Ibogaine

Use and effects

Ibogaine is derived from the root of Tabernanthe iboga, a plant known to exhibit hallucinogenic effects in people who consume it. It is described as having a typical dose range of 1,000 to 1,500mg orally, with these doses producing hallucinogenic effects, and a duration of 18 to 36hours. However, lower doses like 200 to 400mg orally are also active. In addition, very low doses of ibogaine like 8 to 30mg orally have been used and reported to produce stimulant effects. The onset of the drug is 1 to 3hours and peak effects have been described as being reached after 2hours. With full hallucinogenic doses, ibogaine is described as having three different phases of effects. The first phase is the acute or visionary phase, which onsets after 1 to 3hours and has a duration of 4 to 8hours; the second phase is the evaluative or introspective phase, which starts after 4 to 8hours and has a duration of 8 to 20hours; and the third phase is residual stimulation, which onsets after 12 to 24hours and has a duration of 24 to 72hours or longer. Each of these phases is described as having distinct qualitative effects.

The visionary phase is a dream-like, conscious state called oneirophrenia. Visual effects are almost always present and are often described as films or slideshows. These may be accompanied by increases in long-term recall of visual memory, resulting in autobiographical content. Other changes to sensation and perception may occur, including auditory hallucinations or distortions. Nausea and vomiting can be severe. Subjects may experience extreme confusion and/or a depressed mood. The visionary stage typically lasts 4–8 hours, but may last longer with especially high doses.

The introspective is poorly defined, often simply as 24 or 36 hours post-treatment. Sensation and perception return to normal, but nausea, headaches, and other side effects linger. Insomnia, irritability, and mood changes are often seen, including depression and sometimes mania. Depression can persist well after 36 hours, known as a "grey day"; the effect is well-recognized. A persistently low mood can progress into major depressive disorder, a chronic condition. For the treatment of opioid or alcohol addiction, the subjective experiences do not appear to be important, although they are correlated to some secondary measures (e.g. satisfaction in self-assessments).

Adverse effects

Immediate adverse effects of ibogaine ingestion may include nausea, vomiting, tremors leading to ataxia, headaches, and mental confusion. Ibogaine should not be used during pregnancy or breastfeeding.

Ibogaine has potential for adverse interactions with other psychedelic agents and prescription drugs. especially if consumed with opioids or in people with comorbidities such as cardiovascular disease or neurological disorders.

Neurotoxicity

Laboratory studies in rats indicate that ibogaine at high doses may cause degeneration of Purkinje cells in the cerebellum. This also occurred with the related drug harmaline. However, subsequent research found no evidence of this neurotoxicity with ibogaine in a primate. In limited human research, neuropathological examination revealed no evidence of neuronal degenerative changes in an adult female patient who had received four separate doses of ibogaine ranging between 10 and 30 mg/kg over a 15-month interval. A published series of fatalities associated with ibogaine ingestion also found no evidence for consistent neurotoxicity.

Interactions

Ibogaine may interact with monoamine oxidase inhibitors (MAOIs), for instance due to its serotonin reuptake inhibition.

Pharmacology

Pharmacodynamics

Ibogaine affects many different neurotransmitter systems simultaneously and hence has complex pharmacology. The specific targets mediating the effects of ibogaine are not fully clear. The drug is a cyclized derivative of serotonin, and hence may be expected to have serotonergic actions, but shows relatively low affinity for serotonin receptors. In any case, it appears that the serotonin 5-HT2A, 5-HT2C, sigma σ2, and μ- and/or κ-opioid receptors may be involved in the subjective effects of ibogaine based on animal studies. Conversely, the NMDA, serotonin 5-HT1A and 5-HT3, and sigma σ1 receptors do not appear to be involved.

Ibogaine's major active metabolite noribogaine has similar discriminative stimulus properties as ibogaine in rodent drug discrimination tests, but only partially substitutes for ibogaine. It appears that the stimulus properties of ibogaine may be primarily mediated by noribogaine. Noribogaine is most potent as a serotonin reuptake inhibitor. It acts as a moderate κ-opioid receptor agonist and weak μ-opioid receptor agonist or weak partial agonist. It is possible that the action of ibogaine at the κ-opioid receptor may indeed contribute significantly to the psychoactive effects attributed to ibogaine ingestion; Salvia divinorum, another plant recognized for its strong hallucinogenic properties, contains the chemical salvinorin A, which is a highly selective κ-opioid agonist. Noribogaine is more potent than ibogaine in rat drug discrimination assays when tested for the subjective effects of ibogaine.

There has been uncertainty about which biological target interactions mediate the psychoactive and other effects of ibogaine. Rodent drug discrimination studies with ibogaine have been employed to help elucidate these interactions. Ibogaine partially substitutes for the serotonergic psychedelics LSD and DOM and this can be blocked by the serotonin 5-HT2 receptor antagonist pizotifen. Similarly, LSD and DOM partially substitute for ibogaine and this can be blocked by the serotonin 5-HT2A receptor antagonist pirenperone. The serotonin releasing agent and potent serotonin 5-HT2 receptor agonist fenfluramine also partially substitutes for ibogaine. The preferential serotonin 5-HT2C receptor agonists MK-212 and mCPP partially substitute for ibogaine as well and this can be blocked by the serotonin 5-HT2 receptor antagonist metergoline. The preceding findings suggest that serotonin 5-HT2A and 5-HT2C receptor activation are involved in the subjective effects of ibogaine. Conversely, the serotonin 5-HT1A and 5-HT3 receptors do not appear to be involved.

