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Plate 366 of 545Verified

Ibogaine

Also known asEndabuse · (-)-Ibogaine · 12 Methoxyibogamine · 12-Methoxyibogamine · Ibogain · (5beta)-12-methoxyibogamine · Tabernanthe iboga · HJM

(1R,15R,17S,18S)-17-ethyl-7-methoxy-3,13-diazapentacyclo[13.3.1.02,10.04,9.013,18]nonadeca-2(10),4(9),5,7-tetraene

PubChem CID
197060
Measurements
14
InChIKey
HSIBGVUMFOSJPD-CFDPKNGZSA-N

I · Summary

What is known

Published passages, each quoted whole and attributed to the database that published it. Two blocks are written here rather than quoted, and both say so where they stand: the synthesized summary at the top, which may draw only on the passages beneath it, and the history note, which cites the works it came from. Every claim in either carries a marker to its source.

What it is

  • Ibogaine is an organic heteropentacyclic compound that is ibogamine in which the indole hydrogen para to the indole nitrogen has been replaced by a methoxy group. It has a role as a oneirogen, an inhibitor, a hallucinogen and a plant metabolite. It is an aromatic ether, an organic heteropentacyclic compound and a monoterpenoid indole alkaloid. It is functionally related to an ibogamine. It is a conjugate base of an ibogaine(1+).
  • Ibogaine is a DEA Schedule I controlled substance. Substances in the DEA Schedule I have no currently accepted medical use in the United States, a lack of accepted safety for use under medical supervision, and a high potential for abuse. It is a Hallucinogenic substances substance.
  • ibogaine has been reported in Trachelospermum jasminoides, Tabernanthe iboga, and other organisms with data available.
  • endabuse has been reported in Trachelospermum jasminoides, Tabernanthe iboga, and other organisms with data available.

Recognized use

  • /EXPL THER/ Ibogaine is a hallucinogenic indole alkaloid extracted from the West African shrub tabernanthe iboga (Apocynaceae). It has been investigated as an aid to withdrawal from drug addiction.

    Therapeutic Uses

    Hazardous Substances Data Bank (HSDB)SWEETMAN, S.C. (ed.) Martindale-The Complete Drug Reference. 36th ed. London: The Pharmaceutical Press, 2009., p. 2324

  • Schedule I Controlled Substance: (A) The drug or other substance has a high potential for abuse; (B) The drug or other substance has no currently accepted medical use in treatment in the United States; and (C) There is a lack of accepted safety for use of the drug or other substance under medical supervision.

    Use Classification

    Hazardous Substances Data Bank (HSDB)US Department of Justice/Office of Diversion Control; Schedule of Controlled Substances. Available from, as of February 28, 2014: https://www.deadiversion.usdoj.gov/21cfr/21usc/812.htm

  • Iboga extracts said to be used by African natives while stalking game, to enable them to remain motionless for as long as 2 days while retaining mental alertness. /Iboga extracts/

    Use Classification

    Hazardous Substances Data Bank (HSDB)O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Cambridge, UK: Royal Society of Chemistry, 2013., p. 904

  • THERAPEUTIC CATEGORY: Cardiotonic. Diagnostic aid (glaucoma)

    Use Classification

    Hazardous Substances Data Bank (HSDB)O'Neil, M.J. (ed.). The Merck Index - An Encyclopedia of Chemicals, Drugs, and Biologicals. Cambridge, UK: Royal Society of Chemistry, 2013., p. 905

  • In Gabon and elsewhere in West Central Africa, ibogaine is ingested in the form of scrapings of Tabernanthe iboga root bark. The ritual aim of eating iboga has been conceptualized as "binding"' the binding across time through ancestral contact, or binding participants socially on the basis of a common shared experience of a distinctive consciousness and system of belief.

