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Systematic (IUPAC) name
Clinical data
Legal status
  • AU: S4 (Prescription only)
  • CA: Unscheduled
  • NZ: Prescription only
  • UK: Unscheduled
  • US: Schedule I
  • UN: Unscheduled
Routes of
CAS Number 83-74-9 YesY
ATC code None
PubChem CID: 197060
ChemSpider 170667 YesY
UNII 3S814I130U YesY
Chemical data
Formula C20H26N2O
Molecular mass 310.44 g·mol−1
Physical data
Melting point 152 to 153 °C (306 to 307 °F)
 YesY (what is this?)  (verify)

Ibogaine is a naturally occurring psychoactive substance found in plants in the Apocynaceae family such as Tabernanthe iboga, Voacanga africana and Tabernaemontana undulata.[1] A psychedelic with dissociative properties, the substance is banned in some countries; in other countries it is used by proponents of psychedelic therapy to treat addiction to methadone, heroin, ethanol, cocaine, methamphetamine, anabolic steroids, and other drugs. Ibogaine is also used to treat depression and post traumatic stress disorder. Derivatives of ibogaine that lack the substance's psychedelic properties are under development.[2]

Ibogaine-containing preparations are used for medicinal and ritual purposes within African spiritual traditions of the Bwiti, who claim to have learned it from the Pygmy peoples. Although it was first commonly advertised as having anti-addictive properties in 1962 by Howard Lotsof, its Western use predates that by at least a century. In France it was marketed as Lambarène, a medical drug used as a stimulant. Additionally, the U.S. Central Intelligence Agency (CIA) studied the effects of ibogaine in the 1950s.[3]

Ibogaine is an indole alkaloid that is obtained either by extraction from the iboga plant or by semi-synthesis from the precursor compound voacangine,[4][5] another plant alkaloid. A full organic synthesis of ibogaine has been achieved and was published in a patent in 1956.[6] The synthesis process is too expensive and challenging to be used to produce a commercially significant yield. The free base and the HBr salt have both been characterised by X-ray crystallography.[7][8]

While ibogaine's prohibition in several countries has slowed scientific research into its anti-addictive properties, the use of ibogaine for drug treatment has grown in the form of a large worldwide medical subculture.[9] Ibogaine is also used to facilitate psychological introspection and spiritual exploration.

Psychoactive effects[edit]

Ibogaine is a psychedelic.[10] The experience of Ibogaine is broken down in two phases; the visionary phase comes first, then the introspection phase.[11]

The visionary phase has been described as oneirogenic and lasts for 4 to 6 hours. The second phase, the introspection phase, is responsible for the psychotherapeutic effects of ibogaine. It can allow people to conquer their fears and negative emotions.[11]

Ibogaine has been referred to as an oneirogen, referring to the dreamlike nature of its psychedelic effects. Ibogaine catalyzes an altered state of consciousness reminiscent of dreaming while fully conscious and aware so that memories, life experiences, and issues of trauma can be processed.[11]



Ibogaine currently has no accepted medical uses. Ongoing research is investigating potential uses for ibogaine in addiction treatment.[12]


In Bwiti religious ceremonies, the root bark is pulverized and swallowed in large amounts to produce intense psychoactive effects.[13]


In Africa, iboga root bark is sometimes chewed, releasing small amounts of ibogaine to produce a stimulant effect.[13]


Psychiatric medications are strongly contraindicated in ibogaine therapy due to adverse interactions. Some studies also suggest the possibility of adverse interaction with heart conditions.[citation needed]

Adverse effects[edit]


One of the first noticeable effects of large-dose ibogaine ingestion is ataxia, a difficulty in coordinating muscle motion which makes standing and walking difficult without assistance. Xerostomia (dry mouth), nausea, and vomiting may follow. These symptoms may be long in duration, ranging from 4 to 24 hours in some cases. Ibogaine is sometimes administered per rectum to avoid nausea and vomiting.

