaine, alcohol and nicotine dependence and spent three decades campaigning for research.
The US National Institute on Drug Abuse funded preclinical and early clinical work in the 1990s, including studies led by Deborah Mash, but withdrew support amid cardiotoxicity findings and trial-design difficulties. Research continued in the Netherlands, Brazil, New Zealand and Mexico, and a clinic sector grew up around the legal gaps. The 2020s brought renewed institutional attention, driven by veteran advocacy, the broader psychedelic research revival and the opioid overdose crisis.
More detail: Howard Lotsof · Bwiti tradition · Documentaries
Frequently Asked Questions
What is ibogaine?
Ibogaine is a naturally occurring psychoactive indole alkaloid found in the root bark of Tabernanthe iboga, a shrub native to Central Africa. It is studied primarily for its reported ability to interrupt opioid withdrawal and craving, and more recently for trauma-related conditions.
Is ibogaine legal?
Legal status varies by country. Ibogaine is a Schedule I controlled substance in the United States, a prescription medicine in New Zealand, controlled in several European countries, and unregulated in Mexico, Costa Rica and a number of other jurisdictions where most treatment centers operate.
Why is ibogaine considered dangerous?
Ibogaine prolongs the cardiac QT interval and can trigger life-threatening arrhythmias, including torsades de pointes. Deaths have been reported, most often in unmonitored settings or alongside pre-existing heart disease and other drugs. Pre-treatment cardiac screening and continuous ECG monitoring are considered essential.
Does ibogaine cure addiction?
No. Observational studies report large short-term reductions in withdrawal symptoms and craving, but ibogaine is not an approved medicine anywhere for addiction treatment, evidence from randomized controlled trials is lacking, and relapse after treatment is common without ongoing aftercare.
How long does an ibogaine session last?
A single flood dose produces acute effects lasting roughly 24 to 72 hours, with a lingering low-energy recovery phase of several days. Clinic programs typically run 5 to 10 days including screening, dosing and observation.
What does ibogaine treatment cost?
Published clinic pricing generally ranges from about US$6,000 to more than US$30,000 depending on country, medical staffing, program length and aftercare. Costs are almost never covered by insurance because the treatment is not approved.
Is ibogaine being studied in clinical trials?
Yes. Registered studies and state-funded research programs are active, including a 2024 Nature Medicine open-label study of magnesium-ibogaine in veterans with traumatic brain injury and a Texas-funded research consortium established in 2025.[3]
References
Numbered sources cited throughout this page, including peer-reviewed studies, clinical trial registries, government and regulatory material, institutional reports and reputable journalism.
Cherian KN, Keynan JN, Anker L, et al. “Magnesium–ibogaine therapy in veterans with traumatic brain injuries” Nature Medicine, 2024.
Stanford Medicine (Office of Communications) “Ibogaine paired with magnesium may treat traumatic brain injury in veterans” Stanford Medicine News Center, 2024.
Alper KR “Ibogaine: A review” The Alkaloids: Chemistry and Biology, Vol. 56, 2001.
Alper KR, Lotsof HS, Kaplan CD “The ibogaine medical subculture” Journal of Ethnopharmacology, 2008.
Mash DC, Duque L, Page B, Allen-Ferdinand K “Ibogaine detoxification transitions opioid and cocaine abuse into substance-free remission” Frontiers in Pharmacology, 2018.
Brown TK, Alper K “Treatment of opioid use disorder with ibogaine: detoxification and drug use outcomes” The American Journal of Drug and Alcohol Abuse, 2018.
Noller GE, Frampton CM, Yazar-Klosinski B “Ibogaine treatment outcomes for opioid dependence from a twelve-month follow-up observational study” The American Journal of Drug and Alcohol Abuse, 2018.
Knuijver T, Schellekens A, Belgers M, et al. “Safety of ibogaine administration in detoxification of opioid-dependent individuals: a descriptive open-label observational study” Addiction, 2022.[4]
Koenig X, Hilber K “The anti-addiction drug ibogaine and the heart: a delicate relation” Molecules, 2015.