    Use Classification

    Hazardous Substances Data Bank (HSDB)Alper KR et al; J Ethnopharmacol 115 (1): 9-24 (2008)

How it acts

  • ... In this study, /researchers/ first characterized the actions of ibogaine on ethanol self-administration in rodents. Ibogaine decreased ethanol intake by rats in two-bottle choice and operant self-administration paradigms. Ibogaine also reduced operant self-administration of ethanol in a relapse model. Next, /the researchers/ identified a molecular mechanism that mediates the desirable activities of ibogaine on ethanol intake. Microinjection of ibogaine into the ventral tegmental area (VTA), but not the substantia nigra, reduced self-administration of ethanol, and systemic administration of ibogaine increased the expression of glial cell line-derived neurotrophic factor (GDNF) in a midbra…

    Hazardous Substances Data Bank (HSDB)PMID 15659598Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1193648

  • Ibogaine (Endabuse) is a psychoactive indole alkaloid found in the West African shrub, Tabernanthe iboga. This drug interrupts cocaine and amphetamine abuse and has been proposed for treatment of addiction to these stimulants. However, the mechanism of action that explains its pharmacological properties is unclear. Since previous studies demonstrated differential effects of psychotomimetic drugs (cocaine and methamphetamine) on neuropeptides such as neurotensin (NT), the present study was designed to determine: (1) the effects of ibogaine on striatal, nigral, cortical, and accumbens neurotensin-like immunoreactivity (NTLI); (2) the effects of selective dopamine antagonists on ibogaine-induce…

    Hazardous Substances Data Bank (HSDB)PMID 9914442Alburges ME, Hanson GR; Brain Res 818 (1): 96-104 (1999)

Behavior carries the pharmacological classes and the acute-effect durations, with plasma half-life kept separate from duration of effect.

In the body

  • To investigate the pharmacokinetic properties of ibogaine, a putatively anti-addictive alkaloid, levels of this drug were quantified in plasma and tissues for up to 3 hr following i.v. infusion in rats. Immediately following a 31-35 min infusion (20 mg/kg), mean plasma ibogaine levels were 373 ng/mL; these values declined rapidly thereafter in a biexponential manner. The plasma time course in 5 of 7 animals demonstrated an excellent fit to a two-compartment pharmacokinetic model, with alpha and beta half-lives of 7.3 min and 3.3 hr, respectively. Drug clearance was estimated to be 5.9 L/hr (n = 7). Ibogaine levels in brain, liver and kidney 3 hr after the end of drug infusion were 143-170 ng…

    Absorption, Distribution and Excretion

    Hazardous Substances Data Bank (HSDB)PMID 10849889Hough LB et al; Methods Find Exp Clin Pharmacol 22 (2): 77-81 (2000)

  • The distribution of the putative anti-addictive substance ibogaine was measured in plasma, brain, kidney, liver and fat after ip and sc administration in rats. One hr after ip dosing (40 mg/kg), drug levels ranged from 106 ng/ml (plasma) to 11,308 ng/g (fat), with significantly higher values after sc administration of the same dose. Drug levels were 10-20 fold lower 12 hr after the same dose. These results suggest that: 1) ibogaine is subject to a substantial "first pass" effect after ip dosing, demonstrated by higher drug levels following the sc route, 2) ibogaine shows a large accumulation in adipose tissue, consistent with its lipophilic nature, and 3) persistence of the drug in fat may c…

    Absorption, Distribution and Excretion

    Hazardous Substances Data Bank (HSDB)PMID 8632705Hough LB et al; Life Sci 58 (7): PL119-22 (1996)

  • /The authors/ report ... the tissue distribution of ibogaine and noribogaine, the main metabolite of ibogaine, in a 48-year-old Caucasian male, with a history of drug abuse, found dead at his home after a poisoning involving the ingestion of root bark from the shrub Tabernanthe iboga. Ibogaine and noribogaine were quantified in tissues and fluids using a fully validated liquid chromatography-electrospray mass spectrometry method. Apart from cardiac tissue, ibogaine and noribogaine were identified in all matrices investigated. The highest concentrations were found in spleen, liver, brain, and lung. The tissue/subclavian blood concentration ratios averaged 1.78, 3.75, 1.16, and 4.64 for ibogai…

    Absorption, Distribution and Excretion

    Hazardous Substances Data Bank (HSDB)PMID 16959135Kontrimaviciute V et al; J Anal Toxicol 30 (7): 434-40 (2006)

  • Ibogaine is a psychoactive alkaloid that possesses potential as an agent to treat opiate and cocaine addiction. The primary metabolite arises via O-demethylation at the 12-position to yield 12-hydroxyibogamine. In this report, evidence is presented that the O-demethylation of ibogaine observed in human hepatic microsomes is catalyzed primarily by the polymorphically expressed cytochrome P-4502D6 (CYP2D6). An enzyme kinetic examination of ibogaine O-demethylase activity in pooled human liver microsomes suggested that two (or more) enzymes are involved in this reaction: one with a low KMapp (1.1 uM) and the other with a high KMapp (>200 uM). The low KMapp activity comprised >95% of total intri…

