Tabernanthe iboga

'''''Iboga''''' (''Tabernanthe iboga'' Baillon, Apocynaceae) — eboka — is a West and Central African rainforest shrub whose root bark is consumed as a powerful psychoactive preparation. Its principal alkaloid, [[substance:ibogaine]], is a pentacyclic monoterpene [[substance_class:chemical/indole-alkaloid]] with an exceptionally broad multi-target [[glossary:receptor]] profile{{cite|doi=10.1021/jacs.5c06325|anchor=63568f9e}}. Ibogaine produces its effects through simultaneous action on [[glossary:nmda-receptor]], kappa [[substance_class:psychoactive/opioid]], nicotinic, and [[substance_class:pharmacological/serotonin-system|serotonin systems]], generating prolonged visionary and [[substance_class:psychoactive/dissociative]] states. Formally described in 1888{{cite|url=https://powo.science.kew.org/taxon/urn:lsid:ipni.org:names:56090-1|anchor=2140abab}}, ''T. iboga'' is the sacramental plant of the Bwiti religion in Gabon{{cite|doi=10.1007/s12231-018-9410-x|anchor=6c552e7a}}. Western [[glossary:addiction]]-treatment interest began in 1962 when Howard Lotsof reported cessation of opioid [[glossary:withdrawal]] after [[glossary:self-administration]]{{cite|doi=10.1111/dar.13587|anchor=957522d9}}, and the 2024 MISTIC trial demonstrated large [[glossary:effect-size|effect sizes]] for PTSD and traumatic brain injury{{cite|doi=10.1038/s41591-023-02705-w|anchor=5efeb948}}. A 2026 US executive order directed accelerated regulatory review{{cite|doi=10.1038/d41586-026-01286-1|anchor=7312d346}}, though ibogaine remains [[glossary:schedule-i]] at the federal level. [[index:effects|Subjective effects]] include narrative autobiographical visions, dissociative states, [[effect:entity-contact|entity-contact]] phenomena, somatosensory hypersensitivity, and severe [[effect:motor-control-impairment|ataxia]]{{cite|doi=10.1371/journal.pone.0333296|anchor=a3d91df7}}. The experience is predominantly internal and oneirophrenic, lasting 12–24 hours in acute phase with residual effects persisting up to 72 hours due to noribogaine's prolonged [[glossary:half-life]]{{cite|doi=10.1002/jcph.471|anchor=be1dca63}}. Near-universal physical incapacitation, intense [[effect:nausea]], and confrontation with difficult psychological material are characteristic unsought effects{{cite|doi=10.1111/add.15448|anchor=0537e8b1}}. Ibogaine does not produce [[glossary:physical-dependence]], [[glossary:tolerance]], or compulsive [[glossary:redose|redosing]]{{cite|doi=10.1038/tp.2016.71|anchor=a0df3aca}}. The primary safety concern is cardiac: ibogaine and noribogaine block the hERG potassium [[glossary:channel]], producing QTc prolongation that has caused fatal [[glossary:arrhythmia|arrhythmias]] in unsupervised settings{{cite|doi=10.3390/molecules20022208|anchor=42c20d36}}. No controlled dose-response data from randomized trials have been published, and root bark preparations carry additional risk from extreme alkaloid concentration variability (0.6–11.2% ibogaine content){{cite|doi=10.1590/0101-60830000000231|anchor=c616faaf}}.

'''''Iboga''''' (''Tabernanthe iboga'' Baillon, Apocynaceae) — eboka — is a West and Central African rainforest shrub whose root bark is consumed as a powerful psychoactive preparation. Its dominant alkaloid, [[substance:ibogaine]], acts on multiple brain systems simultaneously — including [[glossary:glutamate]], [[substance_class:psychoactive/opioid]], nicotinic, and [[glossary:serotonin]] pathways{{cite|doi=10.1021/jacs.5c06325|anchor=3d5641a2}}. This broad multi-system action produces prolonged visionary and [[substance_class:psychoactive/dissociative]] states unlike any other known plant. Iboga is the sacramental plant of the Bwiti religion in Gabon, where it has been used in initiation and healing ceremonies for generations{{cite|doi=10.1007/s12231-018-9410-x|anchor=15826f58}}. Western interest shifted toward [[glossary:addiction]] medicine in 1962, when Howard Lotsof reported that a single ibogaine dose ended his opioid [[glossary:withdrawal]]{{cite|doi=10.1111/dar.13587|anchor=93fcfb15}}. A landmark 2024 clinical trial showed large reductions in PTSD and [[effect:depression]] in combat veterans, and a 2026 US executive order directed accelerated regulatory review{{cite|doi=10.1038/s41591-023-02705-w|anchor=b1715bf2}}{{cite|doi=10.1038/d41586-026-01286-1|anchor=86967a1e}}. [[index:effects|Subjective effects]] include vivid autobiographical visions, contact with perceived entities, intense body [[glossary:sensitivity]], profound dissociation, and severe [[glossary:motor-coordination|loss of coordination]]{{cite|doi=10.1371/journal.pone.0333296|anchor=39610fcd}}. The experience is predominantly internal and dream-like, lasting 12–24 hours in the acute phase with residual effects persisting up to 72 hours. Near-universal [[effect:nausea]], physical incapacitation, and confrontation with difficult personal memories are characteristic unsought effects{{cite|doi=10.1111/add.15448|anchor=c5b34132}}. Ibogaine does not produce [[glossary:physical-dependence]] or compulsive [[glossary:redose|redosing]]{{cite|doi=10.1038/tp.2016.71|anchor=b26a06d1}}, but the primary [[glossary:acute-risk]] is cardiac — ibogaine slows heart repolarization in a way that can [[glossary:trigger]] fatal [[glossary:arrhythmia|arrhythmias]], particularly without continuous cardiac monitoring{{cite|doi=10.3390/molecules20022208|anchor=e85bc329}}. Co-administration with other heart-affecting drugs or certain [[substance_class:psychoactive/antidepressant|antidepressants]] substantially amplifies this risk. Raw root bark adds unpredictability: ibogaine content varies from 0.6% to 11.2% across samples, making dose control impossible without lab testing{{cite|doi=10.1590/0101-60830000000231|anchor=d7183159}}.

'''''Tabernanthe iboga''''' ('''iboga''', '''eboka''') is a perennial shrub of the family Apocynaceae, native to the rainforest understory of West and Central Africa. Its root bark contains [[substance:ibogaine]], a pentacyclic monoterpene [[substance_class:chemical/indole-alkaloid]] that drives the plant's psychoactive pharmacology through exceptionally broad multi-target [[glossary:receptor-binding|receptor engagement]]. Root bark preparations produce visionary states lasting 12–24 hours in acute phase, with residual effects persisting up to 72 hours due to the prolonged [[glossary:half-life]] of noribogaine, ibogaine's primary [[glossary:active-metabolite]]. First formally described by Baillon in 1888{{cite|url=https://powo.science.kew.org/taxon/urn:lsid:ipni.org:names:56090-1|anchor=bd927c5e}}, ''T. iboga'' is the sacramental plant of the Bwiti religion practiced by the Mitsogho and Fang peoples of Gabon{{cite|doi=10.1007/s12231-018-9410-x|anchor=18acf8fa}}. Western clinical interest began in 1962 when Howard Lotsof reported cessation of [[substance_class:psychoactive/opioid]] [[glossary:withdrawal]] following [[glossary:self-administration]]{{cite|doi=10.1111/dar.13587|anchor=c9ef4e81}}, spurring decades of [[glossary:addiction]] treatment research. The 2024 MISTIC trial demonstrated large [[glossary:effect-size|effect sizes]] for PTSD and traumatic brain injury in veterans{{cite|doi=10.1038/s41591-023-02705-w|anchor=69bd97c7}}, and a 2026 US executive order directed accelerated regulatory review{{cite|doi=10.1038/d41586-026-01286-1|anchor=15609203}} — though ibogaine remains [[glossary:schedule-i]] at the US federal level. Ibogaine acts simultaneously on [[glossary:nmda-receptor|NMDA receptors]] ([[glossary:antagonist]]), kappa opioid [[glossary:receptor|receptors]] ([[glossary:agonist]]), nicotinic α3β4 receptors (antagonist), [[glossary:serotonin-transporter|serotonin transporters]] ([[glossary:inhibitor]]), and [[glossary:vmat2]] (inhibitor) — a profile termed "matrix pharmacology"{{cite|doi=10.1021/jacs.5c06325|anchor=7b7c9e3a}}. [[glossary:cyp2d6]]-mediated O-demethylation produces noribogaine, which has a half-life of 28–48 hours compared to ibogaine's 7–10 hours{{cite|doi=10.1002/jcph.471|anchor=6e0c26af}} and sustains serotonergic and kappa opioid activity well beyond the acute visionary phase. The ibogaine experience is characterized by narrative autobiographical visions, somatosensory hypersensitivity, [[substance_class:psychoactive/dissociative]] states, and transpersonal or [[effect:entity-contact|entity-contact]] phenomena{{cite|doi=10.1371/journal.pone.0333296|anchor=a3940031}}. Severe [[effect:motor-control-impairment|ataxia]] occurs in nearly all subjects at therapeutic doses{{cite|doi=10.1111/add.15448|anchor=be11dad3}}. Effects and duration vary substantially between purified ibogaine HCl and raw root bark, which contains a full alkaloid spectrum at highly variable concentrations. The primary safety concern is cardiac: ibogaine and noribogaine block the hERG potassium [[glossary:channel]], producing clinically significant QTc prolongation — mean maximum 95 ms in one monitored study, with 50% of subjects exceeding QTc 500 ms{{cite|doi=10.1111/add.15448|anchor=7f2c369f}}. Fatal [[glossary:arrhythmia|arrhythmias]] have been reported, predominantly in unsupervised settings{{cite|doi=10.3390/molecules20022208|anchor=92f29c5e}}. Ibogaine does not produce [[glossary:physical-dependence]], [[glossary:tolerance]], or compulsive [[glossary:redose|redosing]] patterns{{cite|doi=10.1038/tp.2016.71|anchor=c06295c4}}. [[glossary:poor-metabolizer|CYP2D6 poor metabolizers]] face approximately double the active [[glossary:moiety]] exposure, making pharmacogenomic screening a prerequisite for safe administration{{cite|doi=10.1002/jcph.471|anchor=e733f8e5}}. Root bark preparations carry additional risk from extreme alkaloid concentration variability (0.6–11.2% ibogaine content) and documented [[glossary:adulterant|adulteration]]{{cite|doi=10.1590/0101-60830000000231|anchor=9640e567}}. No controlled dose-response data from randomized trials have been published, and the long-term neurological effects of therapeutic-dose ibogaine in humans remain uncharacterized.

===Traditional and historical use=== ''Tabernanthe iboga'' was formally described by Henri Ernest Baillon in 1888{{cite|url=https://powo.science.kew.org/taxon/urn:lsid:ipni.org:names:56090-1|anchor=6ffd7599}}. French colonial botanists had encountered the plant in Gabon during the preceding decades, and specimens reached European herbaria before the formal publication. The plant is the sacramental core of the '''Bwiti religion''', practiced primarily by the Mitsogho, Fang, and Babongo peoples of Gabon and neighboring countries{{cite|doi=10.1007/s12231-018-9410-x|anchor=78247bd8}}. Iboga root bark is consumed in two principal traditional contexts{{cite|doi=10.1097/MJT.0000000000001723|anchor=9df14c28}}{{cite|doi=10.1007/s12231-018-9410-x|anchor=ca7f7ebf}}. Large initiation doses are administered over one to three days, producing prolonged visionary states understood as symbolic death-and-rebirth experiences enabling contact with ancestral spirits. Smaller ceremonial doses are taken for healing, guidance, or communal purposes without reaching the full visionary threshold. Sub-visionary doses are also used to combat [[glossary:fatigue]] during extended hunting, treat fever and pain, and as an aphrodisiac{{cite|doi=10.1097/MJT.0000000000001723|anchor=49083cbb}}. No controlled ethnopharmacological studies with quantified alkaloid dosing have been conducted in the traditional Bwiti setting. ===Western discovery and research=== The first alkaloid isolation from ''T. iboga'' root bark is attributed to Dybowsky and Landrin in 1901{{flag|citation-needed}}. The structural chemistry of the four major alkaloids — ibogamine, [[substance:ibogaine]], tabernanthine, and voacangine — was established by Bartlett, Dickel, and Taylor in 1958{{cite|name=bartlett-1958|type=journal|author=Bartlett MF, Dickel DF, Taylor WI|year=1958|title=The Alkaloids of Tabernanthe iboga. Part IV: The Structures of Ibogamine, Ibogaine, Tabernanthine and Voacangine|anchor=27778c8a}}. In the 1930s–1950s, ibogaine was marketed in France as "Lambarene" (5 mg tablets), prescribed as a fatigue remedy and mild [[substance_class:psychoactive/stimulant]]{{flag|citation-needed}}. In 1962, Howard Lotsof, a 19-year-old [[substance:heroin]]-dependent American, self-administered ibogaine and reported cessation of [[substance_class:psychoactive/opioid]] [[effect:craving]] and [[glossary:withdrawal]]{{cite|doi=10.1111/dar.13587|anchor=f83ae0eb}}. He subsequently obtained US patents for ibogaine treatment of multiple substance dependencies. The [[glossary:drug-enforcement-administration|DEA]] classified ibogaine as [[glossary:schedule-i]] in 1967{{flag|citation-needed}}, and in the 1990s Mash et al. initiated Phase I clinical trials at a clinic in St. Kitts, outside US jurisdiction{{cite|pubmed=9668685|anchor=cb7bf586}}{{cite|doi=10.1111/j.1749-6632.2000.tb05213.x|anchor=34680ea8}}. ===Modern era=== Gabon declared ''T. iboga'' a "national cultural heritage strategic reserve" in 2000 and enacted an export ban on wild-harvested iboga in 2019{{cite|url=https://chacruna.net/iboga_conservation/|anchor=6866fba4}}. The 2024 MISTIC trial at Stanford reported large [[glossary:effect-size|effect sizes]] for PTSD (Cohen's ''d'' = 2.54), [[effect:depression]] (''d'' = 2.80), and [[effect:anxiety]] (''d'' = 2.13) in 30 special operations veterans with traumatic brain injury following a magnesium-ibogaine protocol{{cite|doi=10.1038/s41591-023-02705-w|anchor=c4b8002d}}. A 2026 US executive order directed the [[glossary:fda]] and DEA to accelerate ibogaine research and create Right to Try access pathways{{cite|doi=10.1038/d41586-026-01286-1|anchor=10a24b21}}. As of May 2026, nine US states have enacted ibogaine-related legislation, primarily funding clinical research programs{{cite|url=https://www.americansforibogaine.org/legislation/|anchor=fc378f5f}}.

