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    Ibogaine molecular structure

    Ibogaine Stats & Data

    Iboga Endabuse Nih 10567
    NPS DataHub
    MW310.44
    FormulaC20H26N2O
    CAS83-74-9
    IUPAC12-Methoxyibogamine
    SMILESCCC1CC2CN3CCc4c5cc(OC)ccc5nc4C(C2)C13
    InChIKeyHSIBGVUMFOSJPD-CFDPKNGZSA-N
    Chemical Class Iboga alkaloid
    Psychoactive Class Depressant / Dissociative / Psychedelic

    Pharmacology

    DrugBank

    Mechanism of Action

    ... 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),

    Metabolism

    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 micr

    Receptor Profile

    Receptor Actions

    Agonists
    5-HT2A receptor agonist
    Kappa-opioid receptor agonist
    Sigma receptor agonist
    Antagonists
    NMDA receptor antagonist
    Inhibitors
    Serotonin reuptake inhibitor

    Measured Affinities

    Guide to PHARMACOLOGY

    Measured binding and functional data for ibogaine, curated by the IUPHAR/BPS Guide to PHARMACOLOGY. Each row cites the paper it came from. Lower concentrations mean tighter binding — a value in the sub-nanomolar range indicates a very potent interaction.

    Target Action Measure Value Concentration Species Source
    SERT SLC6A4 Inhibition pIC50 6.3 501.19 nM Human PMID 35707155

    Reading this. pKi, pEC50 and pIC50 are negative log molar values, so a higher number means a tighter interaction; the concentration column converts them for you. Values from non-human species are laboratory measurements and do not translate directly to human effect. Receptor affinity is not a dose — it describes what a molecule binds, not how much of it is safe to take.

    Receptor data from the IUPHAR/BPS Guide to PHARMACOLOGY (v2026.2), licensed CC BY-SA 4.0. Matched to this substance by InChIKey.

    History & Culture

    The use of Tabernanthe iboga has been practiced for centuries among Central African foragers in Gabon, Cameroon, and surrounding countries, with this ethnobotanical knowledge eventually passed to the Bwiti tribe of Gabon. Within the Bwiti religion, iboga serves as a sacrament central to numerous spiritual practices, including rites of passage, spiritual communion, resolution of pathological problems, and communication with ancestors. The plant remains fundamental to indigenous society in these regions, holding such cultural significance that in 2000, the Council of Ministers of the Republic of Gabon declared iboga a national treasure.

    1889–1901

    The use of iboga in African spiritual ceremonies was first documented by French and Belgian explorers in the 19th century, with early reports attributed to French naval physician and Gabon explorer Marie-Théophile Griffon du Bellay. The first formal botanical description of Tabernanthe iboga was published in 1889. Twelve years later, in 1901, ibogaine was independently isolated from the plant by two research groups: Dybowski and Landrin, and separately by Haller and Heckel, both working with samples obtained from Gabon.

    1930s–1966

    Total synthesis of ibogaine was achieved in 1956, with its molecular structure subsequently confirmed through X-ray crystallography in 1960. Additional synthetic methodologies continued to be developed, with G. Büchi accomplishing a complete synthesis in 1966. During this period, ibogaine also maintained a commercial presence in France. From the 1930s through 1966, it was marketed as Lambarène, an extract of Tabernanthe manii promoted as a mental and physical stimulant. Each tablet contained approximately 200 mg of extract with relatively low doses of 4 to 8 mg ibogaine. The product gained popularity among post-World War II athletes before being withdrawn from the French market in 1966 when ibogaine-containing products were prohibited. Another formulation marketed during this era was Iperton, which contained Tabernanthe iboga extract at 40 mg per dose unit.

    1962–1992

    Anecdotal observations regarding ibogaine's potential therapeutic effects began emerging in the early 1960s. The compound's anti-addictive properties were discovered serendipitously in 1962 by Howard Lotsof, then 19 years old, when he and five friends—all heroin users—noticed subjective reductions in craving and withdrawal symptoms while taking the substance. Subsequent observations convinced Lotsof of its potential utility in treating substance dependence, leading him to contract with a Belgian company to produce ibogaine tablets for clinical trials in the Netherlands. He was awarded a United States patent for the product in 1985. Beyond addiction treatment, ibogaine was also explored in psychotherapeutic contexts during this period. Researchers documented physician-patient interactions emphasizing early memory recall and the reliving of past experiences, with notable work conducted by Claudio Naranjo. In 1992, Eric Taub established the first ibogaine treatment center at an offshore location near the United States, initiating treatments and advocating for broader recognition of the compound. He was subsequently joined in Costa Rica by Lex Kogan, another prominent figure in the field. Together, they systematized ibogaine administration protocols and established medically monitored treatment clinics across several countries. Since then, clinics have been founded worldwide to serve individuals seeking to reduce or eliminate dependence on other substances, particularly opioids.