Although serotonin 5-HT2A receptor signaling appears to be involved in the effects of ibogaine, neither ibogaine nor its major active metabolite noribogaine appear to act as direct serotonin 5-HT2A receptor agonists. In addition, in contrast to the findings in drug discrimination studies, ibogaine fails to produce the head-twitch response, a behavioral proxy of psychedelic effects, in rodents. As such, it has been said that ibogaine does not appear to be acting primarily or exclusively as a serotonergic psychedelic and that its hallucinogenic effects cannot be ascribed to serotonin 5-HT2A receptor activation. In any case, ibogaine has still been found to have significant in-vivo occupancy of the serotonin 5-HT2A receptor, suggesting that it is still a ligand of the receptor.

The β-carbolines or harmala alkaloids bear a close resemblance to ibogaine both in terms of chemical structure and subjective effects. Relatedly, harmaline and 6-methoxyharmalan fully substitute for ibogaine in drug discrimination tests, whereas harmine, harmane, harmalol, and tryptoline partially substitute for ibogaine. As with the case of ibogaine, the psychedelic DOM partially substitutes for harmaline and this further supports a role of serotonin 5-HT2A receptor activation in the effects of ibogaine as well as of harmala alkaloids. However, like ibogaine, harmala alkaloids like harmaline bound to the serotonin 5-HT2A receptor but failed to act as direct agonists of the receptor even at very high concentrations in vitro. In addition, whereas ibogaine and noribogaine bind to κ-opioid receptors, harmala alkaloids like harmine and harmaline show no affinity for these receptors.

Ibogaine's hallucinogenic effects not being mediated by serotonin 5-HT2A receptor activation has been said to be in accordance with its hallucinogenic effects in humans being qualitatively distinct from and unlike those of serotonergic psychedelics but instead similar to those of harmala alkaloids. It is also in accordance with the fact that unlike serotonergic psychedelics like LSD, neither ibogaine nor harmala alkaloids cause pupil dilation or increase blood pressure in humans. Conversely, unlike serotonergic psychedelics, ibogaine and harmaline are said to cause balance disturbances and vomiting to a greater extent than any other psychoactive drug besides alcohol.

Ibogaine shows appreciable affinity for the NMDA receptor. However, the NMDA receptor antagonists phencyclidine (PCP) and dizocilpine (MK-801) fail to substitute for ibogaine and ibogaine fails to substitute for these NMDA receptor antagonists in rodents and/or monkeys. Hence, NMDA receptor antagonism does not appear to be involved in the subjective effects of ibogaine. Neither μ-opioid receptor agonists nor κ-opioid receptor agonists like U-50,488 substitute for ibogaine. In addition, the opioid antagonist naloxone did not substitute for ibogaine. However, naltrexone partially substitutes for ibogaine. In addition, the mixed opioid agonists and antagonists pentazocine, diprenorphine, and nalorphine partially substituted for ibogaine and this could be antagonized by naloxone. The preceding findings suggest a role of opioid receptors but not the NMDA receptor in the effects of ibogaine.

The non-selective sigma receptor agonists DTG and (+)-3-PPP partially substitute for ibogaine, whereas the σ1 receptor-selective agonists (+)-SKF-10,047 and (+)-pentazocine failed to substitute for ibogaine. These findings suggest a role of σ2 receptor signaling in the effects of ibogaine.

Induction of gamma oscillations with a profile that resembles that of REM sleep may be involved in the hallucinogenic and oneirogenic effects of ibogaine.

Noribogaine, but not ibogaine, produces psychoplastogenic effects in vitro in preclinical research. This can be blocked by the serotonin 5-HT2A receptor antagonist ketanserin, by the mTOR inhibitor rapamycin, and by a TrkB antagonist.

Pharmacokinetics

Ibogaine is metabolized in the human body by cytochrome P450 2D6 (CYP2D6) into noribogaine (more correctly, O-desmethylibogaine or 12-hydroxyibogamine). Both ibogaine and noribogaine have a plasma half-life around 2hours in rats, although the half-life of noribogaine is slightly longer than that of the parent compound. In humans, the elimination half-life of ibogaine is about 7hours whereas the half-life of noribogaine is 24 to 50hours. Ibogaine may be deposited in fat and metabolized into noribogaine as it is released. After ibogaine ingestion in humans, noribogaine shows higher plasma levels than ibogaine and is detected for a longer period of time than ibogaine.

Chemistry

Ibogaine is a substituted tryptamine. It has two separate chiral centers, meaning that four different stereoisomers of ibogaine exist, which are difficult to resolve.

Synthesis

The chemical synthesis of ibogaine has been described.