===Traditional and historical use=== ''Tabernanthe iboga'' was formally described by botanist Henri Ernest Baillon in 1888{{cite|url=https://powo.science.kew.org/taxon/urn:lsid:ipni.org:names:56090-1|anchor=04214e76}}. The plant is the sacramental core of the '''Bwiti religion''', practiced by the Mitsogho, Fang, and Babongo peoples of Gabon and neighboring countries{{cite|doi=10.1007/s12231-018-9410-x|anchor=3e626bfc}}. Large initiation doses are administered over one to three days, producing prolonged visionary states understood as symbolic death-and-rebirth and contact with ancestral spirits; smaller doses serve healing and communal purposes{{cite|doi=10.1097/MJT.0000000000001723|anchor=67d3e6cd}}{{cite|doi=10.1007/s12231-018-9410-x|anchor=425f4b49}}. Sub-visionary doses have also been used to reduce [[glossary:fatigue]] during extended hunting, to treat fever and pain, and as an aphrodisiac{{cite|doi=10.1097/MJT.0000000000001723|anchor=731f3e13}}. No controlled ethnopharmacological studies with quantified alkaloid dosing have been conducted in the traditional Bwiti setting. ===Modern era=== In the 1930s–1950s, [[substance:ibogaine]] was marketed in France as "Lambarene" (5 mg tablets) as a fatigue remedy{{flag|citation-needed}}. In 1962, Howard Lotsof self-administered ibogaine and reported it ended his [[substance_class:psychoactive/opioid]] [[effect:craving]] and [[glossary:withdrawal]]{{cite|doi=10.1111/dar.13587|anchor=c644b9f2}}; the [[glossary:drug-enforcement-administration|DEA]] classified ibogaine as [[glossary:schedule-i]] in 1967{{flag|citation-needed}}. The 2024 MISTIC trial at Stanford reported large reductions in PTSD, [[effect:depression]], and [[effect:anxiety]] in veterans with traumatic brain injury{{cite|doi=10.1038/s41591-023-02705-w|anchor=d6ebbce6}}, and a 2026 US executive order directed accelerated regulatory review{{cite|doi=10.1038/d41586-026-01286-1|anchor=ef60fb72}}. Gabon declared ''T. iboga'' a national cultural heritage strategic reserve in 2000 and banned wild-harvest exports in 2019{{cite|url=https://chacruna.net/iboga_conservation/|anchor=b47ed6d6}}.

===Discovery and early record=== The species was formally described by Henri Ernest Baillon in 1888, published in ''Bulletin Mensuel de la Société Linnéenne de Paris''{{cite|url=https://powo.science.kew.org/taxon/urn:lsid:ipni.org:names:56090-1|anchor=0e03f3e4}}. Baillon established the genus ''Tabernanthe'' to accommodate this plant and related taxa within Apocynaceae. French colonial botanists and pharmacologists had encountered ''T. iboga'' in Gabon during the 1850s–1880s period of Central African exploration, with specimens reaching European herbaria before the formal description. The first alkaloid isolation from ''T. iboga'' root bark is attributed to Dybowsky and Landrin in 1901, working within the French colonial pharmacological tradition{{flag|citation-needed}}. The foundational structural chemistry of the four major alkaloids — ibogamine, [[substance:ibogaine]], tabernanthine, and voacangine — was established by Bartlett, Dickel, and Taylor in 1958{{cite|name=bartlett-1958|type=journal|author=Bartlett MF, Dickel DF, Taylor WI|year=1958|title=The Alkaloids of Tabernanthe iboga. Part IV: The Structures of Ibogamine, Ibogaine, Tabernanthine and Voacangine|anchor=f43ca5cc}}. ===Traditional use=== ''Tabernanthe iboga'' is the sacramental plant of the '''Bwiti religion''', practiced primarily by the Mitsogho and Fang peoples of Gabon and neighboring countries, with significant Babongo participation{{cite|doi=10.1007/s12231-018-9410-x|anchor=33e30056}}. The Bwiti religion integrates ancestral veneration, initiation rites, and healing practices into a complex ceremonial structure in which iboga root bark is central. Iboga is consumed in two primary traditional contexts{{cite|doi=10.1097/MJT.0000000000001723|anchor=c5c6e367}}{{cite|doi=10.1007/s12231-018-9410-x|anchor=28fad66b}}. Large initiation doses involve consumption of root bark over 1–3 days in quantities reported as several hundred grams, producing prolonged visionary states lasting 24–48 hours or more. These initiation rites, conducted for young adults entering the Bwiti tradition, are understood as a symbolic death-and-rebirth experience enabling contact with ancestral spirits. Smaller ceremonial doses are taken in ritual settings for healing, guidance, or community purposes without reaching the full visionary threshold. Traditional medicinal uses at sub-visionary doses include combating [[glossary:fatigue]] and hunger during extended hunting, treatment of fever and pain, and use as an aphrodisiac{{cite|doi=10.1097/MJT.0000000000001723|anchor=4b64a55b}}. No controlled ethnopharmacological studies with quantified alkaloid dosing have been conducted in the traditional Bwiti setting. All traditional-dose accounts derive from ethnographic observation. ===Western encounter and pharmaceutical interest=== In the 1930s–1950s, ibogaine was marketed in France as a neuromuscular tonic under the brand name "Lambarene" (5 mg tablets), prescribed as a fatigue remedy and mild [[substance_class:psychoactive/stimulant]]{{flag|citation-needed}}. In 1962, Howard Lotsof, a 19-year-old [[substance:heroin]]-dependent American, self-administered ibogaine and reported that his [[substance_class:psychoactive/opioid]] [[effect:craving]] and [[glossary:withdrawal]] had ceased; he subsequently observed similar effects in multiple acquaintances{{cite|doi=10.1111/dar.13587|anchor=51d02324}}. Lotsof obtained US patents for ibogaine treatment of multiple substance dependencies in 1985–1986. The US [[glossary:drug-enforcement-administration]] classified ibogaine as [[glossary:schedule-i]] under the [[glossary:controlled-substances-act]] in 1967{{flag|citation-needed}}. In the 1990s, the National Institute on Drug Abuse initiated preclinical studies, and Mash et al. began Phase I clinical trials at a clinic in St. Kitts, outside US jurisdiction{{cite|pubmed=9668685|anchor=f0c3501e}}{{cite|doi=10.1111/j.1749-6632.2000.tb05213.x|anchor=76829a62}}. ===Modern era=== In 2000, Gabon declared ''T. iboga'' a "national cultural heritage strategic reserve," and in 2019 enacted an export ban on wild-harvested iboga{{cite|url=https://chacruna.net/iboga_conservation/|anchor=c54531c7}}. The 2024 MISTIC trial at Stanford University reported large [[glossary:effect-size|effect sizes]] for PTSD (Cohen's ''d'' = 2.54), [[effect:depression]] (''d'' = 2.80), and [[effect:anxiety]] (''d'' = 2.13) in 30 special operations veterans with traumatic brain injury following a magnesium-ibogaine protocol{{cite|doi=10.1038/s41591-023-02705-w|anchor=e22fc921}}. A 2026 US executive order directed the [[glossary:fda]] and DEA to accelerate ibogaine research and create pathways for Right to Try access{{cite|doi=10.1038/d41586-026-01286-1|anchor=0462972f}}. As of May 2026, nine US states have enacted ibogaine-related legislation, primarily funding clinical research programs{{cite|url=https://www.americansforibogaine.org/legislation/|anchor=e2e8329a}}.

''Tabernanthe iboga'' Baillon belongs to the family Apocynaceae (dogbane family), a large family of tropical and subtropical flowering plants that also includes oleander, periwinkle, and several other alkaloid-producing genera. The genus ''Tabernanthe'' is small, containing only a handful of recognized species, of which ''T. iboga'' is by far the most pharmacologically significant. The plant is native to the rainforest understory of West and Central Africa, occurring naturally in Gabon, Cameroon, the Republic of Congo, and the Democratic Republic of Congo. It thrives in the shaded, humid conditions beneath the tropical lowland forest canopy. Wild populations face increasing harvest pressure; Gabon enacted an export ban on wild-harvested material in 2019, though cultivation is permitted with Ministry approval{{cite|url=https://chacruna.net/iboga_conservation/|anchor=92fe8400}}. The plant grows slowly, typically requiring several years before root bark accumulates harvestable alkaloid concentrations. ''T. iboga'' is a small evergreen perennial shrub, typically reaching 1.5–2 metres in height under forest conditions. It produces glossy, dark green opposite leaves with prominent midribs. Small white or pinkish tubular flowers develop into oval orange-yellow fruits. The root system is the pharmacologically important structure — psychoactive alkaloids are concentrated in the root bark, with the inner root bark containing the highest concentrations. Stem bark and leaves contain alkaloids at substantially lower levels. Root bark is traditionally harvested by scraping or shaving the inner bark from excavated roots, which is then dried for ceremonial and medicinal use. Because the root system is the harvested part, destructive harvesting kills or severely damages the parent plant — a key factor in wild population decline and the impetus for Gabon's conservation protections.

''Tabernanthe iboga'' belongs to the family Apocynaceae — the dogbane family — which also includes oleander and periwinkle. The genus ''Tabernanthe'' contains only a handful of species; ''T. iboga'' is by far the most pharmacologically significant. The plant grows natively in the rainforest understory of West and Central Africa — Gabon, Cameroon, the Republic of Congo, and the Democratic Republic of Congo. It thrives in shaded, humid conditions beneath the tropical lowland forest canopy. Wild populations face increasing harvest pressure; Gabon banned wild-harvest exports in 2019, though cultivation with Ministry approval is permitted{{cite|url=https://chacruna.net/iboga_conservation/|anchor=8205ab09}}. ''T. iboga'' is a small evergreen shrub, typically reaching 1.5–2 metres in height. It produces glossy dark green opposite leaves, small white or pinkish tubular flowers, and oval orange-yellow fruits. Psychoactive alkaloids concentrate in the root bark — the inner root bark carries the highest levels. Because roots are the harvested part, collection kills or severely damages the parent plant, a key driver of wild population decline.

''Tabernanthe iboga'' is a perennial shrub or small tree, typically 1.5–2 m tall under forest canopy, belonging to the family Apocynaceae{{cite|url=https://powo.science.kew.org/taxon/urn:lsid:ipni.org:names:56090-1|anchor=c845ca80}}. The genus ''Tabernanthe'' was established by Baillon in 1888 to accommodate this species and related taxa. Seven taxonomic synonyms are recognized by Plants of the World Online: ''Iboga vateriana'' Braun-Blanq. & K.Schum., ''Tabernanthe albiflora'' Stapf, ''T. bocca'' Stapf, ''T. mannii'' Stapf, ''T. pubescens'' Pichon, ''T. subsessilis'' Stapf, and ''T. tenuiflora'' Stapf{{cite|url=https://powo.science.kew.org/taxon/urn:lsid:ipni.org:names:56090-1|anchor=4fe2b3f2}}. The species is native to Cameroon, Central African Republic, Republic of Congo, Democratic Republic of Congo, Gabon, Angola, and Cabinda, growing in wet tropical forest understory, riverine and swamp forest, and relatively wet savannah at [[glossary:elevation|elevations]] of 0–1,500 m{{cite|url=https://powo.science.kew.org/taxon/urn:lsid:ipni.org:names:56090-1|anchor=69be64d2}}. Gabon is the primary source of commercially traded iboga material. ===Morphology=== Leaves are shiny, ovate-oblong, arranged in whorls. Flowers are small, white to light pink. Fruits are orange-yellow, ovoid, and edible. The root and root bark contain the highest alkaloid concentrations; alkaloid content decreases progressively from root bark to stem bark to leaves. ===Cultivation and conservation=== Wild harvesting predominates in the commercial supply. Gabon permits cultivation on private land with Ministry approval, but overcollection driven by global [[substance:ibogaine]] demand has depleted wild populations, particularly in Gabon{{cite|url=https://chacruna.net/iboga_conservation/|anchor=8c95dc4c}}. The IUCN Red List classifies ''T. iboga'' as Least Concern based on its wide distribution, though this assessment predates the acceleration in commercial harvest pressure. In 2000, Gabon declared iboga a national cultural heritage strategic reserve, and in 2019 enacted an export ban on wild-harvested material{{cite|url=https://chacruna.net/iboga_conservation/|anchor=7bb6aea0}}. ===Misidentification risk=== ''Voacanga africana'' (also Apocynaceae) contains voacangine, a chemical precursor used for [[glossary:semi-synthetic]] ibogaine production, and products sold as "iboga" have been identified as ''Voacanga'' material{{cite|doi=10.1590/0101-60830000000231|anchor=e5ec13c4}}. ''Tabernaemontana'' species, a closely related genus, contain iboga-type alkaloids including ibogaine and voacangine at ratios distinct from ''T. iboga''{{cite|doi=10.1007/s00425-026-04987-z|anchor=3cec6f85}}. Analytical verification of any material marketed as iboga is essential before clinical or research use.

===Dominant alkaloid: ibogaine=== [[substance:ibogaine]] is a pentacyclic monoterpene [[substance_class:chemical/indole-alkaloid]] and the primary psychoactive constituent of ''T. iboga'' root bark. Concentrations in root bark vary enormously — from 0.6% to 11.2% of dry weight across samples{{cite|doi=10.1590/0101-60830000000231|anchor=f2590b3e}} — making dose prediction from uncharacterized [[glossary:plant-material]] unreliable. Ibogaine engages an unusually broad set of [[glossary:receptor]] targets simultaneously, a profile described as "matrix pharmacology"{{cite|doi=10.1021/jacs.5c06325|anchor=61efe87c}}: [[glossary:nmda-receptor]] [[glossary:antagonism]], kappa [[substance_class:psychoactive/opioid]] receptor agonism, nicotinic α3β4 receptor antagonism{{cite|doi=10.1021/acs.jmedchem.2c01562|anchor=4c8ddeae}}, [[glossary:serotonin-transporter]] [[glossary:inhibition]], and [[glossary:vmat2]] (VMAT2) inhibition{{cite|doi=10.1021/jacs.5c06325|anchor=6cc718eb}}. ===Noribogaine: the sustained metabolite=== [[glossary:cyp2d6]]-mediated [[glossary:metabolism]] converts ibogaine to noribogaine, its primary [[glossary:active-metabolite]]. Noribogaine shares many of ibogaine's receptor targets — including VMAT2 inhibition, serotonin transporter inhibition, and kappa opioid agonism{{cite|doi=10.1021/jacs.5c06325|anchor=bc374712}}{{cite|doi=10.1111/j.1749-6632.1998.tb08237.x|anchor=480ec776}} — but its [[glossary:half-life]] of 28–48 hours far exceeds ibogaine's 7–10 hours{{cite|doi=10.1002/jcph.471|anchor=210b4d7a}}. This prolonged presence sustains serotonergic and kappa opioid activity well beyond the acute visionary phase and extends the window of cardiac risk. ===Minor alkaloids=== Root bark contains several additional indole alkaloids, including tabernanthine, ibogamine, and voacangine. Voacangine is notable for its hERG [[glossary:channel]] [[glossary:blockade]] [[glossary:potency]]{{cite|doi=10.1007/s12012-015-9311-5|anchor=4bac3581}}. Whether these minor co-alkaloids contribute meaningfully to therapeutic or [[glossary:adverse-effects]] at human exposure concentrations has not been determined. Their presence distinguishes the pharmacology of whole root bark from that of purified ibogaine HCl. ===Concentration variability=== Alkaloid concentrations in ''T. iboga'' root bark vary dramatically across individual plants, growing conditions, plant age, and the specific root section harvested. GC/MS analysis of commercial iboga products found unknown substances in almost all samples tested, and one product labeled as "iboga" contained no detectable iboga alkaloids{{cite|doi=10.1590/0101-60830000000231|anchor=b546c175}}. This variability makes standardized dosing from raw root bark impossible without analytical verification.