Alper KR, Stajić M, Gill JR “Fatalities temporally associated with the ingestion of ibogaine” Journal of Forensic Sciences, 2012.
Litjens RPW, Brunt TM “How toxic is ibogaine?” Clinical Toxicology, 2016.
Cameron LP, Tombari RJ, Lu J, et al. “A non-hallucinogenic psychedelic analogue with therapeutic potential” Nature, 2021.
University of California, San Francisco “Ibogaine inspires new treatments for addiction and depression” UCSF News, 2023.
Glick SD, Maisonneuve IM “Mechanisms of antiaddictive actions of ibogaine” Annals of the New York Academy of Sciences, 1998.
He DY, McGough NNH, Ravindranathan A, et al. “Glial cell line-derived neurotrophic factor mediates the desirable actions of the anti-addiction drug ibogaine against alcohol consumption” The Journal of Neuroscience, 2005.
Maciulaitis R, Kontrimaviciute V, Bressolle FMM, Briedis V “Ibogaine, an anti-addictive drug: pharmacology and time to go further in development” Human & Experimental Toxicology, 2008.
Glue P, Lockhart M, Lam F, et al. “Ascending-dose study of noribogaine in healthy volunteers: pharmacokinetics, pharmacodynamics, safety, and tolerability” The Journal of Clinical Pharmacology, 2015.
Schenberg EE, de Castro Comis MA, Chaves BR, da Silveira DX “Treating drug dependence with the aid of ibogaine: a retrospective study” Journal of Psychopharmacology, 2014.[5]
Corkery JM “Ibogaine as a treatment for substance misuse: potential benefits and practical dangers” Progress in Brain Research, 2018.
Davis AK, Averill LA, Sepeda ND, Barsuglia JP, Amoroso T “Psychedelic treatment for trauma-related psychological and cognitive impairment among US Special Operations Forces veterans” Chronic Stress, 2020.
Barsuglia JP, Polanco M, Palmer R, et al. “A case report SPECT study and theoretical rationale for the sequential administration of ibogaine and 5-MeO-DMT in the treatment of alcohol use disorder” Progress in Brain Research, 2018.
Global Ibogaine Therapy Alliance (GITA) “Clinical Guidelines for Ibogaine-Assisted Detoxification” GITA, 2015.
U.S. Drug Enforcement Administration “Controlled Substances Act — Schedules of controlled substances” DEA Diversion Control Division, 2024.
U.S. National Library of Medicine “Registered clinical studies of ibogaine and noribogaine” ClinicalTrials.gov, 2026.
New Zealand Medicines and Medical Devices Safety Authority “Medicines classification: ibogaine as a prescription medicine” Medsafe (Ministry of Health, New Zealand), 2010.
Texas Legislature “Senate Bill 2308: consortium for ibogaine research and drug development trials” Texas Legislature Online, 89th Legislature, 2025.
European Union Drugs Agency (EUDA/EMCDDA) “Ibogaine drug profile” European Union Drugs Agency, 2024.
UC Berkeley Center for the Science of Psychedelics “Ibogaine: substance overview” BCSP, University of California, Berkeley, 2024.
Mash DC, Kovera CA, Pablo J, et al. “Ibogaine in the treatment of heroin withdrawal” The Alkaloids: Chemistry and Biology, Vol. 56, 2001.
Ona G, Rocha JM, Bouso JC, et al. “The adverse events of ibogaine in humans: an updated systematic review of the literature” Psychopharmacology, 2022.
Malcolm BJ, Polanco M, Barsuglia JP “Changes in withdrawal and craving scores in participants undergoing opioid detoxification utilizing ibogaine” Journal of Psychoactive Drugs, 2018.
Robert F. Worth “Reporting on veterans, trauma and the search for ibogaine treatment abroad” The New York Times Magazine, 2026.