One recent total synthesis of ibogaine and related drugs starts with 2-iodo-4-methoxyaniline which is reacted with triethyl((4-(triethylsilyl)but-3-yn-1-yl)oxy)silane using palladium acetate in DMF to form 2-(triethylsilyl)-3-(2-((triethylsilyl)oxy)ethyl)-1H-indole. This is converted using N-iodosuccinamide and then fluoride to form 2-(2-iodo-1H-indol-3-yl)ethanol. This is treated with iodine, triphenyl phosphine, and imidazole to form 2-iodo-3-(2-iodoethyl)-1H-indole. Then, using 7-ethyl-2-azabicyclo[2.2.2]oct-5-ene and cesium carbonate in acetonitrile, the ibogaine precursor 7-ethyl-2-(2-(2-iodo-1H-indol-3-yl)ethyl)-2-azabicyclo[2.2.2]oct-5-ene is obtained. Using palladium acetate in DMF, the ibogaine is obtained. If the exo ethyl group on the 2-azabicyclo[2.2.2]octane system in ibogaine is replaced with an endo ethyl, then epiibogaine is formed.

Crystalline ibogaine hydrochloride is typically produced by semisynthesis from voacangine in commercial laboratories. It can be prepared from voacangine through one-step demethoxycarbonylation process too.

In 2025, researchers at the University of California, Davis Institute for Psychedelics and Neurotherapeutics reported the total synthesis of ibogaine, ibogaine analogues, and related compounds from pyridine.

Analogues and derivatives

Analogues of ibogaine include noribogaine, ibogamine, ibogaline, tabernanthine, voacangine, coronaridine, oxa-noribogaine, and pinoline, among others.

A synthetic derivative of ibogaine, 18-methoxycoronaridine (18-MC), is a selective α3β4 antagonist that was developed collaboratively by neurologist Stanley D. Glick (Albany) and chemist Martin E. Kuehne (Vermont). This discovery was stimulated by earlier studies on other naturally occurring analogues of ibogaine, such as coronaridine and voacangine, that showed these compounds to have anti-addictive properties.

More recently, non- and less-hallucinogenic analogues, tabernanthalog and ibogainalog, were engineered by scientists attempting to produce non-cardiotoxic ibogaine derivatives by removing the lipophilic isoquinuclidine ring. In animal models, both molecules failed to produce cardiac arrhythmias, and tabernanthalog failed to produce any head twitch response, suggesting psychedelic effects were absent. Other deconstructed analogues of ibogaine, such as 5-MeO-IsoqT, have also been developed and studied.

Biosynthesis

Ibogaine biosynthesis begins with tryptophan undergoing enzymatic decarboxylation by tryptophan decarboxylase (TDC) to form a tryptamine. Secologanin, an iridoid synthesized from isopentenyl pyrophosphate (IPP) and dimethylallyl pyrophosphate (DMAPP), is reacted with tryptamine to make strictosidine. A glycosidic bond cleavage of strictosidine by strictosidine β-deglucosidase (SGD) produces a lactol. The lactol opens and produces an aldehyde, then condenses to form an iminium. Through isomerization and reduction by geissoschizine synthase 1 (GS1), 19E-geissoschizine is yielded. The indole is oxidized and the molecule undergoes intramolecular Mannich reaction and Grob fragmentation to form preakuammicine. Preakuammicine is highly unstable and therefore reduced to stemmadenine by oxidation-reduction reactions (REDOX 1 and REDOX 2). Stemmadine is acylated by stemmadine Ο-acetyltransferase (SAT) to yield stemmadine acetate. Through oxidation by precondylocarpine acetate synthase (PAS) and reduction by dihydroprecondylocarpine acetate synthase (DPAS), an enamine intermediate is formed. The intermediate undergoes fragmentation to produce an iminium that tautomerizes to yield dehydrosecodine. Coronaridine synthase (CorS) catalyzes the isomerization of dehydrosecodine and an unusual cycloaddition is completed. The iminium is reduced by DPAS and NADPH to form (-)-coronaridine.

There are two pathways (-)-coronaridine can take to become (-)-ibogaine. The first pathway begins with a P450 enzyme, ibogamine-10-hydroxylase (I10H), and methylation of noribogaine-10-Ο-methyltransferase (N10OMT) to produce (-)-voacangine. Polyneudridine aldehyde esterase-like 1 (PNAE1) and a spontaneous decarboxylation can convert (-)-voacangine to (-)-ibogaine. The second pathway consists of PNAE1 and the spontaneous decarboxylation occurring first to yield (-)-ibogamine, then the reaction of I10H-mediated hydroxylation and N10OMT-catalyzed O-methylation to produce (-)-ibogaine.

Natural occurrence

Ibogaine occurs naturally in iboga root bark. Ibogaine is also available in a total alkaloid extract of the Tabernanthe iboga plant, which also contains all the other iboga alkaloids and thus has only about half the potency by weight of standardized ibogaine hydrochloride.

Due to environmental concerns and low levels in Tabernanthe iboga, ibogaine is often produced via semi-synthesis starting with voacangine, a naturally-occurring alkaloid in Voacanga africana.

History

The use of iboga in African spiritual ceremonies was first reported by French and Belgian explorers in the 19th century, beginning with the work of French naval physician and explorer of Gabon Marie-Théophile Griffon du Bellay. The first botanical description of the Tabernanthe iboga plant was made in 1889. Ibogaine was first isolated from T. iboga in 1901 by Dybowski and Landrin and independently by Haller and Heckel in the same year using T. iboga samples from Gabon. Complete synthesis of ibogaine was accomplished by G. Büchi in 1966. Since then, several other synthesis methods have been developed.