    Metabolism/Metabolites

    Hazardous Substances Data Bank (HSDB)PMID 9698290Obach RS et al; Drug Metab Dispos 26 (8): 764-8 (1998)

History, discovery and cultural use

Written by this site · every claim referenced

In Gabon and elsewhere in West Central Africa, ibogaine is taken as scrapings of the root bark of Tabernanthe iboga 1. The ritual aim of eating iboga has been described as binding: across time through contact with ancestors, and among participants through a shared experience of a distinctive state of consciousness and system of belief 1.

  1. 1Hazardous Substances Data Bank (HSDB), via PubChem

Both sentences follow the HSDB use-class passage held in this archive, closely and without addition. Nothing above is quoted from Ibogaine’s own database records; those appear as quotations elsewhere on this plate.

Histories of this field

Scholarship on psychedelics generally, not on Ibogaine specifically. Whether any of these treats this compound is a question for the book, not for this page.

  • Mescaline: A Global History of the First Psychedelic

    Traces mescaline and the peyote and San Pedro cacti from pre-Columbian ritual use through nineteenth-century chemistry to twentieth-century psychiatry and the counterculture.

    Jay M. Mescaline: A Global History of the First Psychedelic. Yale University Press, New Haven and London; 2019. ISBN 9780300231076.

  • Expanding Mindscapes: A Global History of Psychedelicsopen access

    Essays on the international and cross-cultural history of psychedelic science, deliberately decentring the standard North American and European account.

    Dyck E, Elcock C, editors. Expanding Mindscapes: A Global History of Psychedelics. The MIT Press, Cambridge MA; 2023. ISBN 9780262546935 (paper), 9780262376891 (open access). doi:10.7551/mitpress/14417.001.0001.

  • Plants of the Gods: Their Sacred, Healing, and Hallucinogenic Powers

    Botany, ethnography and chemistry of the principal hallucinogenic plants, by the founder of modern ethnobotany and the chemist who first synthesized LSD.

    Schultes RE, Hofmann A, Rätsch C. Plants of the Gods: Their Sacred, Healing, and Hallucinogenic Powers. 2nd ed. Healing Arts Press, Rochester VT; 2001. ISBN 9780892819799.

  • Psychonauts: Drugs and the Making of the Modern Mind

    The tradition of scientific self-experimentation with psychoactive drugs, and its part in the emergence of psychology and of modernism.

    Jay M. Psychonauts: Drugs and the Making of the Modern Mind. Yale University Press, New Haven; 2023. ISBN 9780300257946.

  • Ancient Psychoactive Substances

    Archaeological and bioarchaeological evidence for psychoactive plant use across the ancient world.

    Fitzpatrick SM, editor. Ancient Psychoactive Substances. University Press of Florida, Gainesville; 2018. ISBN 9780813056708.

  • History and Current Status of Psychedelics and Entactogens for the Treatment of Psychiatric Disorders

    A chapter tracing psychedelic and entactogen research from earlier ritual use through the mid-century research period to current clinical trials.

    Stroud C, Posey Norris SM, Matney C, editors. History and Current Status of Psychedelics and Entactogens for the Treatment of Psychiatric Disorders. In: Exploring Psychedelics and Entactogens as Treatments for Psychiatric Disorders: Proceedings of a Workshop. National Academies Press, Washington DC; 2022. NBK587225.

    Workshop proceedings record what participants said; they are not a consensus statement of the National Academies.

  • Pharmacokinetic and Pharmacodynamic Aspects of Peyote and Mescaline: Clinical and Forensic Repercussions

    Peer-reviewed review covering the isolation, synthesis, pharmacology and ritual use of peyote and mescaline.

    Dinis-Oliveira RJ, Pereira CL, da Silva DD. Pharmacokinetic and Pharmacodynamic Aspects of Peyote and Mescaline: Clinical and Forensic Repercussions. Current Molecular Pharmacology 12(3):184–194; 2019. doi:10.2174/1874467211666181010154139.