Root bark of ''T. iboga'' contains a complex mixture of monoterpene [[substance_class:chemical/indole-alkaloid|indole alkaloids]] sharing the ibogane skeleton. [[substance:ibogaine]] is the dominant psychoactive constituent, with six additional characterized alkaloids contributing to the plant's full pharmacological profile. ===Dominant constituent: ibogaine=== Ibogaine (C₂₀H₂₆N₂O; MW 310.4 g/mol; 12-methoxyibogamine) is a pentacyclic monoterpene indole alkaloid — an indolethylamine embedded in a cage-like pentacyclic framework. GC/MS analysis of 16 commercial iboga-derived products found ibogaine content of 0.6–11.2% in root bark samples, 8.2–32.9% in total alkaloid extracts, and 61.5–73.4% in purified ibogaine HCl preparations{{cite|doi=10.1590/0101-60830000000231|anchor=9c81318d}}. This nearly 20-fold range in root bark ibogaine concentration reflects variability related to geographic origin, plant age, plant part harvested, season, and post-harvest handling. ===Primary active metabolite: noribogaine=== Noribogaine (12-hydroxyibogamine; C₁₉H₂₄N₂O; MW 296.4 g/mol) is formed [[glossary:in-vivo|in vivo]] by [[glossary:cyp2d6]]-mediated O-demethylation of ibogaine{{cite|doi=10.1002/jcph.471|anchor=1c0ca1c8}}. Though not present in the [[glossary:plant-material]] itself, noribogaine is pharmacologically critical: it has a [[glossary:half-life]] of 28–48 hours compared to ibogaine's 7–10 hours, sustains [[substance_class:pharmacological/serotonin-reuptake-inhibitor]] and kappa [[substance_class:psychoactive/opioid]] agonism, and is responsible for prolonged QTc effects observed 24–72 hours post-administration{{cite|doi=10.1007/s12012-015-9311-5|anchor=18b42dbd}}{{cite|doi=10.1111/add.70319|anchor=ff2cdf96}}. ===Minor alkaloids=== Six additional alkaloids have been characterized in ''T. iboga'' root bark{{cite|doi=10.1590/0101-60830000000231|anchor=d05a337e}}{{cite|name=bartlett-1958|type=journal|author=Bartlett MF, Dickel DF, Taylor WI|year=1958|title=The Alkaloids of Tabernanthe iboga. Part IV: The Structures of Ibogamine, Ibogaine, Tabernanthine and Voacangine|anchor=48fec9bb}}: * '''Tabernanthine''' (C₂₀H₂₆N₂O; MW 310.4) — structural [[glossary:isomer]] of ibogaine differing in methoxy group position (C-6 vs. C-7) * '''Ibogamine''' (C₁₉H₂₄N₂; MW 280.4) — desmethoxy [[glossary:structural-analog]] lacking the methoxy group * '''Voacangine''' — coronaridine carboxymethyl ester; demonstrates hERG [[glossary:blockade]] with IC₅₀ of approximately 2.25 μM{{cite|doi=10.1007/s12012-015-9311-5|anchor=5a298605}}; also serves as a [[glossary:semi-synthetic]] ibogaine precursor * '''Coronaridine''' — biosynthetic precursor to ibogaine in the indole alkaloid pathway; CYP71 family [[glossary:enzyme|enzymes]] catalyze C19-[[glossary:hydroxylation]] of coronaridine in related Apocynaceae species{{cite|doi=10.1007/s00425-026-04987-z|anchor=80e654b8}} * '''Ibogaline''' (6-methoxytabernanthine) — minor alkaloid The in vivo pharmacodynamic contributions of tabernanthine, ibogamine, coronaridine, and ibogaline at typical human exposure concentrations are not well-characterized; published data are largely limited to [[glossary:in-vitro|in vitro]] [[glossary:receptor-binding]] studies. ===Preparation effects on constituent ratios=== Raw root bark delivers the full alkaloid spectrum at highly variable concentrations. Total alkaloid (TA) extracts concentrate all alkaloids proportionally but remain multi-constituent preparations. Purified ibogaine HCl (61.5–73.4% ibogaine content) removes most co-alkaloids, eliminating the voacangine-mediated hERG contribution beyond ibogaine itself{{cite|doi=10.1590/0101-60830000000231|anchor=02e3ed66}}. Aqueous decoctions are not a traditional preparation method for ''T. iboga'' — root bark is typically consumed by chewing or as dried powder{{cite|doi=10.1097/MJT.0000000000001723|anchor=987f529d}}. ===Biosynthesis=== The biosynthetic pathway from strictosidine (common to all monoterpene indole alkaloids) to iboga alkaloids has been substantially elucidated. CYP71 family enzymes (VCOH1-3) catalyze C19-hydroxylation of coronaridine and voacangine in ''Voacanga thouarsii''{{cite|doi=10.1007/s00425-026-04987-z|anchor=deb0c976}}, indicating convergent enzymatic solutions for iboga alkaloid production across Apocynaceae genera.

===Dominant alkaloid: ibogaine=== [[substance:ibogaine]] is the primary psychoactive constituent of ''T. iboga'' root bark. Concentrations vary enormously — from 0.6% to 11.2% of dry weight across samples{{cite|doi=10.1590/0101-60830000000231|anchor=e14ce290}} — making dose prediction from uncharacterized [[glossary:plant-material]] unreliable. Ibogaine acts on [[glossary:serotonin]], [[glossary:glutamate]], kappa [[substance_class:psychoactive/opioid]], and nicotinic systems simultaneously{{cite|doi=10.1021/jacs.5c06325|anchor=8ab5fed3}}{{cite|doi=10.1021/acs.jmedchem.2c01562|anchor=e6d73f5b}}, a profile described as "matrix pharmacology"{{cite|doi=10.1021/jacs.5c06325|anchor=c7f5b70a}} — no single target explains the full experience. ===Noribogaine: the sustained metabolite=== The liver converts ibogaine into noribogaine, its primary [[glossary:active-metabolite]]. Noribogaine shares ibogaine's activity at serotonin and kappa opioid targets{{cite|doi=10.1021/jacs.5c06325|anchor=00e9567d}}{{cite|doi=10.1111/j.1749-6632.1998.tb08237.x|anchor=ac9b84f8}}, but its [[glossary:half-life]] of 28–48 hours far exceeds ibogaine's 7–10 hours{{cite|doi=10.1002/jcph.471|anchor=95e0f1ee}}. Its effects — and cardiac risks — persist well beyond the acute visionary phase. ===Minor alkaloids and variability=== Root bark also contains tabernanthine, ibogamine, and voacangine. Voacangine adds its own cardiac risk through the same [[glossary:channel]]-blocking mechanism{{cite|doi=10.1007/s12012-015-9311-5|anchor=7b135468}}. Whether these minor alkaloids meaningfully alter the therapeutic or adverse effect profile at human doses has not been determined. GC/MS analysis of commercial iboga products found unknown substances in almost all samples tested, and one product labeled "iboga" contained no detectable iboga alkaloids{{cite|doi=10.1590/0101-60830000000231|anchor=3c6af5a9}}.

===Where it acts=== [[substance:ibogaine]]'s broad [[glossary:receptor]] profile produces a convergent assault on multiple [[glossary:neurotransmitter]] systems. It simultaneously modulates [[glossary:serotonin-release]] and [[glossary:reuptake]] through a [[glossary:dual-mechanism]] — inhibiting both [[glossary:vmat2]] (the vesicular [[glossary:transporter]]) and [[glossary:serotonin-transporter]] (the [[glossary:plasma]] membrane transporter) — a pattern termed "SynRI"{{cite|doi=10.1021/jacs.5c06325|anchor=06c0cbeb}}. At the same time, it blocks [[glossary:nmda-receptor]] [[glossary:glutamate]] receptors{{cite|doi=10.1111/j.1749-6632.1998.tb08239.x|anchor=a94a9cbf}}, activates kappa [[substance_class:psychoactive/opioid]] receptors{{cite|doi=10.1111/j.1749-6632.1998.tb08237.x|anchor=dd8547dc}}, antagonizes nicotinic α3β4 receptors{{cite|doi=10.1021/acs.jmedchem.2c01562|anchor=149ca263}}, and functions as a biased [[glossary:partial-agonist]] at [[glossary:mu-opioid-receptor|mu-opioid receptors]]{{cite|doi=10.3390/ph19030397|anchor=1a491223}}. [[glossary:5-ht2a]] receptor involvement is supported by knockout mouse studies{{cite|doi=10.3390/ijms25020687|anchor=fe0ef8d9}}. Noribogaine sustains much of this activity over its 28–48-hour [[glossary:half-life]]{{cite|doi=10.1002/jcph.471|anchor=b38316b5}}. ===What it changes=== The anti-addictive potential of ibogaine appears to arise from several converging mechanisms{{cite|doi=10.1111/j.1749-6632.1998.tb08237.x|anchor=24b5a6c9}}{{cite|doi=10.1017/neu.2026.10059|anchor=852f6648}}: acute suppression of [[glossary:dopamine]] in the [[glossary:nucleus-accumbens]] reduces drug-[[glossary:reward]] [[glossary:reinforcement]]; [[glossary:upregulation]] of glial cell line-derived neurotrophic factor (GDNF) in the [[glossary:ventral-tegmental-area]] reduces [[substance:alcohol]] [[glossary:self-administration]] in [[glossary:animal-model|animal models]]{{cite|doi=10.1523/jneurosci.3959-04.2005|anchor=52b3a0ab}}; and NMDA [[glossary:antagonism]] attenuates opioid and [[substance_class:psychoactive/stimulant]] [[glossary:withdrawal]] through glutamatergic normalization{{cite|doi=10.1111/j.1749-6632.1998.tb08237.x|anchor=4ea59970}}{{cite|doi=10.1111/j.1749-6632.1998.tb08239.x|anchor=b12129c3}}. Structural brain changes in the MISTIC [[glossary:cohort]] at one month post-treatment included increased cortical thickness in 11 regions, subcortical expansion in 8 regions, and a 1.3-year reduction in estimated brain age{{cite|doi=10.1016/j.isci.2026.115121|anchor=76a528d2}}. {{DiscoverMore|Open Questions}} The relative contribution of ibogaine versus noribogaine to anti-addictive [[glossary:efficacy]] remains unresolved — the two compounds have overlapping but distinct receptor profiles and strikingly different durations of action. Whether the minor co-alkaloids in root bark meaningfully alter the therapeutic or adverse effect profile at human doses is unknown. Long-term Purkinje cell effects in humans at therapeutic doses remain uncharacterized, and the remyelination [[glossary:hypothesis]]{{cite|doi=10.1017/neu.2026.10059|anchor=f6cdca6d}} awaits direct human evidence. {{/DiscoverMore}}

===Where it acts=== [[substance:ibogaine]] acts on multiple brain systems at once. It blocks [[glossary:glutamate]] [[glossary:receptor|receptors]]{{cite|doi=10.1111/j.1749-6632.1998.tb08239.x|anchor=c2806245}}, activates kappa [[substance_class:psychoactive/opioid]] receptors{{cite|doi=10.1111/j.1749-6632.1998.tb08237.x|anchor=c6b773a4}}, blocks [[glossary:nicotinic-acetylcholine-receptor|nicotinic receptors]]{{cite|doi=10.1021/acs.jmedchem.2c01562|anchor=f739567f}}, and inhibits [[glossary:reuptake|serotonin reuptake]] through two separate pathways simultaneously{{cite|doi=10.1021/jacs.5c06325|anchor=9cdc0b8e}}. Evidence from knockout mouse studies also points to [[glossary:5-ht2a]] involvement{{cite|doi=10.3390/ijms25020687|anchor=aaac8d9f}}. Noribogaine sustains much of this activity over its 28–48-hour [[glossary:half-life]]{{cite|doi=10.1002/jcph.471|anchor=0b0701d1}}. ===What it changes=== Ibogaine's anti-addictive potential appears to arise from several overlapping mechanisms{{cite|doi=10.1111/j.1749-6632.1998.tb08237.x|anchor=129a9042}}{{cite|doi=10.1017/neu.2026.10059|anchor=9247767d}}: it acutely suppresses [[glossary:dopamine]] in the brain's [[glossary:reward]] center, and it [[glossary:trigger|triggers]] release of a growth factor in a region linked to drug-seeking behavior, reducing [[substance:alcohol]] [[glossary:self-administration]] in [[glossary:animal-model|animal models]]{{cite|doi=10.1523/jneurosci.3959-04.2005|anchor=ec8abe18}}. In the MISTIC trial, brain imaging at one month post-treatment showed increased cortical thickness in 11 regions, subcortical expansion in 8 regions, and an estimated 1.3-year reduction in brain age{{cite|doi=10.1016/j.isci.2026.115121|anchor=2492bf5d}}. {{DiscoverMore|Open Questions}} Whether ibogaine or noribogaine drives the anti-addictive effect remains unresolved — they have overlapping but distinct receptor profiles and very different durations of action. Whether minor co-alkaloids in root bark alter therapeutic or adverse outcomes at human doses is unknown. Long-term effects on cerebellar [[glossary:neuron|neurons]] in humans at therapeutic doses have not been established, and a proposed remyelination mechanism{{cite|doi=10.1017/neu.2026.10059|anchor=461ffb41}} awaits direct human evidence. {{/DiscoverMore}}

The [[substance:ibogaine]] experience is qualitatively unlike either [[glossary:serotonergic-psychedelics|classical serotonergic psychedelics]] or [[substance_class:psychoactive/dissociative]] anesthetics, though it shares features with both. Root bark and purified ibogaine HCl both produce an extended, largely internal visionary state dominated by narrative autobiographical sequences, [[effect:entity-contact|entity encounters]], and intense somatic load{{cite|doi=10.1371/journal.pone.0333296|anchor=c079d289}}. The experience is heavily dose-dependent and preparation-dependent: raw root bark delivers the full alkaloid spectrum at unpredictable concentrations, potentially shifting both character and duration compared to [[glossary:pharmaceutical-grade|pharmaceutical-grade]] ibogaine HCl. Set, setting, and intention strongly modulate the psychological content, though the physical [[glossary:intensity]] — severe [[effect:motor-control-impairment|ataxia]], [[effect:nausea]], [[glossary:sensitivity]] to sound and light — is largely invariant above threshold doses{{cite|doi=10.1111/add.15448|anchor=8a193c21}}. Ibogaine occupies a singular position among psychoactive plants. Its closest pharmacological parallels are [[glossary:synthetic]] analogs (tabernanthalog, oxa-noribogaine) rather than other botanical preparations. The 12–24-hour acute duration, residual effects persisting to 72 hours, severe physical incapacitation, and mandatory cardiac monitoring requirements distinguish it from all commonly discussed [[substance_class:psychoactive/psychedelic]] or dissociative substances.