From the 1930s to 1960s, ibogaine was sold in France in the form of Lambarène, an extract of the Tabernanthe manii plant, and promoted as a mental and physical stimulant. It was formulated at doses of 200mg extract containing low doses of 4 to 8mg ibogaine per tablet. The drug enjoyed some popularity among post-World War II athletes. Lambarène was withdrawn from the market in 1966 when the sale of ibogaine-containing products became illegal in France. Another formulation was Iperton, which contained Tabernanthe iboga extract 40mg per dose unit.

In 2008, Mačiulaitis and colleagues stated that in the late 1960s, the World Health Assembly classified ibogaine as a "substance likely to cause dependency or endanger human health". The U.S. Food and Drug Administration (FDA) also assigned it to a Schedule I classification, and the International Olympic Committee banned it as a potential doping agent.

Anecdotal reports concerning ibogaine's effects appeared in the early 1960s. Its anti-addictive properties were discovered accidentally by Howard Lotsof in 1962, at the age of 19, when he and five friends—all heroin addicts—noted subjective reduction of their craving and withdrawal symptoms while taking it. Further anecdotal observation convinced Lotsof of its potential usefulness in treating substance addictions. He contracted with a Belgian company to produce ibogaine in tablet form for clinical trials in the Netherlands, and was awarded a United States patent for the product in 1985. The first objective, placebo-controlled evidence of ibogaine's ability to attenuate opioid withdrawal in rats was published by Dzoljic et al. in 1988. Diminution of morphine self-administration was reported in preclinical studies by Glick et al. in 1991. Cappendijk et al. demonstrated reduction in cocaine self-administration in rats in 1993, and Rezvani reported reduced alcohol dependence in three strains of "alcohol-preferring" rats in 1995.

As the use of ibogaine spread, its administration varied widely; some groups administered it systematically using well-developed methods and medical personnel, while others employed haphazard and possibly dangerous methodology. Lotsof and his colleagues, committed to the traditional administration of ibogaine, developed treatment regimens themselves. In 1992, Eric Taub brought ibogaine to an offshore location close to the United States, where he began providing treatments and popularizing its use. In Costa Rica, Lex Kogan, another leading proponent, joined Taub in systematizing its administration. The two men established medically monitored treatment clinics in several countries.

In 1981, an unnamed European manufacturer produced 44 kg of iboga extract. The entire stock was purchased by Carl Waltenburg, who distributed it under the name "Indra extract" and used it in 1982 to treat heroin addicts in the community of Christiania. Indra extract was available for sale over the Internet until 2006, when the Indra web presence disappeared. Various products are currently sold in a number of countries as "Indra extract", but it is unclear if any of them are derived from Waltenburg's original stock. Ibogaine and related indole compounds are susceptible to oxidation over time.

The National Institute on Drug Abuse (NIDA) began funding clinical studies of ibogaine in the United States in the early 1990s, but terminated the project in 1995. Data demonstrating ibogaine's efficacy in attenuating opioid withdrawal in drug-dependent human subjects was published by Alper et al. in 1999. A cohort of 33 patients were treated with 6 to 29 mg/kg of ibogaine; 25 displayed resolution of the signs of opioid withdrawal from 24 hours to 72 hours post-treatment, but one 24-year-old female, who received the highest dosage, died. Mash et al. (2000), using lower oral doses (10–12 mg/kg) in 27 patients, demonstrated significantly lower objective opiate withdrawal scores in heroin addicts 36 hours after treatment, with self-reports of decreased cocaine and opiate craving and alleviated depression symptoms. Many of these effects appeared sustainable over a one-month post-discharge follow-up.

Society and culture

Legal status

, the legal status of ibogaine varies widely among countries, as it may be illegal to possess or use, may be legalized, may be decriminalized, or is under consideration for future legislation.

In the United States, although some cities and states have decriminalized psychedelic chemicals, plants and mushrooms, ibogaine has had minimal legislation, and remains illegal under federal law, as of . The US Drug Enforcement Administration enforces ibogaine as a Schedule I substance under the Controlled Substances Act.

Treatment clinics

Ibogaine treatment clinics have emerged in Mexico, Bahamas, Canada, the Netherlands, South Africa, and New Zealand, all operating in what has been described as a "legal gray area". Costa Rica also has treatment centers. While clinical guidelines for ibogaine-assisted detoxification were released by the Global Ibogaine Therapy Alliance in 2015, addiction specialists warn that the treatment of drug dependence with ibogaine in non-medical settings, without expert supervision and unaccompanied by appropriate psychosocial care, can be dangerous — and, in approximately one case in 300, potentially fatal.