Institutional archives

  • Heffter Research Institute Funds and coordinates clinical research on psilocybin, and keeps records of the studies it has supported since 1993. Sponsors the research it archives.
  • Multidisciplinary Association for Psychedelic Studies (MAPS) Sponsors clinical research, chiefly on MDMA-assisted therapy, and publishes an archive of historical and contemporary documents. A sponsor and an advocacy organization, not a disinterested archive; its clinical programme has a commercial arm.

The rest of this dossier

  • Affinity — 14 measurements in this archive, equilibrium constants kept apart from functional readouts.
  • Toxicology — 5 published passages, plus any assay in this archive bearing on toxicity.
  • Legal — DEA Schedule I, with the passage it was read from.
  • Systems — where this compound’s targets are transcribed, by brain region and tissue.

Passages via PubChem descriptive sections, aggregating DrugBank, LiverTox, FDA, DEA, HSDB, EPA. Each is quoted whole and attributed to the database that published it. The only prose written here about Ibogaine is the history note, which says so on its face and carries a reference for every claim in it.

II · Identity

Structure and descriptors

Descriptors are computed here with RDKit from the structure PubChem returns — not from the archive's stored copy, so an edited local structure cannot reach this table.

2D structural depiction of Ibogaine
Depiction served by PubChem for CID 197060. Not redrawn here, so the picture and the identity come from the same record.
Formula
C20H26N2OR
Molecular weight
310.44g/molR
Exact mass
310.2045DaR
cLogP
3.94R
TPSA
28.3ŲR
H-bond donors
1R
H-bond acceptors
2R
Rotatable bonds
2R
Aromatic rings
2R
Heavy atoms
23R
Fraction sp³
0.600R
Formal charge
0R

Computed with RDKit 2025.09.2 from the SMILES returned by PubChem. Audit run 26/09/2026.

Bemis–Murcko scaffold

c1ccc2c3c([nH]c2c1)[C@@H]1C[C@H]2CC[C@@H]1N(CC3)C2

Shared with Ibogaline, Ibogamine, Noribogaine, Tabernanthine. All families

III · Behavior

Behavioral summary

Class, mechanism, and the duration of acute effects — each quoted from the record or trial that publishes it. Duration of effects and plasma half-life are shown separately, because they are different quantities and diverge by a factor of three or four.

Classification

Duration of acute subjective effects

—

No controlled human trial reporting a duration for this compound is cited here. The archive does hold onset and duration ranges for it, inherited from an earlier build, but their source column is empty and so they cannot be shown. A duration is not inferred from a chemical relative.

Plasma elimination half-life

How fast the body clears the drug — not how long the effects last. The two diverge sharply: LSD is cleared with a half-life of about 2.6 h while its subjective effects run 8–12 h.

10.2 h

“Compared with placebo-pretreated subjects, paroxetine-pretreated subjects had rapid (Tmax = 1.5 hours) and substantial absorption of ibogaine, with detectable levels out to 72 hours, and an elimination half-life of 10.2 hours”
Paroxetine-pretreated group, single 20 mg oral dose.Glue P et al., Journal of clinical pharmacology 2015. PMID 25651476

Primary pharmacological drivers

ChEMBL holds no curated mechanism-of-action record for this compound. The measured affinities below are the evidence this archive has for what it binds.

Mechanism, as published

Quoted verbatim from the database named after each passage, never summarized.

  • ... In this study, /researchers/ first characterized the actions of ibogaine on ethanol self-administration in rodents. Ibogaine decreased ethanol intake by rats in two-bottle choice and operant self-administration paradigms. Ibogaine also reduced operant self-administration of ethanol in a relapse model. Next, /the researchers/ identifie…
    Hazardous Substances Data Bank (HSDB)PMID 15659598Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1193648
  • Ibogaine (Endabuse) is a psychoactive indole alkaloid found in the West African shrub, Tabernanthe iboga. This drug interrupts cocaine and amphetamine abuse and has been proposed for treatment of addiction to these stimulants. However, the mechanism of action that explains its pharmacological properties is unclear. Since previous studies…
    Hazardous Substances Data Bank (HSDB)PMID 9914442Alburges ME, Hanson GR; Brain Res 818 (1): 96-104 (1999)
  • Ibogaine, a putative antiaddictive drug, is remarkable in its apparent ability to downgrade withdrawal symptoms and drug craving for extended periods of time after a single dose. Ibogaine acts as a non-competitive NMDA receptor antagonist, while NMDA has been implicated in long lasting changes in neuronal function and in the physiological…
    Hazardous Substances Data Bank (HSDB)PMID 11055745Leal MB e al; Neurochem Res 25 (8): 1083-7 (2000)
  • The iboga alkaloids are a class of small molecules defined structurally on the basis of a common ibogamine skeleton, some of which modify opioid withdrawal and drug self-administration in humans and preclinical models. These compounds may represent an innovative approach to neurobiological investigation and development of addiction pharma…
    Hazardous Substances Data Bank (HSDB)PMID 24204784Full text: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3818563