{{Warning}}[[substance:ibogaine]] preparations carry serious cardiac risk. QTc prolongation exceeding 500 ms occurs in approximately half of subjects at therapeutic doses. All ibogaine administration should occur under continuous cardiac monitoring with immediate access to defibrillation. This section describes preparation forms for informational purposes and does not constitute medical guidance.{{/Warning}} ===Ibogaine HCl (oral, clinical/therapeutic)=== Purified ibogaine hydrochloride is the preparation used in clinical research and most medically supervised treatment settings. Ibogaine content ranges from 61.5–73.4% in commercially available preparations{{cite|doi=10.1590/0101-60830000000231|anchor=3edbe84e}}, with [[glossary:pharmaceutical-grade|pharmaceutical-grade]] material approaching higher purity. '''Ibogaine HCl (oral):''' The therapeutic [[glossary:dose-range]] established in open-label [[glossary:clinical-study|clinical studies]] is 10–20 mg/kg{{cite|doi=10.1111/add.15448|anchor=37047863}}{{cite|doi=10.3389/fphar.2018.00529|anchor=106f7a9c}}. A low exploratory dose of 20 mg total (~0.2–0.3 mg/kg) produced no psychoactive effects in a pharmacokinetic study{{cite|doi=10.1002/jcph.471|anchor=14045d18}}. Doses up to 25 mg/kg have been reported in some [[glossary:addiction]] treatment settings{{cite|doi=10.1177/02698811261443674|anchor=bce662ed}}. Onset: 1–3 h. [[glossary:peak]] effects: 3–8 h. Acute duration: 12–24 h. Residual effects ([[effect:insomnia]], heightened sensory [[glossary:sensitivity]]) may persist 24–48 h. {{flag|safety-citation-needed}} No standardized dose-response data from [[glossary:placebo|placebo-controlled]] randomized trials have been published. The 10–20 mg/kg range derives from open-label observational studies and [[glossary:case-series]]. ===Magnesium-ibogaine (MISTIC protocol)=== The MISTIC study (NCT04313712) administered ibogaine with magnesium co-supplementation as a cardiac risk mitigation strategy in 30 male special operations veterans with traumatic brain injury{{cite|doi=10.1038/s41591-023-02705-w|anchor=38ae65f8}}. Specific ibogaine doses were not reported in the published paper. No unexpected or serious [[glossary:adverse-events]] were observed in this medically supervised setting. Significant improvements were reported in PTSD (Cohen's ''d'' = 2.54), [[effect:depression]] (''d'' = 2.80), and [[effect:anxiety]] (''d'' = 2.13) at one month{{cite|doi=10.1038/s41591-023-02705-w|anchor=fc6ddbb9}}. ===Root bark (oral, traditional and underground use)=== Raw root bark is the traditional preparation consumed in Bwiti ceremonies and in many underground treatment settings. Root bark is typically chewed or taken as dried powder — aqueous decoctions are not a standard preparation method for this plant{{cite|doi=10.1097/MJT.0000000000001723|anchor=b858fbd8}}. Ibogaine content in root bark ranges from 0.6–11.2%{{cite|doi=10.1590/0101-60830000000231|anchor=0b016f30}}, making milligram-equivalent dosing impossible without prior analytical characterization of the specific material. Traditional Bwiti initiation reportedly involves consumption of several hundred grams of root bark over 1–3 days{{cite|doi=10.1007/s12231-018-9410-x|anchor=b3377d3a}}, but no published studies have quantified alkaloid intake during traditional ceremonies. Root bark delivers the full spectrum of iboga alkaloids (ibogaine, tabernanthine, ibogamine, voacangine, coronaridine, ibogaline) at ratios that vary with the source material. {{flag|safety-citation-needed}} No published dose-response data with verified alkaloid content characterize traditional or informal root bark use. Dose values from traditional-use reports cannot be converted to ibogaine milligram equivalents without product-specific analysis. ===Total alkaloid extract (oral)=== Total alkaloid (TA) extracts concentrate all alkaloids present in root bark, with ibogaine content of 8.2–32.9% across analyzed samples{{cite|doi=10.1590/0101-60830000000231|anchor=fafb2078}}. One sample of purified total alkaloids HCl contained 73.7% ibogaine{{cite|doi=10.1590/0101-60830000000231|anchor=1b90f015}}. TA extracts remain multi-constituent preparations that deliver voacangine, coronaridine, and other co-alkaloids alongside ibogaine, potentially modifying both therapeutic and adverse effect profiles relative to purified ibogaine HCl. ===Potency variability=== Commercial iboga products show extreme and unpredictable concentration variability. In a GC/MS analysis of 16 products from treatment providers and online vendors, one sample labeled as "iboga" contained no detectable iboga alkaloids{{cite|doi=10.1590/0101-60830000000231|anchor=57c38fa8}}. Unknown substances were detected in almost all samples. This variability makes dose titration from uncharacterized material a significant [[glossary:overdose]] risk. Analytical verification by GC/MS or HPLC before any clinical use is essential. See the Dose by preparation card for a summary of published dose ranges by preparation type.

The [[substance:ibogaine]] experience is qualitatively unlike either [[glossary:serotonergic-psychedelics|classical psychedelics]] or [[substance_class:psychoactive/dissociative]] anesthetics, though it shares features with both. It is predominantly internal — narrative autobiographical visions, encounters with perceived entities, and intense [[glossary:body-load]] dominate the acute phase{{cite|doi=10.1371/journal.pone.0333296|anchor=55f2fd03}}. The physical [[glossary:intensity]] — severe [[glossary:motor-coordination|loss of coordination]], [[effect:nausea]], and [[glossary:sensitivity]] to sound and light — is largely constant above threshold doses, regardless of set or setting{{cite|doi=10.1111/add.15448|anchor=42fd136f}}. No commonly used [[substance_class:psychoactive/psychedelic]] plant shares ibogaine's overall profile. Its closest pharmacological parallels are [[glossary:synthetic]] analogs, not other botanicals. The 12–24-hour acute duration, residual effects stretching to 72 hours, near-total physical incapacitation, and cardiac monitoring requirements distinguish it from all other substances discussed on this platform.

Raw root bark, total alkaloid extract, and purified [[substance:ibogaine]] HCl are pharmacologically distinct products with non-overlapping [[glossary:dose-range|dose ranges]]. Preparation type strongly determines onset, duration, gastrointestinal burden, and cardiac risk profile. ====Raw root bark (oral)==== Dried inner root bark is chewed or swallowed as shavings or coarse powder. Ibogaine content ranges from 0.6% to 11.2% of dry weight{{cite|doi=10.1590/0101-60830000000231|anchor=0f57a249}} — dose prediction from uncharacterized bark is impossible. Traditional Bwiti initiation doses involve consumption over 1–3 days in quantities reported as several hundred grams{{cite|doi=10.1097/MJT.0000000000001723|anchor=89302abe}}. Onset is gradual (1–3 hours); acute visionary phase lasts 12–24 hours; residual effects persist up to 72 hours. [[effect:nausea]] and [[effect:vomiting]] are near-universal. Taste is intensely bitter. ====Total alkaloid extract (oral)==== '''Total alkaloid extract''' (TA) concentrates the full alkaloid spectrum, typically at roughly 15–35% total alkaloid content by weight. Doses are lower by weight than raw bark, but batch-to-batch variability in alkaloid ratios and total [[glossary:potency]] remains. Onset, duration, and effect character resemble raw bark. Gastrointestinal [[glossary:distress]] is somewhat reduced due to lower material volume. The full minor alkaloid profile — including voacangine — is retained. ====Purified ibogaine HCl (oral)==== '''Ibogaine hydrochloride''' is the [[glossary:pharmaceutical-grade|pharmaceutical-grade]] preparation used in clinical settings. [[glossary:clinical-study|Clinical studies]] have used doses of 10–20 mg/kg{{cite|doi=10.1111/add.15448|anchor=4b72f1b8}}{{cite|doi=10.1002/jcph.471|anchor=ad6a419f}}. Onset occurs approximately 1.5–4 hours after [[glossary:ingestion]]{{cite|doi=10.1002/jcph.471|anchor=3dc75f0d}}{{cite|doi=10.1177/02698811241237873|anchor=8aaa81d2}}, with an acute phase lasting 12–24 hours. Cardiac risk (QTc prolongation) requires continuous monitoring{{cite|doi=10.1111/add.15448|anchor=aa251732}}. The experience tends to be described as "cleaner" than raw bark — less gastrointestinal distress, equivalent visionary [[glossary:intensity]] at equivalent ibogaine doses. ====Magnesium-ibogaine combination==== The MISTIC trial co-administered magnesium with ibogaine{{cite|doi=10.1038/s41591-023-02705-w|anchor=cf872ec3}}. Magnesium may modulate the same cardiac [[glossary:channel]] ibogaine blocks, potentially providing a cardioprotective effect — though this specific combination has not been independently validated in controlled cardiac safety studies. Per-preparation dose tiers, timelines, and [[glossary:bioavailability]] data are in the '''Dose · by preparation''' card on this page.

====Toxicity==== '''Cardiac toxicity''' is the primary [[glossary:acute-risk]] across all [[substance:ibogaine]]-containing preparations. Ibogaine and noribogaine block the cardiac [[glossary:channel]] that governs heart repolarization{{cite|doi=10.1007/s12012-015-9311-5|anchor=9f825566}}. In a [[glossary:clinical-study]] of 14 patients receiving 10 mg/kg ibogaine HCl, average maximum QT interval prolongation was 95 ms (range 29–146 ms), and 50% of subjects exceeded the dangerous 500 ms threshold{{cite|doi=10.1111/add.15448|anchor=06b49be1}}. In 6 of 14 subjects, elevated QT prolongation persisted beyond 24 hours{{cite|doi=10.1111/add.15448|anchor=aba555e1}}. Fatal [[glossary:arrhythmia|cardiac arrhythmias]] have occurred, predominantly in unsupervised settings without cardiac monitoring{{cite|doi=10.3390/molecules20022208|anchor=daaf667a}}{{cite|doi=10.1111/add.70319|anchor=f291bc8e}}. Sudden death has been reported up to 72 hours after [[glossary:ingestion]]{{cite|doi=10.3390/molecules20022208|anchor=18605df7}}{{cite|doi=10.1007/s12012-015-9311-5|anchor=c6cf81e0}} — the cardiac risk window extends far beyond the visionary phase. The UK National Poisons Information Service documents real-world ibogaine [[glossary:toxicity]] presentations over a 10-year [[glossary:case-series]]{{cite|doi=10.1080/15563650.2024.2447500|anchor=6375133c}}. Commercial iboga products present significant quality concerns. GC/MS analysis of 16 products found unknown substances in almost all samples, and one product labeled "iboga" contained no detectable iboga alkaloids{{cite|doi=10.1590/0101-60830000000231|anchor=7e98a7fa}}. No jurisdiction mandates certified laboratory testing or Certificate of Analysis requirements for iboga products. Independent analytical verification is the only available risk mitigation{{cite|doi=10.1590/0101-60830000000231|anchor=4b5ee02f}}.{{flag|safety-citation-needed}} In rats, ibogaine causes degeneration of cerebellar [[glossary:neuron|neurons]] at high doses{{cite|pubmed=9348351|anchor=1c9d539b}}{{cite|pubmed=8377927|anchor=5cd00663}}. At 40 mg/kg — within the anti-addictive [[glossary:dose-range]] in [[glossary:rodent-model|rodents]] — this effect was not observed{{cite|pubmed=8930373|anchor=b01931e6}}. In humans, severe transient [[glossary:motor-coordination|loss of coordination]] was observed in all 14 patients in the clinical safety study{{cite|doi=10.1111/add.15448|anchor=63476bfe}}. The MISTIC [[glossary:cohort]] showed structural brain improvements rather than deterioration at one month{{cite|doi=10.1016/j.isci.2026.115121|anchor=3e0fd60c}}; long-term effects at therapeutic doses have not been established. ====Psychological Risks==== [[effect:anxiety]], fear, and confrontation with difficult autobiographical material are commonly reported during the acute phase{{cite|doi=10.1080/02791072.2019.1598603|anchor=f19f053f}}. These experiences form a documented factor in the Ibogaine Experience Scale (N=499){{cite|doi=10.1371/journal.pone.0333296|anchor=83f351d0}}. Individuals with pre-existing psychotic spectrum [[glossary:disorder|disorders]] face risk of acute psychological decompensation. [[effect:delirium]]-like states may occur at high doses, and an exaggerated startle response has been reported during the residual phase. Long-term [[glossary:psychological-risk|psychological risks]] in the general population remain uncharacterized beyond [[glossary:case-report|case reports]] and observational cohorts.{{flag|safety-citation-needed}} ====Tolerance & Dependence==== Ibogaine does not produce classical [[glossary:tolerance]] or [[glossary:physical-dependence]]. No [[glossary:withdrawal]] has been documented in humans{{cite|doi=10.1016/j.jsat.2021.108717|anchor=356076e7}}{{cite|doi=10.1111/j.1749-6632.1998.tb08237.x|anchor=dbe63452}}. Traditional Bwiti use is intermittent — not daily. [[glossary:animal-model|Animal studies]] do not show [[glossary:self-administration]], and no compulsive [[glossary:redose|redosing]] patterns have been observed{{cite|doi=10.1038/tp.2016.71|anchor=76bae5ff}}. The experience is typically described as physically demanding rather than recreationally reinforcing. ====Drug Interactions==== '''CYP2D6 inhibitors''' (paroxetine, fluoxetine, bupropion, quinidine) approximately double combined ibogaine + noribogaine exposure, proportionally increasing cardiac risk{{cite|doi=10.1002/jcph.471|anchor=c7269fea}}. '''QT-prolonging drugs''' ([[substance:methadone]], tricyclic [[substance_class:psychoactive/antidepressant|antidepressants]], [[substance_class:psychoactive/antipsychotic|antipsychotics]], certain SSRIs, some antihistamines) compound ibogaine's cardiac effect and elevate risk of a dangerous arrhythmia called torsades de pointes{{cite|doi=10.3390/molecules20022208|anchor=0ecc6e9e}}{{cite|doi=10.1111/add.70319|anchor=32d3ca9b}}. '''Opioids''' interact in a timing-dependent and complex way. Ibogaine may precipitate or attenuate [[substance_class:psychoactive/opioid]] withdrawal depending on timing relative to last opioid dose{{cite|doi=10.1111/j.1749-6632.1998.tb08237.x|anchor=dd8f64b2}}{{cite|doi=10.3389/fphar.2018.00529|anchor=d2323619}}. Post-ibogaine loss of opioid tolerance increases [[glossary:overdose]] risk on resumption{{cite|doi=10.1097/ADM.0000000000001645|anchor=8333867e}}. '''Serotonergic agents:''' Ibogaine's [[substance_class:pharmacological/serotonin-reuptake-inhibitor]] creates a theoretical risk of a dangerous overheating and [[glossary:seizure]] response when combined with MAOIs or [[glossary:serotonin]] [[glossary:releasing-agent|releasers]]{{cite|doi=10.1021/jacs.5c06325|anchor=27725eff}}. {{flag|safety-citation-needed}} No published clinical case report of ibogaine-induced [[glossary:serotonin-syndrome]] was identified. ====Contraindications==== Pre-existing cardiac conditions — QT prolongation, arrhythmia, structural heart disease, or heart failure — are absolute [[glossary:contraindication|contraindications]]{{cite|doi=10.1007/s12012-015-9311-5|anchor=4bfab0a7}}{{cite|doi=10.1111/add.15448|anchor=dec1a30c}}. [[glossary:poor-metabolizer|CYP2D6 poor metabolizers]] face approximately double the active compound exposure, substantially increasing cardiac and neurological risk{{cite|doi=10.1002/jcph.471|anchor=78af9b09}}{{cite|doi=10.1111/add.70319|anchor=ad5a7a3a}}. Severe [[glossary:hepatic-impairment|liver impairment]], uncorrected electrolyte abnormalities (particularly low potassium or magnesium){{cite|doi=10.1007/s00406-023-01590-1|anchor=31c16e35}}, personal or family history of psychotic spectrum disorders{{cite|doi=10.1007/s00406-023-01590-1|anchor=cf8bf1a1}}, [[glossary:pregnancy]], and active opioid maintenance therapy without supervised tapering{{cite|doi=10.1097/ADM.0000000000001645|anchor=e6120741}} are additional contraindications. Concurrent QT-prolonging [[glossary:medication|medications]] must be discontinued with appropriate washout periods before any ibogaine administration.