Media

Documentary films

• (2004). Directed by David Graham Scott. Scott begins videotaping his heroin-addicted friends. Before long, he himself is addicted to the drug. He eventually turns the camera on himself and his family. After 12 years of debilitating, painful dependence on methadone, Scott turns to ibogaine. Filmed in Scotland and England, and broadcast on BBC One as the third installment in the documentary series One Life.
• (2004). Directed by Ben Deloenen. Cy, a 34-year-old heroin addict, undergoes ibogaine treatment with Dr. Martin Polanco at the Ibogaine Association, a clinic in Rosarito, Mexico. Deloenen interviews people formerly addicted to heroin, cocaine, and methamphetamine, who share their perspectives about ibogaine treatment. In Gabon, a Babongo woman receives iboga root for her depressive malaise. Deloenen visually contrasts this Western, clinical use of ibogaine with the Bwiti use of iboga root, but emphasizes the Western context.
• (2007). Directed by Magnolia Martin. Martin's subject is a former millionaire and stockbroker who travels to Mexico for ibogaine treatment for heroin addiction.
• Tripping in Amsterdam (2008). In this short film directed by Jan Bednarz, Simon "Swany" Wan visits Sara Glatt's iboga treatment center in Amsterdam. Current TV broadcast the documentary in 2008 as part of their "Quarter-life Crisis" programming roster.
• (2009). Directed by Michel Negroponte. Negroponte examines Dimitri Mobengo Mugianis's long, clandestine career of treating heroin addicts with ibogaine.
• One of the five segments of "Hallucinogens DMT" (2012), Season 2, Episode 4 of Drugs, Inc. on National Geographic Channel, a former heroin user treats addicts with ibogaine in Canada. He himself used ibogaine to stop his abuse of narcotics.
• The "Underground Heroin Clinic" segment of "Addiction" (2013). Season 1, episode 7 of the HBO documentary series Vice examines the use of ibogaine to interrupt heroin addiction.
• The Ibogaine Safari (2014). A documentary by filmmaker Pierre le Roux which investigates the claims of painless withdrawal from opiates such as nyaope/heroin in South Africa by taking several addicts on an adventure "safari" while taking ibogaine. The documentary won the award for 'Best Documentary Short' at the 2014 Canada International Film Festival.
• (2014). Directed by David Graham Scott.
• (2019). A documentary by Tyler Chandler and Nicholas Meyers. Synopsis- After years of no success with prescription drugs, a suicidal Adrianne seeks help from underground healers with her depression, anxiety, and opioid addiction by utilizing illegal psychedelics like magic mushrooms and iboga.
• "Synthetic Ibogaine - Natural Tramadol" (2021). This episode of the documentary series Hamilton's Pharmacopeia on Vice on TV, follows a struggling local addict to an ibogaine ritual.
• (2022). A documentary by Mike "Zappy" Zapolin, in which famous NBA athlete (and former Keeping Up With the Kardashians star) Lamar Odom seeks out ibogaine and other therapies to heal PTSD, anxiety, and addiction.
• (2025). A Netflix documentary in which Navy SEALS with PTSD seek therapy using ibogaine through a program run by Stanford University.

Print media

• While in Wisconsin covering the primary campaign for the United States presidential election of 1972, gonzo journalist Hunter S. Thompson submitted a satirical article to Rolling Stone accusing Democratic Party candidate Edmund Muskie of being addicted to ibogaine. Many readers, and even other journalists, did not realize that the Rolling Stone piece was facetious. The ibogaine assertion, which was completely unfounded, did significant damage to Muskie's reputation, and was cited as a factor in his loss of the nomination to George McGovern. Thompson later said he was surprised that anyone believed it. The article is included in Thompson's post-election anthology, Fear and Loathing on the Campaign Trail '72 (1973).
• Author and Yippie Dana Beal co-wrote the 1997 book The Ibogaine Story.
• American author Daniel Pinchbeck wrote about his own experience of ibogaine in his book Breaking Open the Head (2002), and in a 2003 article for The Guardian titled "Ten years of therapy in one night".
• Author and musician Geoff Rickly based his debut novel Someone Who Isn't Me on his real-life experiences with heroin addiction and an ibogaine clinic in Mexico.
• American investigative journalist, Rachel Nuwer, published a comprehensive feature for Reason magazine titled Can This Psychedelic Help Cure Opioid Addiction? In the article, Rachel speaks with experts in the field of opioid use disorder (OUD) and how ibogaine shows promising results for effective treatment and recovery. This is particularly true for those patients that also suffer from traumatic brain injuries (TBI).

Television drama

Ibogaine factors into the stories of these episodes from television drama series:

Radio and podcasts

• — A former heroin addict realizes that he wants to help other addicts kick their habits. The problem is, he wants to do this using a hallucinogenic drug - ibogaine - that is completely illegal, and which requires medical expertise he doesn't have.
• In January 2025, former Texas Governor Rick Perry and W. Bryan Hubbard, appeared on The Joe Rogan Experience. The trio discussed advances in public policy towards ibogaine and eventual FDA clinical trials. Hubbard was the former Chairman and Executive Director of the Kentucky Opioid Abatement Advisory Commission until he was asked to resign in December 2023. Since 2024, Hubbard has continued his campaign outside Kentucky and now works with the REID Foundation as the Executive Director of the American Ibogaine Initiative.

Research

Ibogaine has been studied for its potential medical use in treating substance use disorders, particularly opioid addiction, by reducing withdrawal symptoms and cravings, though its use and clinical development have been limited by regulatory restrictions and serious safety concerns including cardiac risks.

Psychotherapy

Ibogaine was used as an adjunct to psychotherapy by Claudio Naranjo, documented in his 1973 book The Healing Journey: New Approaches to Consciousness. He was awarded patent in 1974.