    2025–present

    Interest in ibogaine as a potential treatment for addiction has continued to grow. In 2025, the state of Texas allocated $50 million to fund clinical research on ibogaine, with the stated goal of developing FDA-approved treatments for opioid use disorder, co-occurring substance use disorders, and other ibogaine-responsive conditions. The initiative, supported by former Governor Rick Perry, established a consortium of universities, hospitals, and drug developers, positioning Texas as a potential center for psychedelic medicine research.

    Ibogaine has appeared in various cultural and media contexts over the decades. In 1972, gonzo journalist Hunter S. Thompson published a satirical article in Rolling Stone while covering the Democratic primary campaign, falsely asserting that candidate Edmund Muskie was addicted to ibogaine. The piece was not recognized as satire by many readers and other journalists, and the unfounded accusation reportedly damaged Muskie's reputation—Thompson later expressed surprise that anyone had believed it. The substance has also been the subject of several books. Author and Yippie activist Dana Beal co-authored "The Ibogaine Story" in 1997. Daniel Pinchbeck described his personal ibogaine experience in "Breaking Open the Head" (2002) and a subsequent Guardian article titled "Ten years of therapy in one night" (2003). More recently, musician and author Geoff Rickly based his debut novel "Someone Who Isn't Me" on his experiences with heroin addiction and treatment at an ibogaine clinic in Mexico.

    Toxicity

    Ibogaine's toxicity is cardiac, and it is well documented: it blocks hERG potassium channels at the same concentrations used to treat addiction (IC50 around 3–4 µM against human plasma levels that reach up to 11 µM), prolonging the QT interval and setting up ventricular arrhythmias. Alper's forensic series counted 19 deaths temporally associated with ibogaine over 1990–2008; most involved pre-existing (mainly cardiovascular) disease or other drugs, and deaths occurred up to three days after dosing. That delay is the signature of noribogaine, the active metabolite: it blocks hERG about as potently as ibogaine and its half-life is 28–49 hours, so the danger window outlasts the trip by days — one documented case's QTc stayed prolonged for 12 days. Arrhythmias are also documented in people with no cardiac history. The clinical screening standards exist for good reason: a resting 12-lead ECG (exclusion at QTc 450 ms in males / 470 ms in females), potassium and magnesium checked and corrected before dosing (low levels independently prolong QT), no significant cardiac history, and continuous ECG monitoring during treatment. Unsupervised use is where the deaths concentrate.

    Effect Profile

    Curated + 50 Reports
    Psychedelic 8.6

    Strong visuals, headspace, and auditory effects with strong body load

    Visual Intensity×3
    10104.2
    Headspace Depth×3
    10103.8
    Auditory Effects×1
    8105.3
    Body Load / Somatic Effects×1
    96.35.9
    Catalog Erowid BlueLight
    Dissociative 4.1

    Moderate insight with strong motor impairment, moderate mania, mild dissociative depth

    Dissociative Depth×3
    44.53.5
    Mania / Compulsion×1
    63.5
    Insight / Novel Thought×2
    61.2
    Motor / Sensory Impairment×1
    99.42.4
    Catalog Erowid BlueLight

    Tolerance & Pharmacokinetics

    drugs.wiki
    Half-Life
    Ibogaine: ~4–7 h; noribogaine: ~28–49 h (human plasma)
    Addiction Potential
    Ibogaine is not considered addictive and is not a substitute agonist therapy. It is often administered once (‘single administration modality’) in addiction-interruption contexts. However, post-ibogaine opioid tolerance may be reduced, increasing overdose risk if relapse occurs; extended psychosocial follow-up is critical.

    Tolerance Decay

    Half tolerance 1d Baseline ~7d

    Acute tachyphylaxis to re-dosing is common due to persistent noribogaine; functional sensitivity returns over days–weeks. Repeated high-dose use is uncommon due to intensity and cardiotoxic window.