====Raw root bark (oral)==== The traditional preparation is dried inner root bark, consumed by chewing or swallowing as shavings or coarse powder. [[substance:ibogaine]] content ranges from 0.6% to 11.2% of dry weight{{cite|doi=10.1590/0101-60830000000231|anchor=cd7c28e9}}, making dose prediction from uncharacterized bark impossible. Traditional Bwiti initiation doses involve consumption of root bark over 1–3 days in quantities reported as several hundred grams{{cite|doi=10.1097/MJT.0000000000001723|anchor=6fe3634e}}. Onset is gradual (1–3 hours), with the acute visionary phase lasting 12–24 hours and residual effects persisting up to 72 hours. [[effect:nausea]] and [[effect:vomiting]] are near-universal with raw bark due to the volume of [[glossary:plant-material]] required and the presence of the full alkaloid spectrum. The taste is intensely bitter. ====Total alkaloid extract (oral)==== '''Total alkaloid extract''' (sometimes labeled "TA") is a semi-purified preparation that concentrates the full alkaloid spectrum of the root bark, typically reported at roughly 15–35% total alkaloid content by weight. TA delivers a pharmacological profile closer to whole root bark than to purified ibogaine HCl, retaining the minor co-alkaloids (tabernanthine, ibogamine, voacangine). Doses are substantially lower by weight than raw bark due to concentration, but the same variability problem applies — alkaloid ratios and total [[glossary:potency]] differ between batches. Onset, duration, and effect character resemble root bark, with somewhat reduced gastrointestinal [[glossary:distress]] due to lower material volume. ====Purified ibogaine HCl (oral)==== '''Ibogaine hydrochloride''' is the [[glossary:pharmaceutical-grade|pharmaceutical-grade]] preparation used in most clinical and clinic settings. It delivers a single pharmacokinetically defined compound, eliminating the variability introduced by minor co-alkaloids and batch inconsistency. [[glossary:clinical-study|Clinical studies]] have used doses in the range of 10–20 mg/kg{{cite|doi=10.1111/add.15448|anchor=638616c3}}{{cite|doi=10.1002/jcph.471|anchor=1c0648f0}}. Onset occurs at approximately 1.5–4 hours post-[[glossary:ingestion]]{{cite|doi=10.1002/jcph.471|anchor=ab83e4cb}}{{cite|doi=10.1177/02698811241237873|anchor=34c13058}}, with the acute phase lasting 12–24 hours. Cardiac risk (QTc prolongation) is present with purified ibogaine HCl and requires continuous monitoring{{cite|doi=10.1111/add.15448|anchor=6b39deb5}}. The experience tends to be described as "cleaner" than raw bark, with less gastrointestinal distress but equivalent visionary [[glossary:intensity]] at equivalent ibogaine doses. ====Magnesium-ibogaine combination==== The MISTIC trial protocol co-administered magnesium with ibogaine in a supervised clinical setting{{cite|doi=10.1038/s41591-023-02705-w|anchor=456ee742}}. The rationale for magnesium co-administration includes its role as a natural hERG [[glossary:channel]] modulator and potential cardioprotective effect, though this specific combination has not been independently validated in controlled cardiac safety studies. Per-preparation dose tiers, timelines, and [[glossary:bioavailability]] data are in the '''Dose · by preparation''' card on this page.

====Toxicity==== '''Cardiac toxicity''' is the primary acute safety concern for all [[substance:ibogaine]]-containing preparations. Ibogaine and noribogaine block the hERG potassium [[glossary:channel]] that governs cardiac repolarization{{cite|doi=10.1007/s12012-015-9311-5|anchor=e662b577}}. In an open-label study of 14 [[substance_class:psychoactive/opioid]]-dependent patients receiving 10 mg/kg ibogaine HCl, mean maximum QTc prolongation was 95 ms (range 29–146 ms), and 50% of subjects exceeded QTc 500 ms{{cite|doi=10.1111/add.15448|anchor=572f28fe}}. In 6 of 14 subjects, QTc remained above 450 ms beyond 24 hours post-administration{{cite|doi=10.1111/add.15448|anchor=03fc954d}}. Fatal [[glossary:arrhythmia|cardiac arrhythmias]] have been reported, with deaths occurring predominantly in unsupervised settings without continuous cardiac monitoring{{cite|doi=10.3390/molecules20022208|anchor=4123a985}}{{cite|doi=10.1111/add.70319|anchor=dd973a61}}. The UK National Poisons Information Service documents real-world ibogaine [[glossary:toxicity]] presentations over a 10-year [[glossary:case-series]]{{cite|doi=10.1080/15563650.2024.2447500|anchor=a2f4de0e}}. Because noribogaine's [[glossary:half-life]] extends to 28–48 hours, cardiac risk persists well beyond the visionary phase — sudden death has been reported up to 72 hours after [[glossary:ingestion]]{{cite|doi=10.3390/molecules20022208|anchor=6750d798}}{{cite|doi=10.1007/s12012-015-9311-5|anchor=e24cd7b1}}. '''Neurotoxicity:''' In rats, ibogaine causes indirect excitotoxic degeneration of Purkinje cells in the cerebellar vermis at high doses{{cite|pubmed=9348351|anchor=0db665dc}}{{cite|pubmed=8377927|anchor=7fe2bd2b}}. At 40 mg/kg — within the anti-addictive [[glossary:dose-range]] in [[glossary:rodent-model|rodents]] — this effect was not observed{{cite|pubmed=8930373|anchor=68099c8a}}, suggesting anti-addictive and neurotoxic thresholds may be separable. In humans, severe transient [[effect:motor-control-impairment|ataxia]] was observed in all 14 patients in a clinical safety study{{cite|doi=10.1111/add.15448|anchor=96693751}}. Long-term Purkinje cell effects in humans at therapeutic doses have not been established; the MISTIC [[glossary:cohort]] showed structural brain improvements rather than deterioration at one month{{cite|doi=10.1016/j.isci.2026.115121|anchor=e6fa2577}}. '''Contaminant and adulterant risk:''' Commercial iboga products present significant quality concerns. GC/MS analysis of 16 products found unknown substances in almost all samples, and one product labeled as "iboga" contained no detectable iboga alkaloids{{cite|doi=10.1590/0101-60830000000231|anchor=17503d5a}}. No published analytical data on heavy metal [[glossary:contamination]] (lead, cadmium, arsenic, mercury), pesticide residues, or mycotoxin levels in commercial iboga products were identified. {{flag|safety-citation-needed}} Unlike regulated [[substance:cannabis]] markets, no jurisdiction mandates ISO/IEC-accredited laboratory testing or Certificate of Analysis requirements for iboga products. Independent analytical verification before use is the only available risk mitigation for product quality{{cite|doi=10.1590/0101-60830000000231|anchor=29348f68}}. ====Psychological Risks==== Challenging and dysphoric experiences are a documented component, identified as one of seven empirically-derived factors ("Discomfort and challenge") in the Ibogaine Experience Scale (N=499){{cite|doi=10.1371/journal.pone.0333296|anchor=c86ea2b7}}. [[effect:anxiety]], fear, confrontation with difficult autobiographical material, and [[effect:nausea]]-related [[glossary:distress]] are commonly reported during the acute phase{{cite|doi=10.1080/02791072.2019.1598603|anchor=fc84f49e}}. Risk of acute psychological decompensation exists in individuals with pre-existing psychotic spectrum [[glossary:disorder|disorders]]. [[effect:delirium]]-like states may occur at high doses, and hyperekplexia (exaggerated startle response) has been reported during the residual phase. No [[glossary:prevalence]] estimates for ibogaine-associated acute [[glossary:psychosis]] have been published. {{flag|safety-citation-needed}} Long-term [[glossary:psychological-risk|psychological risks]] of ibogaine in the general population remain uncharacterized beyond [[glossary:case-report|case reports]] and observational cohorts. ====Tolerance & Dependence==== Ibogaine does not produce classical pharmacological [[glossary:tolerance]]. It is typically administered as a single dose in therapeutic contexts, and no published evidence documents [[glossary:dose-escalation]] or tolerance development{{cite|doi=10.1016/j.jsat.2021.108717|anchor=bd6d9b46}}{{cite|doi=10.1111/j.1749-6632.1998.tb08237.x|anchor=b25af513}}. Ibogaine does not appear to produce [[glossary:physical-dependence]]. No [[glossary:withdrawal]] has been documented in humans. Traditional Bwiti ceremonial use is intermittent (initiation rites, periodic ceremonies), not daily. Animal [[glossary:self-administration]] models do not show ibogaine self-administration, and no compulsive [[glossary:redose|redosing]] patterns have been observed{{cite|doi=10.1038/tp.2016.71|anchor=16612d67}}. [[glossary:abuse-liability]] is considered negligible. The experience is typically described as challenging and physically demanding rather than recreationally reinforcing. ====Drug Interactions==== '''CYP2D6 inhibitors''' represent the most clinically significant herb-[[glossary:drug-interaction]]. Co-administration of any potent [[glossary:cyp2d6]] [[glossary:inhibitor]] (paroxetine, fluoxetine, bupropion, quinidine) approximately doubles the combined active [[glossary:moiety]] (ibogaine + noribogaine) exposure and proportionally increases cardiac risk{{cite|doi=10.1002/jcph.471|anchor=8d8a2962}}. '''QT-prolonging agents''' compound ibogaine's hERG [[glossary:blockade]]. Co-administration with [[substance:methadone]], tricyclic [[substance_class:psychoactive/antidepressant|antidepressants]], [[substance_class:psychoactive/antipsychotic|antipsychotics]], certain SSRIs, or some antihistamines elevates risk of torsades de pointes{{cite|doi=10.3390/molecules20022208|anchor=86a3d504}}{{cite|doi=10.1111/add.70319|anchor=0581ce76}}. '''Opioid interactions''' are complex and timing-dependent. Ibogaine may precipitate opioid withdrawal or attenuate it depending on the timing relative to last opioid dose{{cite|doi=10.1111/j.1749-6632.1998.tb08237.x|anchor=6b6f44b8}}{{cite|doi=10.3389/fphar.2018.00529|anchor=25376531}}. [[glossary:discontinuation]] of methadone or [[substance:buprenorphine]] for ibogaine treatment creates a dual hazard: incomplete tapering risks precipitated withdrawal, while post-ibogaine loss of opioid tolerance increases [[glossary:overdose]] risk{{cite|doi=10.1097/ADM.0000000000001645|anchor=1978c4f9}}. '''Serotonergic agents:''' Ibogaine's [[glossary:serotonin-transporter]] [[glossary:inhibition]] creates a theoretical [[glossary:serotonin-syndrome]] risk when combined with MAOIs or [[glossary:serotonin]] [[glossary:releasing-agent|releasers]]{{cite|doi=10.1021/jacs.5c06325|anchor=31d7c647}}. {{flag|safety-citation-needed}} No published clinical case report of ibogaine-induced serotonin syndrome was identified. ====Contraindications==== '''Pre-existing cardiac conditions''' constitute an absolute [[glossary:contraindication]]. Any history of QT prolongation, cardiac arrhythmia, structural heart disease, or heart failure precludes ibogaine administration{{cite|doi=10.1007/s12012-015-9311-5|anchor=85733eea}}{{cite|doi=10.1111/add.15448|anchor=1784834c}}. '''CYP2D6 poor metabolizer genotype''' is a major risk factor. These individuals experience approximately double the active moiety exposure, substantially increasing cardiac and neurological risk{{cite|doi=10.1002/jcph.471|anchor=acb97039}}{{cite|doi=10.1111/add.70319|anchor=6a29930a}}. CYP2D6 genotyping is recommended before any ibogaine administration. '''Concurrent QT-prolonging medications''' must be discontinued with appropriate washout periods. This includes methadone, many antipsychotics, tricyclic antidepressants, and certain antibiotics (macrolides, fluoroquinolones). '''Severe hepatic impairment''' compromises CYP-mediated ibogaine [[glossary:metabolism]], potentially resulting in unpredictable drug exposure. '''Personal or family history of psychotic spectrum disorders''' (schizophrenia, schizoaffective disorder) constitutes a relative contraindication due to risk of precipitated psychosis{{cite|doi=10.1007/s00406-023-01590-1|anchor=405244f7}}. '''Pregnancy''' is an absolute contraindication. No reproductive safety data have been published. '''Active opioid maintenance therapy without supervised tapering''' creates a dual risk: precipitated withdrawal during ibogaine treatment and post-treatment overdose from reduced tolerance{{cite|doi=10.1097/ADM.0000000000001645|anchor=70f47924}}. '''Electrolyte abnormalities''' — particularly hypokalemia and hypomagnesemia — [[glossary:potentiation|potentiate]] QT prolongation and must be corrected before ibogaine administration{{cite|doi=10.1007/s00406-023-01590-1|anchor=af07dedd}}.