Addiction treatment

A 2022 systematic review of 24 studies involving 705 participants suggests that ibogaine and noribogaine show promise in treating substance use disorders and comorbid depressive symptoms and psychological trauma, but carry serious safety risks, necessitating rigorous clinical oversight.

Texas research initiative

In 2025, the state of Texas allocated $50 million to fund clinical research on ibogaine, aiming to develop a U.S. Food and Drug Administration-approved treatment for opioid use disorder, co-occurring substance use disorders, and other ibogaine-responsive conditions. The initiative, supported by former Governor Rick Perry, established a consortium of universities, hospitals, and drug developers, with the goal of positioning Texas as a leading center for psychedelic medicine research.

References

References

1. (March 2022). "Trips and neurotransmitters: Discovering principled patterns across 6850 hallucinogenic experiences". Sci Adv.
2. (12 May 2017). "Notice - Prescription Drug List (PDL): Multiple additions". Government of Canada, Health.
3. (March 2011). "Ibogaine--be informed before you promote or prescribe". Journal of Primary Health Care.
4. "Ibogaine". U.S. National Library of Medicine.
5. (July 2022). "A systematic literature review of clinical trials and therapeutic applications of ibogaine". Journal of Substance Abuse Treatment.
6. (2001). "A contemporary history of ibogaine in the United States and Europe". Academic Press.
7. (July 2017). "Indoles as therapeutics of interest in medicinal chemistry: Bird's eye view". Elsevier BV.
8. (September 2016). "Ibogaine for treating drug dependence. What is a safe dose?". Drug and Alcohol Dependence.
9. "Ibogaine".
10. (November 2017). "Subjective effectiveness of ibogaine treatment for problematic opioid consumption: Short- and long-term outcomes and current psychological functioning". Journal of Psychedelic Studies.
11. (2018-01-02). "Treatment of opioid use disorder with ibogaine: detoxification and drug use outcomes". The American Journal of Drug and Alcohol Abuse.
12. (January 2016). "hERG Blockade by Iboga Alkaloids". Cardiovascular Toxicology.
13. (2024). "Psychedelic Therapy: A Primer for Primary Care Clinicians-Ibogaine". Am J Ther.
14. (September 2025). "Old Dog, New Tricks: Ibogaine and Its Analogs as Potential Neurotherapeutics". J Med Chem.
15. (May 1998). "Medication development of ibogaine as a pharmacotherapy for drug dependence". Annals of the New York Academy of Sciences.
16. (March 2012). "Fatalities temporally associated with the ingestion of ibogaine". Journal of Forensic Sciences.
17. (January 2026). "Safety and Efficacy of Monoamine Oxidase Inhibitors in Patients Who Use Psychoactive Substances: Potential Drug Interactions and Substance Use Disorder Treatment Data". CNS Drugs.
18. (18 June 2025). "Kᵢ Database".
19. (October 2018). "DARK Classics in Chemical Neuroscience: Ibogaine". ACS Chem Neurosci.
20. (2001). "Mechanisms of action of ibogaine: Relevance to putative therapeutic effects and development of a safer iboga alkaloid congener". The Alkaloids: Chemistry and Biology.
21. (September 2000). "18-Methoxycoronaridine (18-MC) and ibogaine: comparison of antiaddictive efficacy, toxicity, and mechanisms of action". Ann N Y Acad Sci.
22. (2016). "How toxic is ibogaine?". Clin Toxicol (Phila).
23. (June 1995). "100 years of ibogaine: neurochemical and pharmacological actions of a putative anti-addictive drug". Pharmacol Rev.
24. (February 2010). "Psychedelics and the human receptorome". PLOS ONE.
25. (January 2021). "A non-hallucinogenic psychedelic analogue with therapeutic potential". Nature.
26. (March 1998). "Standard binding and functional assays related to medications development division testing for potential cocaine and opiate narcotic treatment medications". NIDA Res Monogr.
27. (December 2015). "Noribogaine is a G-protein biased κ-opioid receptor agonist". Neuropharmacology.
28. (June 1995). "Properties of ibogaine and its principal metabolite (12-hydroxyibogamine) at the MK-801 binding site of the NMDA receptor complex". Neurosci Lett.
29. (January 2023). "What We Have Gained from Ibogaine: α3β4 Nicotinic Acetylcholine Receptor Inhibitors as Treatments for Substance Use Disorders". J Med Chem.
30. (September 2010). "Interaction of ibogaine with human alpha3beta4-nicotinic acetylcholine receptors in different conformational states". Int J Biochem Cell Biol.
31. (September 2011). "Structure-activity relationship of ibogaine analogs interacting with nicotinic acetylcholine receptors in different conformational states". Int J Biochem Cell Biol.
32. (April 1999). "The effects of ibogaine on dopamine and serotonin transport in rat brain synaptosomes". Brain Res Bull.
33. (10 March 2025). "Deciphering Ibogaine's Matrix Pharmacology: Multiple Transporter Modulation at Serotonin Synapses".