IV · Clinical

Clinical description

Where this compound's substance class sits in ICD-11 and DSM-5-TR, and how much of the recorded literature speaks to each domain of a mental status examination.

Filed under Hallucinogens

  • 6C49Disorders due to use of hallucinogens

Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, Text Revision (DSM-5-TR): Hallucinogen-Related Disorders. Category names only — the manual is in copyright and no diagnostic criterion is reproduced here.

How much has been written about each domain

The clinical domains, and how many of the records this archive holds for this compound say something under each. What the terms mean, and the word list behind every spoke, are set out in the method.

Affect0Mood1Perception1Cognition3Thought process0Thought content0Psychomotor activity0Insight and judgment0
This measures the literature, not the compound. Each spoke counts how many of the 11 records this archive holds for this compound say something under that domain — 3 at the widest ring. A long spoke means the subject has been written about, not that the effect is strong, and a spoke at the center means nothing here discusses it rather than that nothing happens. The terms behind each domain are listed in the method.
Mood 1
matched on “elation” · in PMID 23123541
Perception 1
matched on “hallucinogen” · in PMID 23919354
Cognition 3
matched on “concentrat” · in PMID 9914442; PMID 23919354; PMID 24112325

V · Systems

Systems physiology

Where the targets this compound binds are transcribed — brain regions on the left, peripheral and autonomic tissues on the right. A join of two measurements, not a claim about what the compound does to either.

093 nTPM

Square-root ramp · shared scale across both plates

Shading is transcript level — not affinity, and not affinity combined with expression. Outlined but unshaded organs hold none of this compound’s resolved targets above the atlas’s detection threshold. Anatomy from EMBL-EBI Anatomogram (Apache License 2.0); regions identified by Uberon (uberon.org), CC BY 3.0.

Brain regions

Regions where this compound's measured targets are transcribed. Linked from the plate above.

  1. midbrain

    92.9 nTPM
  2. pituitary gland

    41.5 nTPM
  3. cerebellum

    32.4 nTPM
  4. hypothalamus

    14.4 nTPM
  5. basal ganglia

    14.0 nTPM
  6. cerebral cortex

    10.0 nTPM
  7. hippocampal formation

    8.9 nTPM
  8. amygdala

    7.5 nTPM
  9. retina

    5.3 nTPM
  10. spinal cord

    4.0 nTPM

Peripheral & autonomic

Tissues outside the CNS expressing the same targets — where a compound's bodily effects become possible.

  1. small intestine

    38.0 nTPM
  2. colon

    36.0 nTPM
  3. heart muscle

    28.4 nTPM
  4. lung

    27.2 nTPM
  5. urinary bladder

    13.4 nTPM
  6. stomach 1

    10.6 nTPM
  7. duodenum

    9.7 nTPM
  8. smooth muscle

    7.0 nTPM
  9. adrenal gland

    3.4 nTPM
  10. pancreas

    3.2 nTPM
  11. spleen

    1.7 nTPM
  12. kidney

    1.1 nTPM
  13. skeletal muscle

    1.0 nTPM
  14. salivary gland

    0.9 nTPM
  15. thyroid gland

    0.7 nTPM
  16. liver

    0.2 nTPM

Each row joins two published measurements and nothing else: the affinity this archive holds for the compound at that target, and the transcript level the Human Protein Atlas reports for that target’s gene in that region. Bars scale with expression only. Expression is not activation — a receptor transcribed in a region is a receptor available to be bound there, which is a weaker and more defensible claim than saying the region is affected.

3 of this compound’s targets could not be resolved to a gene and are absent from both columns: NMDA, Sigma 1, Sigma 2.

Expression data from Human Protein Atlas (CC BY-SA 3.0), RNA expression, nTPM (normalized transcripts per million), consensus tissue dataset. Uhlén M, et al. Tissue-based map of the human proteome. Science. 2015;347(6220):1260419.