===Forms & Identification=== Iboga preparations vary enormously in [[glossary:potency]] and purity. Raw root bark, total alkaloid extracts, and purified [[substance:ibogaine]] HCl are pharmacologically distinct products with non-overlapping [[glossary:dose-range|dose ranges]]. GC/MS analysis of commercial products found unknown [[glossary:adulterant|adulterants]] in almost all samples tested, and one product labeled "iboga" contained no iboga alkaloids at all{{cite|doi=10.1590/0101-60830000000231|anchor=bb332e4e}}. No jurisdiction mandates certified laboratory testing for iboga products. Obtain independent analytical verification by GC/MS or HPLC before use. For purified ibogaine HCl, request a Certificate of Analysis specifying ibogaine content and absence of voacangine. For raw root bark or total alkaloid extract, treat every batch as an unknown quantity. ===Set & Setting=== Ibogaine sessions are not recreational events. The acute phase lasts 12–24 hours; residual effects extend to 72 hours. Near-total physical incapacitation is expected throughout. A supervised clinical or ceremonial setting with continuous cardiac monitoring is the minimum safe environment. The session space should be quiet and dimly lit — an exaggerated startle response is reported during the residual phase. A [[glossary:sitter]] or medical attendant must be present for the entire acute phase and should remain available through the 72-hour cardiac risk window. Ambulatory movement without assistance is unsafe due to severe [[glossary:motor-coordination|loss of coordination]]{{cite|doi=10.1111/add.15448|anchor=540e50ec}}. {{Guideline}} ===Guidelines=== * '''Cardiac screening is non-negotiable.''' Obtain a baseline 12-lead ECG with QTc measurement before any ibogaine administration. Individuals with QTc above 450 ms, any history of [[glossary:arrhythmia]], or structural heart disease should not proceed{{cite|doi=10.1007/s12012-015-9311-5|anchor=6fb5e0cc}}{{cite|doi=10.1111/add.15448|anchor=8353480b}}. * '''CYP2D6 genotyping''' should be completed before administration. [[glossary:poor-metabolizer|Poor metabolizers]] face approximately double the active compound exposure{{cite|doi=10.1002/jcph.471|anchor=83bba31e}}. * '''Discontinue all CYP2D6 inhibitors and QT-prolonging medications''' with appropriate washout periods before any session. This includes paroxetine, fluoxetine, bupropion, [[substance:methadone]], tricyclic [[substance_class:psychoactive/antidepressant|antidepressants]], and many [[substance_class:psychoactive/antipsychotic|antipsychotics]]. * '''Correct electrolyte imbalances''' — particularly potassium and magnesium — before administration{{cite|doi=10.1007/s00406-023-01590-1|anchor=41735cd6}}. * '''Continuous cardiac monitoring''' (telemetry or repeated 12-lead ECGs) should be maintained for at least 24 hours post-administration and ideally through 72 hours, given noribogaine's prolonged [[glossary:half-life]]. * '''Start with the lowest effective preparation.''' For root bark or total alkaloid extract, begin with a small test dose and wait at least 2 hours before any additional consumption. Never estimate dose from uncharacterized bark. * '''Maintain hydration.''' [[effect:nausea]] and [[effect:vomiting]] are near-universal; anti-emetics should be available. * '''Opioid tapering:''' Complete any taper from [[substance_class:psychoactive/opioid]] maintenance therapy under medical supervision before the session. Post-ibogaine loss of opioid [[glossary:tolerance]] increases [[glossary:overdose]] risk on resumption{{cite|doi=10.1097/ADM.0000000000001645|anchor=ef2a6b59}}. {{/Guideline}} {{Emergency}} ===Emergency Response=== '''Recognizing an emergency:''' * Irregular heartbeat, [[glossary:chest-pain]], or palpitations during or after a session * [[glossary:loss-of-consciousness]] or unresponsiveness * [[glossary:seizure]] activity * Breathing difficulty or cessation * Severe [[effect:confusion]] or [[glossary:psychosis|psychotic symptoms]] persisting beyond the expected acute phase '''Immediate steps:''' * '''1.''' Call emergency services immediately if cardiac symptoms, loss of consciousness, or breathing difficulty occur. * '''2.''' Place an unresponsive person in the [[glossary:recovery-position]]. * '''3.''' Do not leave the person alone — cardiac events can occur up to 72 hours post-[[glossary:ingestion]]. * '''4.''' If available, attach an AED (automated external defibrillator) and follow its prompts. * '''5.''' Monitor breathing and pulse continuously until paramedics arrive. '''What to tell the dispatcher:''' * The person took ibogaine (spell it out: I-B-O-G-A-I-N-E) * Approximate dose and preparation type (root bark, extract, or ibogaine HCl) if known * Time of ingestion * Current symptoms, especially any cardiac irregularity * Note: [[glossary:good-samaritan-law|Good Samaritan laws]] exist in many jurisdictions and provide legal protection for reporting drug-related emergencies '''Reversal agents:''' No specific reversal agent for ibogaine exists. Treatment is supportive: cardiac monitoring, electrolyte correction, and management of arrhythmias per standard ACLS protocols. Noribogaine's prolonged half-life means monitoring must continue well beyond symptom resolution. {{/Emergency}} {{Aftercare}} ===Aftercare & Integration=== The afterglow period extends 24–72 hours beyond the acute visionary phase. During this window, noribogaine continues to exert pharmacological activity, and cardiac monitoring should be maintained. Physical recovery priorities include rehydration, gentle reintroduction of food, and rest. Loss of coordination and physical weakness may persist for 24–48 hours after the visionary phase resolves. Avoid driving, operating machinery, or any activity requiring coordination during this period. Psychological [[glossary:integration]] is widely considered a critical component of therapeutic ibogaine use. The visionary content is often dense, emotionally charged, and autobiographical. Structured integration sessions with a trained [[glossary:therapist]] or experienced facilitator — beginning 1–3 days after the session and continuing over subsequent weeks — help translate [[glossary:insight|insights]] into sustained behavioral change. {{/Aftercare}} {{Recovery}} ===Recovery & Support=== Ibogaine does not produce [[glossary:dependence]] or a [[glossary:withdrawal]]. Recovery support in the ibogaine context typically addresses the underlying condition that motivated treatment — most commonly [[glossary:substance-use-disorder|opioid use disorder]], alcohol use disorder, or trauma-related conditions. Post-ibogaine opioid safety is critical: opioid tolerance is substantially reduced after ibogaine treatment, and resumption of [[glossary:pretreatment|pre-treatment]] opioid doses can be fatal{{cite|doi=10.1097/ADM.0000000000001645|anchor=ac3863e2}}. Ongoing [[glossary:addiction]] medicine support, including consideration of maintenance therapy, should be arranged before the session. '''Resources:''' * SAMHSA National Helpline: 1-800-662-4357 (US, free, confidential, 24/7) * Global Ibogaine Therapy Alliance (GITA): provider directory and safety information * Crisis Text Line: text HOME to 741741 (US) {{/Recovery}}

===Forms & Identification=== Iboga preparations vary enormously in [[glossary:potency]] and purity. Raw root bark, total alkaloid extracts, and purified [[substance:ibogaine]] HCl are pharmacologically distinct products with non-overlapping [[glossary:dose-range|dose ranges]]. GC/MS analysis of commercial products found unknown [[glossary:adulterant|adulterants]] in almost all samples tested, and one product labeled "iboga" contained no iboga alkaloids at all{{cite|doi=10.1590/0101-60830000000231|anchor=4697d535}}. No jurisdiction currently mandates ISO/IEC-accredited laboratory testing or Certificate of Analysis requirements for iboga products. Independent analytical verification by GC/MS or HPLC is the only reliable way to confirm identity, purity, and alkaloid concentration before use. For purified ibogaine HCl, a Certificate of Analysis from the supplier specifying ibogaine content and absence of voacangine (which adds cardiac risk) is the minimum standard. For raw root bark or total alkaloid extract, assume extreme batch-to-batch variability and treat every new batch as an unknown quantity. ===Set & Setting=== Ibogaine sessions are not recreational events. The experience lasts 12–24 hours in acute phase with residual effects to 72 hours, involves near-total physical incapacitation, and frequently surfaces difficult psychological material. A supervised clinical or ceremonial setting with continuous cardiac monitoring is the minimum safe environment. The session space should be quiet, dimly lit, and free from sudden stimuli — hyperekplexia (exaggerated startle response) is reported during the residual phase. A [[glossary:sitter]] or medical attendant must be present for the entire acute phase and should remain available through the 72-hour cardiac risk window. Ambulatory movement without assistance is unsafe during the acute phase due to severe [[effect:motor-control-impairment|ataxia]]{{cite|doi=10.1111/add.15448|anchor=0399e763}}. {{Guideline}} ===Guidelines=== * '''Cardiac screening is non-negotiable.''' A baseline 12-lead ECG with QTc measurement must be obtained before any ibogaine administration. Individuals with QTc above 450 ms, any history of [[glossary:arrhythmia]], or structural heart disease should not proceed{{cite|doi=10.1007/s12012-015-9311-5|anchor=f27b96dd}}{{cite|doi=10.1111/add.15448|anchor=07719822}}. * '''CYP2D6 genotyping''' should be completed before administration. [[glossary:poor-metabolizer|Poor metabolizers]] face approximately double the active [[glossary:moiety]] exposure{{cite|doi=10.1002/jcph.471|anchor=db131e5d}}. * '''Discontinue all CYP2D6 inhibitors and QT-prolonging medications''' with appropriate washout periods before any ibogaine session. This includes paroxetine, fluoxetine, bupropion, [[substance:methadone]], tricyclic [[substance_class:psychoactive/antidepressant|antidepressants]], and many [[substance_class:psychoactive/antipsychotic|antipsychotics]]. * '''Correct electrolyte imbalances''' — particularly potassium and magnesium — before administration{{cite|doi=10.1007/s00406-023-01590-1|anchor=cdf25723}}. * '''Continuous cardiac monitoring''' (telemetry or repeated 12-lead ECGs) should be maintained for at least 24 hours post-administration and ideally through 72 hours, given noribogaine's prolonged [[glossary:half-life]]. * '''Start with the lowest effective preparation.''' If using root bark or total alkaloid extract, begin with a small test dose and wait at least 2 hours before any additional consumption. Never estimate dose from uncharacterized bark. * '''Hydration and nutrition:''' Maintain IV or oral [[glossary:hydration]] access. [[effect:nausea]] and [[effect:vomiting]] are near-universal; anti-emetics should be available. * '''Opioid tapering:''' If discontinuing [[substance_class:psychoactive/opioid]] maintenance therapy for ibogaine treatment, complete the taper under medical supervision. Incomplete tapering risks precipitated [[glossary:withdrawal]]; post-ibogaine loss of opioid [[glossary:tolerance]] increases [[glossary:overdose]] risk on resumption{{cite|doi=10.1097/ADM.0000000000001645|anchor=f6c5fbd4}}. {{/Guideline}} {{Emergency}} ===Emergency Response=== '''Recognizing an emergency:''' * Irregular heartbeat, [[glossary:chest-pain]], or palpitations during or after an ibogaine session * [[glossary:loss-of-consciousness]] or unresponsiveness * [[glossary:seizure]] activity * Breathing difficulty or cessation * Severe [[effect:confusion]] or [[glossary:psychosis|psychotic symptoms]] persisting beyond the expected acute phase '''Immediate steps:''' * '''1.''' Call emergency services immediately if cardiac symptoms, loss of consciousness, or breathing difficulty occur. * '''2.''' Place an unresponsive person in the [[glossary:recovery-position]]. * '''3.''' Do not leave the person alone — cardiac events can occur up to 72 hours post-[[glossary:ingestion]]. * '''4.''' If available, attach an AED (automated external defibrillator) and follow its prompts. * '''5.''' Monitor breathing and pulse continuously until paramedics arrive. '''What to tell the dispatcher:''' * The person took ibogaine (spell it out: I-B-O-G-A-I-N-E) * Approximate dose and preparation type (root bark, extract, or ibogaine HCl) if known * Time of ingestion * Current symptoms, especially any cardiac irregularity * Note: [[glossary:good-samaritan-law|Good Samaritan laws]] exist in many jurisdictions and provide legal protection for reporting drug-related emergencies '''Reversal agents:''' No specific reversal agent for ibogaine exists. Treatment is supportive: cardiac monitoring, electrolyte correction, and management of arrhythmias per standard ACLS protocols. The prolonged half-life of noribogaine means monitoring must continue well beyond symptom resolution. {{/Emergency}} {{Aftercare}} ===Aftercare & Integration=== The ibogaine afterglow period extends 24–72 hours beyond the acute visionary phase. During this window, noribogaine continues to exert pharmacological activity, and cardiac monitoring should be maintained. Physical recovery priorities include rehydration (oral fluids or IV if vomiting was severe), gentle reintroduction of food, and rest. Ataxia and physical weakness may persist for 24–48 hours after the visionary phase resolves. Avoid driving, operating machinery, or any activity requiring [[glossary:motor-coordination|coordination]] during this period. Psychological [[glossary:integration]] is widely considered a critical component of therapeutic ibogaine use. The visionary content is often dense, emotionally charged, and autobiographical. Structured integration sessions with a trained [[glossary:therapist]] or experienced facilitator — beginning 1–3 days after the session and continuing over subsequent weeks — help process the material and translate [[glossary:insight|insights]] into sustained behavioral change. {{/Aftercare}} {{Recovery}} ===Recovery & Support=== Ibogaine itself does not produce [[glossary:dependence]] or a withdrawal syndrome. Recovery support in the ibogaine context typically addresses the underlying condition that motivated treatment — most commonly [[glossary:substance-use-disorder|opioid use disorder]], alcohol use disorder, or trauma-related conditions. '''Post-ibogaine opioid safety:''' Individuals who used ibogaine to interrupt opioid dependence face a critical risk period. Opioid tolerance is substantially reduced after ibogaine treatment, and resumption of [[glossary:pretreatment|pre-treatment]] opioid doses can be fatal{{cite|doi=10.1097/ADM.0000000000001645|anchor=1f9c04f0}}. Ongoing [[glossary:addiction]] medicine support, including consideration of maintenance therapy, should be arranged before the ibogaine session. '''Resources:''' * SAMHSA National Helpline: 1-800-662-4357 (US, free, confidential, 24/7) * Global Ibogaine Therapy Alliance (GITA): provider directory and safety information * Crisis Text Line: text HOME to 741741 (US) {{/Recovery}}