Cardiovascular and respiratory[edit]

In one study of canine subjects, ibogaine was observed to increase sinus arrhythmia (the normal change in heart rate during respiration).[14] It was proposed that there is a risk of QT-interval prolongation following ibogaine administration.[15] This risk was further demonstrated by a case reported in the New England Journal of Medicine documenting prolonged QT interval and ventricular tachycardia after initial use.[16] Fatalities following ibogaine ingestion are documented in the medical literature.[17] Lethal respiratory and cardiac effects are associated with use.[18]


In humans, ibogaine is used in dosages anywhere from 5 mg/kg of body weight for a minor effect to 30 mg/kg in the treatment of strong polysubstance addiction. Efficacy (and risk) of dosages higher than 30 mg/kg in humans is unknown. In animal neurotoxicity studies, there was no observable neurotoxicity of ibogaine at 25 mg/kg, but at 50 mg/kg, one-third of the rats had developed patches of neurodegeneration, and at doses of 75 mg/kg or above, all rats showed a characteristic pattern of degeneration of Purkinje neurons, mainly in the cerebellum.[19] While caution should be exercised when extrapolating animal studies to humans, these results suggest that neurotoxicity of ibogaine is likely to be minimal when ibogaine is used in the 10–20 mg/kg range typical of drug addiction interruption treatment regimens.[20]


Because ibogaine is one of the many drugs that are partly metabolized by the cytochrome P450 complex, caution must be exercised to avoid foods or drugs that are similarly metabolized by CP450, in particular foods containing bergamottin or bergamot oil, such as grapefruit juice.[21]


Ki-values in μM[22] (a smaller value demonstrates higher binding affinity)
Receptor Ibogaine Noribogaine
κ-opioid 2.2 0.61
μ-opioid 2.0 0.68
δ-opioid >10 5.2
NMDA 3.1 15
5-HT2A 16 >100
5-HT2C >10 >10
5-HT3 2.6 >100
σ1 2.5 11
σ2 0.4 19


Ibogaine affects many different neurotransmitter systems simultaneously.[23][24]


Ibogaine is metabolized in the human body by cytochrome P450 2D6 into noribogaine (12-hydroxyibogamine). Noribogaine is most potent as a serotonin reuptake inhibitor. It acts as a moderate κ-opioid receptor antagonist[citation needed] and weak µ-opioid receptor antagonist or weak partial agonist.[25] It is possible that the action of ibogaine at the kappa opioid receptor may indeed contribute significantly to the psychoactive effects attributed to ibogaine ingestion (citation needed); Salvia divinorum, another plant recognized for its strong hallucinogenic properties, contains the chemical salvinorin A which is a highly selective kappa opioid agonist. Both ibogaine and noribogaine have a plasma half-life of around two hours in the rat,[26] although the half-life of noribogaine is slightly longer than that of the parent compound. It is proposed that ibogaine is deposited in fat and metabolized into noribogaine as it is released.[27] After ibogaine ingestion in humans, noribogaine shows higher plasma levels than ibogaine and is detected for a longer period of time than ibogaine.[28] Noribogaine is also more potent than ibogaine in rat drug discrimination assays when tested for the subjective effects of ibogaine.[29]

Physical and chemical properties[edit]

The general structure of tryptamines.

Ibogaine is a tryptamine. It has two separate chiral centers, meaning that there are four different stereoisomers of ibogaine. These four isomers are difficult to resolve.[30]


One recent total synthesis[31] 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.