VI · Profile

Affinity rosette

The strongest measurement at each of 8 molecular targets. Cell-line and whole-organism screens are excluded here — they carry no affinity — and appear in the table below.

KOR — Ki 5.57 pXMOR — Ki 5.36 pXSigma 2 — Ki 6.69 pXSigma 1 — Ki 6.60 pXSERT — IC50 6.23 pXDAT — IC50 5.39 pXNMDA — Ki 5.70 pXhERG — Ki 6.15 pXKORMORSigma 2Sigma 1SERTDATNMDAhERG579
Fig. Radius is pX = −log₁₀(value in M), that is 9 − log₁₀(value in nM), computed from the normalized measurement. Hatched wedges are equilibrium binding constants (Ki, Kd); dashed outlines are functional readouts (IC₅₀, EC₅₀, AC₅₀, potency), which answer a different question and are not pooled with them. Rings mark whole pX units from 5 to 10, labeled every second ring in the gutter at the top. Where a target carries several measurements, the strongest is drawn.

VII · Toxicology

Toxicological profile

What has been measured, and what has been published — kept apart, and neither scored. There is no risk rating on this page; the archive once carried one, identical for every compound, produced by a stub.

Measured in this archive

Assays that bear on toxicity, drawn from the same ChEMBL records as everything else on this page. They are measurements of what a compound binds or does to cells — not verdicts about what it does to a person.

hERG / cardiac ion channel 1

Block of the hERG potassium channel (KCNH2) is the standard in-vitro flag for QT prolongation. A measured affinity is not an arrhythmia risk, and this archive does not convert one into the other.

  • hERGKi710nMno origin

As published

Quoted verbatim from the database named after each passage, never summarized — a summary of a toxicology statement is a new claim.

Human Toxicity Excerpts

  • /CASE REPORTS/ /The authors/ report the case of a man who died twelve hours after ingesting powdered iboga root, commonly taken for its stimulant and hallucinogenic properties. Ibogaine and ibogamine were quantified in the powder ingested and the victim's body fluids by GC-MS/MS after liquid-liquid extraction. The concentrations of ibogaine measured in the blood samples taken at the scene and in the peripheral blood,…

    Hazardous Substances Data Bank (HSDB)PMID 23919354Mazoyer C et al; J Forensic Sci. 2013 Nov;58(6):1666-72 (2013)

  • /CASE REPORTS/ Ibogaine is a naturally occurring alkaloid derived from the roots of the rain forest shrub Tabernanthe iboga. Deaths have occurred temporarily related to the use of ibogaine. However, although not licensed as therapeutic drug, and despite evidence that ibogaine may disturb the rhythm of the heart, this alkaloid is currently used as an anti-addiction drug in alternative medicine for detoxification purpo…

    Hazardous Substances Data Bank (HSDB)PMID 24112325Papadodima SA et al; J Forensic Leg Med. 2013 Oct;20(7):809-11 (2013)

  • /CASE REPORTS/ Ibogaine is a naturally occurring psychoactive plant alkaloid that is used globally in medical and nonmedical settings for opioid detoxification and other substance use indications. All available autopsy, toxicological, and investigative reports were systematically reviewed for the consecutive series of all known fatalities outside of West Central Africa temporally related to the use of ibogaine from 1…

    Hazardous Substances Data Bank (HSDB)PMID 22268458Alper KR et al; J Forensic Sci 57 (2): 398-412 (2012)

  • /CASE REPORTS/ Ibogaine is a naturally occurring psychoactive alkaloid extracted from the roots of the Tabernanthe iboga plant, which in alternative medicine is used to treat drug dependency. However, this upcoming, online advocated therapy can be dangerous due to its potentially lethal adverse effects. We present three cases in which toxic side effects were noted. /The authors/ used the Naranjo scale to estimate the…

    Hazardous Substances Data Bank (HSDB)PMID 23123541Paling FP et al; Neth J Med. 2012 Nov;70(9):422-4 (2012)

  • /OTHER TOXICITY INFORMATION/ Ibogaine is the most important alkaloid of the Central African Iboga-shrub. It is the central drug in Gabonian initiation ceremonies in which it is used to cause a near-death experience. In Western countries it is used in private clinics to treat addiction. However, in the United States and most European countries it is classified as an illegal drug because at least eight persons have die…

    Hazardous Substances Data Bank (HSDB)PMID 16698188Maas U, Strubelt S; Med Hypotheses 67 (4): 960-4 (2006)

Published passages via PubChem toxicology sections, aggregating Hazardous Substances Data Bank (HSDB), RTECS, LiverTox. No figure on this page is scored, ranked or combined into a risk level.