34. (January 2016). "hERG Blockade by Iboga Alkaloids". Cardiovasc Toxicol.
35. (March 2014). "Anti-addiction drug ibogaine inhibits hERG channels: a cardiac arrhythmia risk". Addict Biol.
36. (1999). "Pharmacology of Ibogaine and Ibogaine-Related Alkaloids". Academic Press.
37. (2001). "Ibogaine: A Review". Academic.
38. (2013). "Effect of Iboga alkaloids on µ-opioid receptor-coupled G protein activation". PLOS ONE.
39. (July 1999). "Noribogaine generalization to the ibogaine stimulus: correlation with noribogaine concentration in rat brain". Neuropsychopharmacology.
40. (2001). "The Alkaloids: Chemistry and Biology". Elsevier.
41. (February 1998). "Behavioral and biochemical evidence for a nonessential 5-HT2A component of the ibogaine-induced discriminative stimulus". Pharmacol Biochem Behav.
42. (2018). "Ibogaine Acute Administration in Rats Promotes Wakefulness, Long-Lasting REM Sleep Suppression, and a Distinctive Motor Profile". Front Pharmacol.
43. (December 2003). "Binding of beta-carbolines at 5-HT(2) serotonin receptors". Bioorganic & Medicinal Chemistry Letters.
44. (February 1992). "Mechanisms of action of ibogaine and harmaline congeners based on radioligand binding studies". Brain Res.
45. Naranjo, Claudio. (1969). "Psycotherapeutic Possibilities of New Fantasy-Enhancing Drugs". Clinical Toxicology.
46. (April 2021). "EEG Gamma Band Alterations and REM-like Traits Underpin the Acute Effect of the Atypical Psychedelic Ibogaine in the Rat". ACS Pharmacol Transl Sci.
47. (December 2023). "Main targets of ibogaine and noribogaine associated with its putative anti-addictive effects: A mechanistic overview". J Psychopharmacol.
48. (October 2025). "Changing your mind: neuroplastic mechanisms underlying the therapeutic effect of psychedelics in depression, PTSD, and addiction". Prog Neuropsychopharmacol Biol Psychiatry.
49. (June 2018). "Psychedelics Promote Structural and Functional Neural Plasticity". Cell Rep.
50. (May 2001). "In vivo neurobiological effects of ibogaine and its O-desmethyl metabolite, 12-hydroxyibogamine (noribogaine), in rats". The Journal of Pharmacology and Experimental Therapeutics.
51. (February 2015). "Ascending-dose study of noribogaine in healthy volunteers: pharmacokinetics, pharmacodynamics, safety, and tolerability". J Clin Pharmacol.
52. (November 2016). "Ascending Single-Dose, Double-Blind, Placebo-Controlled Safety Study of Noribogaine in Opioid-Dependent Patients". Clin Pharmacol Drug Dev.
53. (March 2000). "Pharmacokinetic characterization of the indole alkaloid ibogaine in rats". Methods and Findings in Experimental and Clinical Pharmacology.
54. (September 2000). "Ibogaine: complex pharmacokinetics, concerns for safety, and preliminary efficacy measures". Annals of the New York Academy of Sciences.
55. (1997). "Tihkal: the continuation". Transform Press.
56. (2012). "Total synthesis of ibogaine, epiibogaine and their analogues". Tetrahedron.
57. (February 2002). "Extraction studies of Tabernanthe iboga and Voacanga africana". Natural Product Letters.
58. "Voacanga Extraction Manual: Phase 4: Production and Purification of Ibogaine".
59. (July 2019). "Extraction and Conversion Studies of the Antiaddictive Alkaloids Coronaridine, Ibogamine, Voacangine, and Ibogaine from Two Mexican Tabernaemontana Species (Apocynaceae)". Chemistry & Biodiversity.
60. (2025-02-06). "UC Davis Researchers Achieve Total Synthesis of Ibogaine".
61. (February 2025). "Efficient and modular synthesis of ibogaine and related alkaloids". Nature Chemistry.
62. (May 2004). "Novel iboga alkaloid congeners block nicotinic receptors and reduce drug self-administration". European Journal of Pharmacology.
63. (September 1994). "Effects of iboga alkaloids on morphine and cocaine self-administration in rats: relationship to tremorigenic effects and to effects on dopamine release in nucleus accumbens and striatum". Brain Research.
64. (28 January 2006). "Antiaddictive indole alkaloids in Ervatamia yunnanensis and their bioactivity". Academic Journal of Second Military Medical University.
65. (2020-12-09). "Progress Toward A Safer Psychedelic Drug To Treat Depression And Addiction".
66. (June 2024). "Structural pharmacology and therapeutic potential of 5-methoxytryptamines". Nature.
67. (March 2021). "The iboga enigma: the chemistry and neuropharmacology of iboga alkaloids and related analogs". Natural Product Reports.
68. (2023-02-05). "Marie Théophile GRIFFON du BELLAY (1829–1908)".
69. (1901). "PLANT CHEMISTRY. Concerning Iboga, its excitement-producing properties, its composition, and the new alkaloid it contains, ibogaine". C. R. Acad. Sci..
70. (1966). "The Total Synthesis of Iboga Alkaloids". J. Am. Chem. Soc..
71. (1999). "Ph.D.".
72. (April 2023). "IUPHAR - invited review - Ibogaine - A legacy within the current renaissance of psychedelic therapy". Pharmacol Res.