Currently, pure crystalline ibogaine hydrochloride is the most standardized formulation. It is typically produced by semi-synthesis from voacangine in commercial laboratories.[13]


A synthetic derivative of ibogaine, 18-methoxycoronaridine (18-MC), is a selective α3β4 antagonist that was developed collaboratively by the neurologist Stanley D. Glick (Albany) and the chemist Martin E. Kuehne (Vermont).[32] This discovery was stimulated by earlier studies on other naturally occurring analogues of ibogaine such as coronaridine and voacangine that showed these compounds also have anti-addictive properties.[33][34]

Natural occurrence[edit]

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 as standardized ibogaine hydrochloride.[13]


The use of iboga in African spiritual ceremonies was first observed by French and Belgian explorers in the 19th century. 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[35] 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.[36] Since then, several other synthesis methods have been developed.[37]

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. 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.[38]

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) assigned it Schedule I classification, and the International Olympic Committee banned it as a potential doping agent.[39]

Anecdotal reports concerning ibogaine's effects appeared in the early 1960s.[40] 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.[41] 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.[42] Diminution of morphine self-administration was reported in preclinical studies by Glick et al. in 1991.[43] Cappendijk et al. demonstrated reduction in cocaine self-administration in rats in 1993,[44] and Rezvani reported reduced alcohol dependence in three strains of "alcohol preferring" rats in 1995.[45]

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.[46] 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.[47]

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 Christiania, Denmark, a squatter village where heroin addiction was widespread.[48] 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.[20][49]

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.[50] Data demonstrating ibogaine's efficacy in attenuating opioid withdrawal in drug-dependent human subjects was published by Alper et al. in 1999.[51] 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.[52]

Society and culture[edit]

Legal status[edit]

As of 2009, ibogaine is unregulated in Canada[53][54] and Mexico.[2]

As of 2015 in the United Kingdom, ibogaine is not listed under the Misuse of Drugs Act and so is legal to possess, however distribution is illegal.[55][56]

Ibogaine is schedule I in Sweden.[57]

Ibogaine is classified as a as a Schedule I-controlled substance in the United States,[58] and is not approved there for addiction treatment (or any other therapeutic use) because of its hallucinogenic, neurotoxic, and cardiovascular side effects, as well as the scarcity of safety and efficacy data in human subjects.[59]

Ibogaine is illegal in Norway (as are all tryptamine derivatives).[60]

Ibogaine is unregulated in Germany, but for medical use it can be regulated by the pharmacy rules (AMG).

Ibogaine was gazetted in New Zealand in 2009 as a non-approved prescription medicine.[61]

In most other countries it remains unregulated and unlicensed.[62][63]

Treatment clinics[edit]

Ibogaine treatment clinics have emerged in Mexico, Canada, the Netherlands, South Africa, and New Zealand, all operating in what has been described as a "legal gray area".[62][64] Costa Rica also has treatment centers, most notably one run by Lex Kogan, a leading proponent of ibogaine.[65] Covert, illegal neighborhood clinics are known to exist in the United States, despite active DEA surveillance.[66] 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.[64] However, Clinical Guidelines for Ibogaine-Assisted Detoxification,[67] hosted by the Global Ibogaine Therapy Alliance,[68] were carefully crafted by prominent treatment providers and medical professionals and released in 2015. When practiced, these living Guidelines are intended to minimize the medical and psychological risk associated with ibogaine treatmemt, and to maximize its efficacy.


Documentary films[edit]

Detox or Die (2004)

Directed by David Graham Scott.[69] David Graham Scott begins videotaping his heroin-addicted friends. Before long, he himself is addicted to the drug. He eventually turns the camera to 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 instalment in the documentary series One Life.[70]

Ibogaine: Rite of Passage (2004)

Directed by Ben Deloenen.[71] 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.

Facing the Habit (2007)

Directed by Magnolia Martin.[72] 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.[73] Current TV broadcast the documentary in 2008, as part of their "Quarter-life Crisis" programming roster.

I'm Dangerous with Love (2009)

Directed by Michel Negroponte.[74] Negroponte examines Dimitri Mugianis's long, clandestine career of treating heroin addicts with ibogaine.

"Hallucinogens" (2012)

In one of five segments from this episode 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.:[75]

"Addiction" (2013)

This episode of the HBO documentary series Vice[76] devotes a segment to the use of ibogaine to interrupt heroin addiction.