VIII · Evidence

Every measurement

One row per published value. The identifier in the last column resolves to the ChEMBL assay record it was read from.

Equilibrium binding constants 10

Ki and Kd — a concentration at equilibrium. Directly comparable across rows at the same target.

TargetClassTypeValue (nM)pXOrganismAssay
UncheckedUnclassifiedKi2016.70— organism not recordedCHEMBL3238653
Sigma 2Sigma receptorsKi2066.69HUMANPMID 20126400
Sigma 1Sigma receptorsKi2506.60Cavia porcellusCHEMBL915240
hERGIon channelsKi7106.15HAMSTERPMID 25636206
NMDAGlutamate receptorsKi2,0015.70RATPMID 20126400
KOROpioid receptorsKi2,7175.57HUMANPMID 20126400
MOROpioid receptorsKi4,3625.36HUMANPMID 20126400
Sigma 1Sigma receptorsKi5,8395.23HUMANPMID 20126400
Sigma 1Sigma receptorsKi8,5545.07Homo sapiensCHEMBL3238652
UncheckedUnclassifiedKi9,3105.03— organism not recordedCHEMBL915241

Functional readouts 4

IC₅₀, EC₅₀, AC₅₀ and potency. Assay-dependent, and not interchangeable with a binding constant.

TargetClassTypeValue (nM)pXOrganismAssay
SERTMonoamine transportersIC505906.23Rattus norvegicusCHEMBL803045
DATMonoamine transportersIC504,1105.39Rattus norvegicusCHEMBL675227
NMDAGlutamate receptorsIC505,2005.28Rattus norvegicusCHEMBL751794
KOROpioid receptorsIC5025,0004.60Rattus norvegicusCHEMBL753903
P
PubChem
C
ChEMBL
R
Computed here with RDKit
D
Derived here from the stored measurement

IX · Trials

Registered clinical trials

Studies filed with ClinicalTrials.gov that name this compound as an intervention. A registered trial is a protocol, not a result — status and enrollment are printed beside every row, and withdrawn studies are counted rather than hidden.

5T

Registered studies

2T

Open or ongoing

3T

With a phase recorded

By phase

A study may carry two phase codes at once, so these count studies bearing each phase and do not sum to the total.

  • Phase 23

By status

The registry’s own status for each record. Withdrawn and terminated studies are counted here rather than hidden — a stopped trial is part of what is known.

  • Completed2
  • Active, not recruiting2
  • Withdrawn1

Every matched study

Newest first by start date. Each identifier opens the registry record it came from; the title is the sponsor’s own, quoted.

  • NCT06810765Withdrawn · Phase 2

    Trifecta Research Study

    Enrollment
    0Tactual
    Started
    2025-09
    Sponsor
    Johns Hopkins University

    Conditions PTSD - Post Traumatic Stress Disorder · Cognitive Dysfunction · Brain Trauma · Brain Injuries

    Matched “Ibogaine” in the study’s intervention “ibogaine with magnesium treatment”

  • NCT03380728Completed · Phase 2

    Ibogaine in the Treatment of Alcoholism: an Open-label Escalating-dose Trial

    Enrollment
    9Tactual
    Started
    2022-10-30
    Sponsor
    University of Sao Paulo

    Conditions Alcoholism

    Matched “Ibogaine” in the study’s intervention “Ibogaine Hydrochloride”

  • NCT07717866Active, not recruiting

    Trifecta Research Study

    Enrollment
    52Tactual
    Started
    2022-08-01
    Sponsor
    Axial Therapeutic Research

    Conditions PTSD - Post Traumatic Stress Disorder · Cognitive Dysfunction · Brain Injury · Depression - Major Depressive Disorder · Suicidal Ideation

    Matched “Ibogaine” in the study’s intervention “Ibogaine Hydrochloride with Magnesium Sulfate”

  • NCT04313712Active, not recruiting

    Pre-post Evaluation of the Safety and Efficacy of Ibogaine-Magnesium Therapy in Veterans With Repeated Blast Exposure