73. (March 2008). "Ibogaine, an anti-addictive drug: pharmacology and time to go further in development. A narrative review". Hum Exp Toxicol.
74. (2003). "Ibogaine: a Comprehensive Literature Review". Nova Science Publishers.
75. (1999). "Treatment of acute opioid withdrawal with ibogaine". The American Journal on Addictions.
76. (17 February 2010). "Howard Lotsof Dies at 66; Saw Drug Cure in a Plant". The New York Times.
77. (1988). "Effect of ibogaine on naloxone-precipitated withdrawal syndrome in chronic morphine-dependent rats". Archives Internationales de Pharmacodynamie et de Therapie.
78. (April 1991). "Effects and aftereffects of ibogaine on morphine self-administration in rats". European Journal of Pharmacology.
79. (September 1993). "Inhibitory effects of ibogaine on cocaine self-administration in rats". European Journal of Pharmacology.
80. (November 1995). "Attenuation of alcohol intake by ibogaine in three strains of alcohol-preferring rats". Pharmacology, Biochemistry, and Behavior.
81. (17 July 2007). "A Home for Ibogaine in Barcelona".
82. (11 September 2012). "Costa Rican Center a Leader in Alternative Ibogaine Therapy".
83. (September 2006). "Distribution of ibogaine and noribogaine in a man following a poisoning involving root bark of the ''Tabernanthe iboga'' shrub". Journal of Analytical Toxicology.
84. (1965). "The Alkaloids: Chemistry and Physiology". Elsevier.
85. (2003-05-12). "A Non-Profit Approach to Developing Ibogaine into an FDA-Approved Medication".
86. (1999). "Treatment of Acute Opioid Withdrawal with Ibogaine". The American Journal on Addictions.
87. (September 2000). "Ibogaine: Complex Pharmacokinetics, Concerns for Safety, and Preliminary Efficacy Measures". Annals of the New York Academy of Sciences.
88. (22 March 2024). "What psychedelics legalisation and decriminalisation looks like around the world". BBC.
89. (January 2023). "Psychedelic Drug Legislative Reform and Legalization in the United States". JAMA Psychiatry.
90. (21 April 2023). "Iboga (ibogaine)". Drugs.com.
91. (2012-04-10). "Can a hallucinogen from Africa cure addiction?".
92. (1979-04-19). "Ibogaine Therapy".
93. (2005-12-13). "Busted for Iboga".
94. (2020-10-28). "Clinical Guidelines for Ibogaine-Assisted Detoxification".
95. "The Global Ibogaine Therapy Alliance (GITA)".
96. (2004-06-08). "Detox or Die".
97. (January–February 2005). "Ibogaine: Rite of Passage".
98. (2007-07-13). "The 2007 FFF Winners".
99. . (23 June 2008). ["Tripping in Amsterdam"](http://current.com/green/89043771_tripping-in-amsterdam.htm). *Current.com*.
100. (2011-01-10). "Review: I'm Dangerous with Love".
101. (2013-05-17). "A New Episode of Our TV Show Is Airing Tonight".
102. "Tobaccoland & Underground Heroin Clinic {{!".
103. (2019-11-13). "Ibogaine Media".
104. "The Ibogaine Safari".
105. (2015-07-31). "Iboga Nights".
106. (2020-03-19). "'Dosed' Review: The Case for Plant-Based Recovery".
107. (2021-06-21). "Hulu's 'Hamilton's Pharmacopeia' Shows That We Can No Longer Ignore Connections Between Religion and Drugs".
108. (2021-06-10). "Lamar Odom prepares to fight Aaron Carter, but first he fought PTSD".
109. (1999-02-03). "Online NewsHour: Remembering Ed Muskie".
110. (2008). "[[Gonzo: The Life and Work of Dr. Hunter S. Thompson]]".
111. (1973). "Fear and Loathing on the Campaign Trail '72". Straight Arrow Books.
112. (1997). "The Ibogaine Story: Report on the Staten Island Project". Autonomedia.
113. (2002). "Breaking Open the Head: A Psychedelic Journey into the Heart of Contemporary Shamanism". Broadway Books.
114. (19 September 2003). "Ten years of therapy in one night". [[The Guardian]].
115. "Someone Who Isn't Me".
116. (2024-09-15). "Can this psychedelic help cure opioid addiction?".
117. (5 January 2024). "Psychoactive drug ibogaine effectively treats traumatic brain injury in special ops military vets".
118. (1 December 2006). "Sink or Swim. Act Two. I'm Not A Doctor But I Play One At The Holiday Inn.".
119. PowerfulJRE. (2025-01-02). "Joe Rogan Experience #2251 - Rick Perry & W. Bryan Hubbard".
120. "W. Bryan Hubbard {{!}} Exec. Director of American Ibogaine Initiative".
121. "The Sabotage of Bryan Hubbard's Kentucky Ibogaine Initiative".
122. "Texas Ibogaine Initiative".
123. (March 2013). "Ibogaine in the treatment of substance dependence". Current Drug Abuse Reviews.
124. Naranjo, Claudio. (1973). "The Healing Journey: New Approaches to Consciousness". Parthenon Books.
125. (July 2022). "A systematic literature review of clinical trials and therapeutic applications of ibogaine". Journal of Substance Abuse Treatment.
126. (2025-06-11). "With Rick Perry's backing and $50 million from the state, Texas set to become a leader in psychedelics research".
127. "Texas Legislature Online - 89(R) History for SB 2308".