"The Ibogaine Safari" (2014)

A documentary by film maker Pierre le Roux, investigating the claims of painless withdrawal from Opiates such as Njope/Heroin in South Africa by taking several addicts on an adventure 'safari' while taking Ibogaine. The documentary won the award of excellence for 'Best documentary short' at the 2014 Canada International film festival.[77]

Print media[edit]

While in Wisconsin covering the primary election for the United States presidential election of 1972, gonzo journalist Hunter S. Thompson submitted a satirical article to his editor at Rolling Stone accusing presidential nominee Edmund Muskie of being addicted to ibogaine. When Rolling Stone published the piece, many readers, and even other journalists, did not realize that Thompson's assertion was facetious. The claim was completely unfounded, and Thompson was surprised that anyone believed it.[78]

After the election, Thompson republished the article (slightly modified) in his article anthology Fear and Loathing on the Campaign Trail '72 (1973).[79] Muskie was not elected to the Presidency.

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),[80] and in a 2003 article for The Guardian titled "Ten years of therapy in one night".[81]

Television drama[edit]

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


  • "Sink or Swim. Act Two. I'm Not A Doctor But I Play One At The Holiday Inn.". This American Life. Episode 321. 1 December 2006.  — 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.[88]


Addiction treatment[edit]

The most-studied therapeutic effect of ibogaine is the reduction or elimination of addiction to opioids. An integral effect is the alleviation of symptoms of opioid withdrawal. Research also suggests that ibogaine may be useful in treating dependence on other substances such as alcohol, methamphetamine, and nicotine and may affect compulsive behavioral patterns not involving substance abuse or chemical dependence. Researchers note that there remains a "need for systematic investigation in a conventional clinical research setting."[40]

Many users of ibogaine report experiencing visual phenomena during a waking dream state, such as instructive replays of life events that led to their addiction, while others report therapeutic shamanic visions that help them conquer the fears and negative emotions that might drive their addiction. It is proposed that intensive counseling, therapy and aftercare during the interruption period following treatment is of significant value. Some individuals require a second or third treatment session with ibogaine over the course of the next 12 to 18 months. A minority of individuals relapse completely into opiate addiction within days or weeks. A comprehensive article (Lotsof 1995) on the subject of ibogaine therapy detailing the procedure, effects and aftereffects is found in "Ibogaine in the Treatment of Chemical Dependence Disorders: Clinical Perspectives".[89] Ibogaine has also been reported in multiple small-study cohorts to reduce cravings for methamphetamine.[90]

There is also evidence that this type of treatment works with LSD, which has been shown to have a therapeutic effect on alcoholism. Both ibogaine and LSD appear to be effective for encouraging introspection and giving the user occasion to reflect on the sources of their addiction, while also producing an intense, transformative experience that can put established patterns of behaviour into perspective;[91] ibogaine has the added benefit of preventing withdrawal effects.[40]

Shredded bark of tabernanthe iboga for consumption. Contains ibogaine.

Chronic pain management[edit]

In 1957, Jurg Schneider, a pharmacologist at CIBA (now a division of Novartis), found that ibogaine potentiated morphine analgesia.[92] No additional data was ever published by CIBA researchers on ibogaine–opioid interactions. Almost 50 years later, Patrick Kroupa and Hattie Wells released the first treatment protocol for concomitant administration of ibogaine with opioids in human subjects, indicating that ibogaine reduced tolerance to opioid drugs. Their paper in the Multidisciplinary Association for Psychedelic Studies Journal demonstrated that administration of low "maintenance" doses of ibogaine HCl with opioids decreases tolerance, but noted that ibogaine's potentiating action could make this a risky procedure.[93]


Ibogaine has been used as an adjunct to psychotherapy by Claudio Naranjo, documented in his book The Healing Journey.[94] He was awarded patent CA 939266  in 1974.

See also[edit]


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