===Multi-target receptor pharmacology=== [[substance:ibogaine]] exhibits an exceptionally broad [[glossary:receptor]] profile, engaging multiple [[glossary:neurotransmitter]] systems simultaneously — a pattern described as "matrix pharmacology"{{cite|doi=10.1021/jacs.5c06325|anchor=23cb34b9}}. At the molecular level, ibogaine inhibits [[glossary:vmat2]] (VMAT2) at submicromolar concentrations, producing partial [[glossary:serotonin-release]] from synaptic vesicles{{cite|doi=10.1021/jacs.5c06325|anchor=521ebb3e}}. It simultaneously inhibits the [[glossary:serotonin-transporter]] (SERT), creating a dual vesicular and [[glossary:plasma]] membrane [[glossary:serotonin]] transport [[glossary:modulation]] termed "SynRI"{{cite|doi=10.1021/jacs.5c06325|anchor=f2e44355}}. Ibogaine antagonizes [[glossary:nmda-receptor|NMDA receptors]] at the [[substance:pcp]]/[[glossary:channel]] site (K_i 0.01–0.05 μM in [[glossary:cortex]]){{cite|doi=10.1111/j.1749-6632.1998.tb08239.x|anchor=bd5d6b4d}}, antagonizes α3β4 [[glossary:nicotinic-acetylcholine-receptor|nicotinic acetylcholine receptors]]{{cite|doi=10.1021/acs.jmedchem.2c01562|anchor=8f4be474}}, acts as a kappa [[substance_class:psychoactive/opioid]] [[glossary:agonist|receptor agonist]]{{cite|doi=10.1111/j.1749-6632.1998.tb08237.x|anchor=27a97a0d}}, binds [[glossary:sigma-1-receptor]] and sigma-2 receptors (K_i 1.5–3 μM){{cite|doi=10.1111/j.1749-6632.1998.tb08239.x|anchor=7f2a0b9a}}, and functions as a biased [[glossary:partial-agonist]] at [[glossary:mu-opioid-receptor|mu-opioid receptors]] with low [[glossary:beta-arrestin-recruitment|beta-arrestin recruitment]]{{cite|doi=10.3390/ph19030397|anchor=3f68f6dc}}. [[glossary:5-ht2a]] receptor involvement is supported by knockout mouse studies showing sex-dependent effects on NMDA [[glossary:transmission]] in medial [[glossary:prefrontal-cortex]]{{cite|doi=10.3390/ijms25020687|anchor=1b30fc54}}. Noribogaine shares many of these targets but with distinct pharmacokinetic properties: submicromolar VMAT2 [[glossary:inhibition]], SERT inhibition, and kappa opioid agonism{{cite|doi=10.1021/jacs.5c06325|anchor=870acc0d}}{{cite|doi=10.1111/j.1749-6632.1998.tb08237.x|anchor=31606bb4}}, sustained over a 28–48-hour [[glossary:half-life]] compared to ibogaine's 7–10 hours{{cite|doi=10.1002/jcph.471|anchor=e1ca8b0b}}. ===Anti-addictive mechanisms=== Multiple converging pathways have been identified{{cite|doi=10.1111/j.1749-6632.1998.tb08237.x|anchor=a49adf60}}{{cite|doi=10.1017/neu.2026.10059|anchor=5fb92e98}}: * '''Acute dopamine suppression:''' Ibogaine and noribogaine decrease extracellular [[glossary:dopamine]] in [[glossary:nucleus-accumbens]], acutely reducing drug [[glossary:reward]] [[glossary:reinforcement]] * '''GDNF upregulation:''' Microinjection into the [[glossary:ventral-tegmental-area]] reduces ethanol [[glossary:self-administration]] through glial cell line-derived neurotrophic factor signaling and Ret receptor [[glossary:phosphorylation]]{{cite|doi=10.1523/jneurosci.3959-04.2005|anchor=68f40f33}} * '''NMDA antagonism:''' Attenuates opioid and [[substance_class:psychoactive/stimulant]] [[glossary:withdrawal]] through glutamatergic normalization{{cite|doi=10.1111/j.1749-6632.1998.tb08237.x|anchor=c01f703a}}{{cite|doi=10.1111/j.1749-6632.1998.tb08239.x|anchor=ff525d3e}} * '''Kappa opioid agonism:''' Contributes to modulation of opioid and stimulant self-administration{{cite|doi=10.1111/j.1749-6632.1998.tb08237.x|anchor=04066a11}} * '''Neuroplasticity:''' Structural brain changes observed in humans at one month post-treatment include increased cortical thickness in 11 brain regions, subcortical expansion in 8 regions, and a 1.3-year reduction in estimated brain age{{cite|doi=10.1016/j.isci.2026.115121|anchor=d75feb45}} ===Pharmacokinetics=== Ibogaine is rapidly absorbed orally with T_max of 1.5–4 hours{{cite|doi=10.1002/jcph.471|anchor=173a0cea}}{{cite|doi=10.1177/02698811241237873|anchor=c9d09f29}}. [[glossary:first-pass-metabolism|First-pass]] [[glossary:cyp2d6]]-mediated [[glossary:metabolism]] substantially converts ibogaine to noribogaine, with the [[glossary:metabolite]] reaching [[glossary:cmax|peak plasma concentration]] at approximately 3–4 hours post-administration{{cite|doi=10.1002/jcph.471|anchor=b5933c3d}}. Ibogaine is highly lipophilic, with significant adipose tissue sequestration and slow release contributing to prolonged duration. Elimination half-life is approximately 7–10 hours in CYP2D6 normal metabolizers; substantially longer in [[glossary:poor-metabolizer|poor metabolizers]]. CYP2D6 phenotype is the dominant pharmacokinetic variable. In a [[glossary:controlled-study]] of a single 20 mg dose in 21 healthy volunteers, CYP2D6 activity correlated strongly with ibogaine exposure (r = 0.82){{cite|doi=10.1002/jcph.471|anchor=50b2d13d}}. [[glossary:pretreatment]] with paroxetine (a CYP2D6 [[glossary:inhibitor]]) substantially elevated ibogaine AUC, with poor metabolizers demonstrating approximately double the combined active [[glossary:moiety]] (ibogaine + noribogaine) exposure compared to normal metabolizers{{cite|doi=10.1002/jcph.471|anchor=0b6214df}}. ===Neuroimaging evidence=== The MISTIC [[glossary:cohort]] (30 veterans with traumatic brain injury) has produced the most extensive neuroimaging data following ibogaine administration. Structural MRI revealed increased cortical thickness and subcortical volume at one month{{cite|doi=10.1016/j.isci.2026.115121|anchor=994f40d4}}. Functional MRI demonstrated measurable neural correlates of treatment response{{cite|doi=10.1016/j.bpsc.2026.02.001|anchor=22f77fcf}}. Mystical experience [[glossary:intensity]] during the ibogaine session predicted both PTSD symptom improvement and EEG changes{{cite|doi=10.1016/j.jad.2025.120722|anchor=69dc4ed6}}. ===Open questions=== The relative contribution of ibogaine versus noribogaine to anti-addictive [[glossary:efficacy]] remains unresolved — the two compounds have overlapping but distinct receptor profiles and strikingly different half-lives. Whether the minor co-alkaloids in root bark preparations (tabernanthine, ibogamine, voacangine) contribute meaningfully to therapeutic or [[glossary:adverse-effects]] at human exposure concentrations has not been determined. Long-term Purkinje cell effects in humans at therapeutic doses remain uncharacterized, and the remyelination [[glossary:hypothesis]]{{cite|doi=10.1017/neu.2026.10059|anchor=2b92f2cc}} awaits direct human evidence.

[[substance:ibogaine]] is not listed in any of the three UN drug convention schedules (1961, 1971, 1988), so national laws govern independently. The result is a fragmented international landscape: ibogaine is a [[glossary:schedule-i]] controlled substance in the United States at the federal level, yet legal or unregulated in several countries where treatment clinics operate openly. A 2026 US executive order directed accelerated regulatory review{{cite|doi=10.1038/d41586-026-01286-1|anchor=05779004}}, and nine US states have enacted ibogaine-related legislation as of May 2026{{cite|url=https://www.americansforibogaine.org/legislation/|anchor=5e7c02f3}}, making the legal environment unusually dynamic.

Jurisdiction	Status	Notes
United States (federal)	Schedule I	Classified under the Controlled Substances Act since 1967. No accepted medical use at federal level. A 2026 executive order directed FDA and DEA to accelerate research and create Right to Try pathways{{cite|doi=10.1038/d41586-026-01286-1|anchor=350cc3c7}}.
United States (state level)	Varies	Nine states enacted ibogaine-related legislation as of May 2026, including Texas ($50M clinical research), Kentucky ($21M/year SUD research), Oregon (first regulated ibogaine program), and Louisiana (psychedelic-assisted therapy program). Nine additional states have active bills{{cite|url=https://www.americansforibogaine.org/legislation/|anchor=515b95ed}}.
Mexico	Unscheduled	Physician-supervised administration is lawful. Most international ibogaine treatment clinics operate in Mexico{{cite|url=https://www.mindscaperetreat.com/ibogaine-legal-status|anchor=61312ee5}}.
Brazil	Licensed medical use	Licensed clinics operate under ANVISA oversight{{cite|url=https://www.mindscaperetreat.com/ibogaine-legal-status|anchor=c12f8162}}.
New Zealand	Class C controlled drug	Prescription required for lawful possession or use{{cite|url=https://www.mindscaperetreat.com/ibogaine-legal-status|anchor=ed8960d6}}.
Netherlands	Not prohibited	Therapeutic use permitted; several licensed clinics operate{{cite|url=https://www.mindscaperetreat.com/ibogaine-legal-status|anchor=09607af0}}.
South Africa	Medical supervision required	Not specifically prohibited; medical oversight required for administration{{cite|url=https://www.mindscaperetreat.com/ibogaine-legal-status|anchor=9f42df6c}}.
Costa Rica	Unregulated	No specific prohibition; ibogaine treatment openly practiced{{cite|url=https://www.mindscaperetreat.com/ibogaine-legal-status|anchor=96e6631e}}.
United Kingdom	Controlled substance	Not licensed for medical use. NPIS monitors toxicity cases{{cite|doi=10.1080/15563650.2024.2447500|anchor=fc9cb188}}. {{flag|citation-needed}} Exact Misuse of Drugs Act schedule placement requires verification.
Gabon	National heritage plant	Declared "national cultural heritage strategic reserve" in 2000. Wild harvest export banned in 2019. Cultivation permitted with Ministry approval{{cite|url=https://chacruna.net/iboga_conservation/|anchor=e37b6591}}.
European Union	Varies by member state	No EU-wide scheduling. Generally not approved for medical use in most member states. {{flag|citation-needed}} Member-state-level scheduling requires jurisdiction-specific verification.
Australia	Controlled	{{flag|citation-needed}} Specific TGA scheduling and state-level provisions require verification.

===Treaty and analog considerations=== Because ibogaine is absent from all three UN drug convention schedules, nations are under no treaty obligation to control ''T. iboga'' or ibogaine. This regulatory gap explains why countries such as Mexico, Brazil, and the Netherlands permit ibogaine use without violating international commitments. The plant ''T. iboga'' itself carries additional legal complexity in Gabon, where it is protected as cultural heritage irrespective of drug scheduling. {{flag|safety-citation-needed}} US legal status is rapidly evolving. The 2026 executive order and multiple state-level bills may substantially alter ibogaine's regulatory status before the next scheduled review of this article.

[[substance:ibogaine]] is not listed in any of the three UN drug convention schedules, so national laws govern independently. In the United States, ibogaine remains a [[glossary:schedule-i]] controlled substance at the federal level, though a 2026 executive order directed the [[glossary:fda]] and [[glossary:drug-enforcement-administration|DEA]] to accelerate research and create Right to Try access pathways{{cite|doi=10.1038/d41586-026-01286-1|anchor=d4548763}}. Nine US states have enacted ibogaine-related legislation as of May 2026, including Texas, Kentucky, Oregon, and Louisiana{{cite|url=https://www.americansforibogaine.org/legislation/|anchor=9cb1610a}}. Internationally, ibogaine is legal or unregulated in Mexico (where most international treatment clinics operate), the Netherlands, and Costa Rica; licensed medical use is permitted in Brazil; New Zealand and the United Kingdom treat it as a controlled drug requiring medical oversight{{cite|url=https://www.mindscaperetreat.com/ibogaine-legal-status|anchor=84d679a5}}. In Gabon, the plant itself is protected as a national cultural heritage strategic reserve, with wild-harvest exports banned since 2019{{cite|url=https://chacruna.net/iboga_conservation/|anchor=30c47f60}}. The legal environment is unusually dynamic — multiple jurisdictions are actively legislating, and the US federal status may change before the next review of this article. {{Warning}} Legal status changes frequently. This overview reflects the status as of the article's last update and is not legal advice. Verify current law in the relevant jurisdiction before acting on this information. {{/Warning}}

The [[substance:ibogaine]] experience is qualitatively distinct from [[glossary:serotonergic-psychedelics|classical serotonergic psychedelics]] and [[substance_class:psychoactive/dissociative]] anesthetics, though it shares features with both classes. Ibogaine imposes an extended, largely internal visionary state dominated by autobiographical narrative sequences, [[effect:entity-contact|entity encounters]], and pronounced somatic [[glossary:intensity]] — a phenomenological topology some researchers classify as oneirophrenic. Preparation type is the primary modifier: purified ibogaine HCl delivers a pharmacokinetically defined single-compound experience, while raw root bark introduces the full alkaloid spectrum at unpredictable concentrations, potentially altering both character and duration. Ibogaine occupies a singular position among psychoactive plants. Its closest pharmacological parallels are [[glossary:synthetic]] analogs (tabernanthalog, oxa-noribogaine) rather than other botanical preparations. The extended duration (12–24 hours acute, residual effects persisting to 72 hours), severe physical incapacitation during the experience, and mandatory cardiac monitoring requirements distinguish it from all commonly discussed [[substance_class:psychoactive/psychedelic]] or dissociative substances.