    Enrollment
    30Testimated
    Started
    2021-11-15
    Sponsor
    Stanford University

    Conditions Blast or Combat Exposure · Head Injury Trauma

    Matched “Ibogaine” in the study’s intervention “ibogaine with magnesium treatment”

  • NCT04003948Completed · Phase 2

    Preliminary Efficacy and Safety of Ibogaine in the Treatment of Methadone Detoxification

    Enrollment
    20Tactual
    Started
    2020-10-28
    Sponsor
    International Center for Ethnobotanical Education, Research, and Service

    Conditions Drug Dependence · Drug Use Disorders · Opioid Dependence

    Matched “Ibogaine” in the study’s intervention “Ibogaine Hydrochloride”

Records from ClinicalTrials.gov (U.S. National Library of Medicine, NIH), API v2. A study is listed against a compound only when a verified name for that compound appears as a whole word in one of the study's own intervention names. A short code must appear as written, and a name the registry uses for something else (Aleph, a vaccine maker) is not matched. Title matches are not accepted. The matched name and the intervention text it matched are shown with every row.

Searched as Ibogaine · (-)-Ibogaine · 12 Methoxyibogamine. Run this search at the registry — it returns the unfiltered result, including studies this page rejected as belonging to a different molecule.

A registered trial is a protocol somebody filed with the registry. It is not a result, and nothing on this plate says whether Ibogaine worked.

XI · Literature

Sources behind this dossier

The papers this compound's values were read from, ranked by what each contributed. Not a review of the field.

Every paper below is one some value on this page came from — a binding constant, a passage of pharmacology or toxicology, or a measured duration. Each entry says what this archive took from it. Nothing else is claimed about any of them: the title is the study’s own account of itself, and a summary written here would be an assertion with no source behind it.

  1. 01

    Psychedelics and the human receptorome

    Ray TS · PloS one 2010

    • · 5 measurements at 5 targets (Ki), strongest Sigma 2 at 6.69 pX

    PMID 20126400

  2. 02

    hERG Blockade by Iboga Alkaloids

    Alper K, Bai R, Liu N et al. · Cardiovascular toxicology 2016

    • · 1 measurement at 1 target (Ki), strongest hERG at 6.15 pX

    PMID 25636206

  3. 03

    Influence of CYP2D6 activity on the pharmacokinetics and pharmacodynamics of a single 20 mg dose of ibogaine in healthy volunteers

    Glue P, Winter H, Garbe K et al. · Journal of clinical pharmacology 2015

    • · Plasma elimination half-life

    PMID 25651476

  4. 04

    Effect of Iboga alkaloids on µ-opioid receptor-coupled G protein activation

    Antonio T, Childers SR, Rothman RB et al. · PloS one 2013

    • · Mechanism of Action

    PMID 24204784

  5. 05
  6. 06

    Ibogaine related sudden death: a case report

    Papadodima SA, Dona A, Evaggelakos CI et al. · Journal of forensic and legal medicine 2013

    • · Human Toxicity Excerpts

    PMID 24112325

  7. 07

    Fatalities temporally associated with the ingestion of ibogaine

    Alper KR, Stajić M, Gill JR · Journal of forensic sciences 2012

    • · Human Toxicity Excerpts

    PMID 22268458

  8. 08

    Life-threatening complications of ibogaine: three case reports

    Paling FP, Andrews LM, Valk GD et al. · The Netherlands journal of medicine 2012

    • · Human Toxicity Excerpts

    PMID 23123541

  9. 09
  10. 10

    Glial cell line-derived neurotrophic factor mediates the desirable actions of the anti-addiction drug ibogaine against alcohol consumption

    He DY, McGough NN, Ravindranathan A et al. · The Journal of neuroscience : the official journal of the Society for Neuroscience 2005

    • · Mechanism of Action

    PMID 15659598

  11. 11

    Long-lasting ibogaine protection against NMDA-induced convulsions in mice

    Leal MB, de Souza DO, Elisabetsky E · Neurochemical research 2000

    • · Mechanism of Action

    PMID 11055745

  12. 12

    Pharmacokinetic characterization of the indole alkaloid ibogaine in rats

    Hough LB, Bagal AA, Glick SD · Methods and findings in experimental and clinical pharmacology 2000

    • · Biological Half-Life

    PMID 10849889

  13. 13