===Toxicity=== ====Cardiac toxicity==== Cardiac [[glossary:toxicity]] is the primary acute safety concern for all [[substance:ibogaine]]-containing preparations. Ibogaine and noribogaine block the hERG potassium [[glossary:channel]] (I_Kr), which governs cardiac repolarization{{cite|doi=10.1007/s12012-015-9311-5|anchor=e833f38e}}. Published IC₅₀ values for hERG [[glossary:blockade]] are: ibogaine 3.53 μM, noribogaine 2.86 μM, and voacangine 2.25 μM{{cite|doi=10.1007/s12012-015-9311-5|anchor=ede74a0a}}. By comparison, 18-methoxycoronaridine (18-MC), an experimental safer [[glossary:structural-analog]], shows IC₅₀ greater than 50 μM{{cite|doi=10.1007/s12012-015-9311-5|anchor=dac60cea}}. In an open-label safety study of 14 [[substance_class:psychoactive/opioid]]-dependent patients receiving 10 mg/kg ibogaine HCl, mean maximum QTc prolongation was 95 ms (range 29–146 ms), and 50% of subjects reached QTc greater than 500 ms during the monitoring period{{cite|doi=10.1111/add.15448|anchor=3eaafcaf}}. In 6 of 14 subjects, QTc remained above 450 ms beyond 24 hours post-administration{{cite|doi=10.1111/add.15448|anchor=e8cba609}}. No torsades de pointes (TdP) occurred in this monitored clinical setting. Fatal [[glossary:arrhythmia|cardiac arrhythmias]] attributed to ibogaine have been reported, with deaths primarily occurring in unsupervised settings where continuous cardiac monitoring was absent{{cite|doi=10.3390/molecules20022208|anchor=57d739a0}}{{cite|doi=10.1111/add.70319|anchor=e0602c8a}}. The 10-year UK National Poisons Information Service [[glossary:case-series]] documents real-world ibogaine toxicity presentations{{cite|doi=10.1080/15563650.2024.2447500|anchor=fde16895}}. Noribogaine's prolonged [[glossary:half-life]] (28–48 hours) means cardiac risk extends well beyond the visionary phase — sudden death has been reported up to 72 hours after ibogaine [[glossary:ingestion]]{{cite|doi=10.3390/molecules20022208|anchor=3ee368c4}}{{cite|doi=10.1007/s12012-015-9311-5|anchor=741697a5}}. ====Neurotoxicity==== In rats, ibogaine causes indirect (trans-synaptic) excitotoxic degeneration of Purkinje cells in the cerebellar vermis via [[glossary:activation]] of the olivocerebellar projection{{cite|pubmed=9348351|anchor=65504907}}{{cite|pubmed=8377927|anchor=7dca7c4c}}. Dose-response studies established 100 mg/kg (i.p.) as consistently neurotoxic and 25 mg/kg as the no-observed-adverse-effect level (NOAEL){{cite|pubmed=10966515|anchor=60e2d954}}. At 40 mg/kg — within the anti-addictive [[glossary:dose-range]] in [[glossary:rodent-model|rodents]] — ibogaine did not cause Purkinje cell degeneration{{cite|pubmed=8930373|anchor=c343b054}}, suggesting that anti-addictive and neurotoxic properties may be dissociable at the dose level. In humans, severe transient [[effect:motor-control-impairment|ataxia]] (inability to walk without support) was observed in all 14 patients in a clinical safety study{{cite|doi=10.1111/add.15448|anchor=482ae5ee}}. Long-term Purkinje cell effects in humans at therapeutic doses have not been established. The MISTIC cohort showed structural brain improvements (increased cortical thickness, decreased brain age) rather than deterioration at one month{{cite|doi=10.1016/j.isci.2026.115121|anchor=3ab1852d}}. ====Acute toxicity thresholds==== No published mammalian [[glossary:lethal-dose|LD50]] for ibogaine was identified in structured database searches. Rat [[glossary:toxicology]] studies used single intraperitoneal doses of 25–100 mg/kg; translation to human oral dosing is uncertain given species differences and [[glossary:route-of-administration]]. {{flag|safety-citation-needed}} Human lethal dose has not been established. ====Contaminant and adulterant risk==== Commercial iboga products present significant [[glossary:contamination|contaminant]] and [[glossary:adulterant]] risks. GC/MS analysis of 16 products found unknown substances in almost all samples, and one product labeled as "iboga" contained no detectable iboga alkaloids{{cite|doi=10.1590/0101-60830000000231|anchor=05f06a73}}{{flag|additional-citations-needed}}. The extreme variability in ibogaine content across root bark samples (0.6–11.2%) makes dose prediction from uncharacterized material impossible. No published analytical data on heavy metal contamination (lead, cadmium, arsenic, mercury), pesticide residues, or mycotoxin levels in commercial iboga products were identified in this research. This represents a significant safety data gap. Unlike regulated [[substance:cannabis]] markets in some US states, no jurisdiction mandates ISO/IEC-accredited laboratory testing or Certificate of Analysis requirements for iboga products. Independent analytical verification by GC/MS or HPLC before clinical use is the only available risk mitigation for product quality{{cite|doi=10.1590/0101-60830000000231|anchor=b14dfdd3}}{{flag|additional-citations-needed}}. ===Psychological risks=== Challenging and dysphoric experiences are a documented component of the ibogaine experience, identified as one of seven empirically-derived factors ("Discomfort and challenge") in the Ibogaine Experience Scale (N=499){{cite|doi=10.1371/journal.pone.0333296|anchor=31ee6fa2}}. [[effect:anxiety]], fear, confrontation with difficult autobiographical material, and [[effect:nausea]]-related [[glossary:distress]] are commonly reported during the acute phase{{cite|doi=10.1080/02791072.2019.1598603|anchor=578327de}}. Risk of acute psychological decompensation exists in individuals with pre-existing psychotic spectrum [[glossary:disorder|disorders]]. [[effect:delirium]]-like states may occur at high doses. Hyperekplexia (exaggerated startle response) has been reported during the residual phase. No [[glossary:prevalence]] estimates for ibogaine-associated acute [[glossary:psychosis]] have been published. {{flag|safety-citation-needed}} Long-term [[glossary:psychological-risk|psychological risks]] of ibogaine in the general population remain uncharacterized beyond [[glossary:case-report|case reports]] and observational cohorts. ===Tolerance & dependence=== Ibogaine does not produce classical pharmacological [[glossary:tolerance]]. It is typically administered as a single dose in therapeutic contexts, and no published evidence documents [[glossary:dose-escalation]] or tolerance development in humans{{cite|doi=10.1016/j.jsat.2021.108717|anchor=63187f42}}{{cite|doi=10.1111/j.1749-6632.1998.tb08237.x|anchor=cc3333dd}}. Ibogaine does not appear to produce physical dependence. No [[glossary:withdrawal]] from ibogaine has been documented in humans. Traditional Bwiti ceremonial use is intermittent (initiation rites, periodic ceremonies), not daily. Animal [[glossary:self-administration]] models do not show ibogaine self-administration, and no compulsive [[glossary:redose|redosing]] patterns have been documented{{cite|doi=10.1038/tp.2016.71|anchor=48ecf290}}{{flag|additional-citations-needed}}. Ibogaine's abuse liability is considered negligible. The experience is typically described as challenging and physically demanding rather than recreationally reinforcing. ===Drug Interactions=== The most clinically significant herb-[[glossary:drug-interaction]] involves '''CYP2D6 inhibition'''. In a controlled human pharmacokinetic study, pretreatment with paroxetine (a potent [[glossary:cyp2d6]] [[glossary:inhibitor]]) substantially elevated ibogaine AUC, with a strong correlation (r = 0.82) between CYP2D6 phenotype and ibogaine exposure{{cite|doi=10.1002/jcph.471|anchor=583e6127}}{{flag|additional-citations-needed}}. Co-administration of any CYP2D6 inhibitor (paroxetine, fluoxetine, bupropion, quinidine) with ibogaine approximately doubles active moiety exposure and proportionally increases cardiac risk. '''Additive QT prolongation''' represents a [[glossary:pharmacodynamic-interaction]] mechanism. Co-administration of ibogaine with any QT-prolonging agent — including [[substance:methadone]], tricyclic [[substance_class:psychoactive/antidepressant|antidepressants]], [[substance_class:psychoactive/antipsychotic|antipsychotics]], certain SSRIs, and some antihistamines — compounds the hERG blockade effect and elevates risk of torsades de pointes{{cite|doi=10.3390/molecules20022208|anchor=f0c3c6b2}}{{cite|doi=10.1111/add.70319|anchor=9a930ab3}}. '''Opioid interactions''' are complex and timing-dependent. Ibogaine may precipitate opioid withdrawal or attenuate withdrawal depending on the timing relative to last opioid dose{{cite|doi=10.1111/j.1749-6632.1998.tb08237.x|anchor=18a20e4d}}{{cite|doi=10.3389/fphar.2018.00529|anchor=3b39e226}}. Discontinuation of [[glossary:medication|medications]] for [[glossary:substance-use-disorder|opioid use disorder]] (methadone, [[substance:buprenorphine]]) for ibogaine treatment creates a dangerous scenario: incomplete tapering risks precipitated withdrawal, while loss of opioid tolerance after ibogaine treatment increases post-session [[glossary:overdose]] risk{{cite|doi=10.1097/ADM.0000000000001645|anchor=291b4e9b}}. '''Serotonergic interactions''' are mechanism-based. Ibogaine's [[glossary:serotonin-transporter]] [[glossary:inhibition]] creates a theoretical [[glossary:serotonin-syndrome]] risk when combined with MAOIs or [[glossary:serotonin]] [[glossary:releasing-agent|releasers]]{{cite|doi=10.1021/jacs.5c06325|anchor=335a6d43}}{{flag|additional-citations-needed}}. {{flag|safety-citation-needed}} No published clinical case report of ibogaine-induced serotonin syndrome was identified. ===Contraindications=== '''Pre-existing cardiac conditions''' constitute an absolute [[glossary:contraindication]]. Any history of QT prolongation, cardiac arrhythmia, structural heart disease, or heart failure precludes ibogaine administration due to the established hERG blockade mechanism{{cite|doi=10.1007/s12012-015-9311-5|anchor=09e414b0}}{{cite|doi=10.1111/add.15448|anchor=d05224fd}}. '''CYP2D6 poor metabolizer genotype''' is a major risk factor. Individuals with reduced CYP2D6 activity experience approximately double the active moiety exposure, substantially increasing cardiac and neurological adverse event risk{{cite|doi=10.1002/jcph.471|anchor=628ae284}}{{cite|doi=10.1111/add.70319|anchor=97b92ff5}}. CYP2D6 genotyping is recommended before any ibogaine administration. '''Concurrent QT-prolonging medications''' must be discontinued with appropriate washout periods before ibogaine treatment. This includes methadone, many antipsychotics, tricyclic antidepressants, and certain antibiotics (macrolides, fluoroquinolones). '''Severe hepatic impairment''' compromises CYP-mediated ibogaine [[glossary:metabolism]], potentially resulting in unpredictable drug exposure. '''Personal or family history of psychotic spectrum disorders''' (schizophrenia, schizoaffective disorder) constitutes a relative contraindication due to risk of precipitated psychosis{{cite|doi=10.1007/s00406-023-01590-1|anchor=39b5e76e}}{{flag|additional-citations-needed}}. '''Pregnancy''' is an absolute contraindication. No reproductive safety data have been published. '''Active opioid maintenance therapy without supervised tapering''' creates a dual risk: precipitated withdrawal during ibogaine treatment and post-treatment opioid overdose from reduced tolerance{{cite|doi=10.1097/ADM.0000000000001645|anchor=4e557335}}{{flag|additional-citations-needed}}. '''Electrolyte abnormalities''' — particularly hypokalemia and hypomagnesemia — [[glossary:potentiation|potentiate]] QT prolongation and must be corrected before ibogaine administration{{cite|doi=10.1007/s00406-023-01590-1|anchor=0fa9680b}}{{flag|additional-citations-needed}}.

[[substance:ibogaine]] is not listed in the schedules of the 1961 Single Convention on Narcotic Drugs, the 1971 [[glossary:convention-on-psychotropic-substances]], or the 1988 UN Convention Against Illicit Traffic in Narcotic Drugs and Psychotropic Substances. National laws therefore govern independently, producing a fragmented international regulatory landscape.

Jurisdiction	Classification	Key provisions
United States (federal)	Schedule I (Controlled Substances Act, 1967)	No accepted medical use recognized at federal level. Ibogaine HCl is also Schedule I. A 2026 executive order directed FDA and DEA to accelerate research and create Right to Try pathways{{cite|doi=10.1038/d41586-026-01286-1|anchor=cf528947}}.
United States (state level)	Varies by state	Nine states enacted ibogaine-related legislation as of May 2026: Texas ($50M clinical research, SB 2308, June 2025), Arizona ($5M Phase I trials, HB 2871, June 2025), Kentucky ($21M/year SUD research, SB 77, April 2026), Louisiana (psychedelic-assisted therapy program, SB 43, effective August 2026), Mississippi ($5M FDA consortium, HB 314), Oklahoma (clinical trial framework, HB 3834), Oregon (first regulated ibogaine program, HB 4110), plus Indiana, California, and Tennessee. Nine additional states have active bills{{cite|url=https://www.americansforibogaine.org/legislation/|anchor=8cdde155}}.
Mexico	Unscheduled	Physician-supervised administration is lawful. Most international ibogaine treatment clinics operate in Mexico{{cite|url=https://www.mindscaperetreat.com/ibogaine-legal-status|anchor=eb6b8fad}}.
Brazil	Licensed medical use	Licensed clinics operate under ANVISA oversight{{cite|url=https://www.mindscaperetreat.com/ibogaine-legal-status|anchor=7f5593a6}}.
New Zealand	Class C controlled drug	Prescription required for lawful possession or use{{cite|url=https://www.mindscaperetreat.com/ibogaine-legal-status|anchor=f265b319}}.
Netherlands	Not prohibited	Therapeutic use permitted; several licensed clinics operate{{cite|url=https://www.mindscaperetreat.com/ibogaine-legal-status|anchor=af00fc6c}}.
South Africa	Medical supervision required	Not specifically prohibited; medical oversight required for administration{{cite|url=https://www.mindscaperetreat.com/ibogaine-legal-status|anchor=858cd519}}.
Costa Rica	Unregulated	No specific prohibition; ibogaine treatment openly practiced{{cite|url=https://www.mindscaperetreat.com/ibogaine-legal-status|anchor=91bf919d}}.
United Kingdom	Controlled substance (specific schedule unconfirmed)	Not licensed for medical use. NPIS monitors toxicity cases{{cite|doi=10.1080/15563650.2024.2447500|anchor=8c78f2d4}}. {{flag|citation-needed}} Exact Misuse of Drugs Act schedule placement requires verification.
Gabon	National heritage plant	Declared "national cultural heritage strategic reserve" in 2000. Wild harvest export banned in 2019. Cultivation permitted with Ministry approval{{cite|url=https://chacruna.net/iboga_conservation/|anchor=0cb2d853}}.
European Union	Varies by member state	No EU-wide scheduling. Generally not approved for medical use in most member states. {{flag|citation-needed}} Member-state-level scheduling requires jurisdiction-specific verification.
Australia	Controlled	{{flag|citation-needed}} Specific TGA scheduling and state-level provisions require verification.

===Treaty and analog considerations=== Because ibogaine is absent from all three UN drug convention schedules, nations are under no treaty obligation to control ''T. iboga'' or ibogaine. This regulatory gap explains why countries such as Mexico, Brazil, and the Netherlands can permit ibogaine use without violating international treaty commitments. The plant ''T. iboga'' itself carries additional legal complexity in Gabon, where it is protected as cultural heritage irrespective of drug scheduling considerations. {{flag|safety-citation-needed}} US legal status is rapidly evolving. The 2026 executive order and multiple state-level bills may substantially alter ibogaine's regulatory status before the next scheduled review of this article.