    Cross-Tolerances

    Classical psychedelics (5-HT2A agonists)

    Experience Report Analysis

    Erowid BlueLight
    46 Reports
    33 Single-substance
    1997–2023 Date Range
    27 With Age Data
    23 Effects Detected

    Demographics

    Gender Distribution

    Age Distribution

    Reports Over Time

    Effect Analysis

    Erowid + Bluelight

    Effects aggregated from 50 experience reports (33 single-substance Erowid + 17 Bluelight)

    50 Reports
    84 Effects Detected
    31 Positive
    36 Adverse
    17 Neutral

    Effect Sentiment Distribution

    Confidence Distribution

    Each bar is the share of reports mentioning the effect; its whisker, and the band on the rows below, is the 95% interval: where the share could plausibly be with other reports of the same kind.

    Rows resting on fewer than 20 reports show a count (“3 of 7”) instead of a bar. Why 20?

    Positive Effects 31

    Color Enhancement 63.6% (95% interval 47 to 78 percent) 70%
    Stimulation 45.5% (95% interval 30 to 62 percent) 70%
    Empathy 40.0% (95% interval 28 to 54 percent) 85%
    Introspection 40.0% (95% interval 28 to 54 percent) 78%
    Euphoria 30.0% (95% interval 19 to 44 percent) 90%
    Body High 28.0% (95% interval 18 to 42 percent) 70%
    Music Enhancement 24.0% (95% interval 14 to 37 percent) 81%
    Focus Enhancement 20.0% (95% interval 11 to 33 percent) 75%
    Tactile Enhancement 12.0% (95% interval 6 to 24 percent) 70%
    Sedation 12.0% (95% interval 6 to 24 percent) 75%
    Insight 4 of 17 86%
    Mystical Quality 3 of 17 83%
    Awe 3 of 17 77%
    Out-Of-Body Experience 3 of 17 87%
    Emotional Release 2 of 17 82%
    Empathogenic Connection 2 of 17 78%
    Geometric Imagery 2 of 17 82%
    Contentment 2 of 17 80%
    Mood Elevation 2 of 17 85%
    Contact-With-Presence 1 of 17 70%

    Adverse Effects 36

    Anxiety 54.0% (95% interval 40 to 67 percent) 82%
    Nausea 38.0% (95% interval 26 to 52 percent) 85%
    Confusion 32.0% (95% interval 21 to 46 percent) 80%
    Motor Impairment 32.0% (95% interval 21 to 46 percent) 79%
    Increased Heart Rate 15.2% (95% interval 7 to 31 percent) 70%
    Body Load 9 of 17 84%
    Fear 8 of 17 84%
    Dizziness 6 of 17 85%
    Insomnia 5 of 17 86%
    Visual Trails 3 of 17 83%
    Heaviness 3 of 17 78%
    Depersonalization 3 of 17 72%
    Vomiting 3 of 17 88%
    Restlessness 3 of 17 80%
    Vertigo 2 of 17 88%
    Memory Suppression 2 of 17 88%
    Thought Loops 2 of 17 72%
    Depression 2 of 17 82%
    Emotional Blunting 2 of 17 78%
    Ataxia 2 of 17 85%
    Show 16 more adverse effects
    Pain Enhancement 2 of 17 80%
    Visual Vibration 2 of 17 85%
    Thought Deceleration 2 of 17 80%
    Guilt 1 of 17 85%
    Anhedonia 1 of 17 90%
    Hot Flashes 1 of 17 80%
    Cold Flashes 1 of 17 80%
    Body Temperature Change 1 of 17 75%
    Vibrating 1 of 17 90%
    Tremor 1 of 17 85%
    Appetite Suppression 1 of 17 75%
    Afterimages 1 of 17 90%
    Headache 1 of 17 85%
    Amnesia 1 of 17 95%
    Numbness 1 of 17 70%
    Dry Mouth 1 of 17 75%
    Show 17 neutral or unclassified mentions
    Visual Distortions 63.6% (95% interval 47 to 78 percent)
    Auditory Effects 44.0% (95% interval 31 to 58 percent)
    Closed-Eye Visuals 34.0% (95% interval 22 to 48 percent)
    Dissociation 27.3% (95% interval 15 to 44 percent)
    Hospital 15.2% (95% interval 7 to 31 percent)
    Time Distortion 12.1% (95% interval 5 to 27 percent)
    Ego Dissolution 12.0% (95% interval 6 to 24 percent)
    Open-Eye Visuals 8.0% (95% interval 3 to 19 percent)
    Entity Imagery 7 of 17
    Time Dilation 5 of 17
    Brightness Enhancement 2 of 17
    Peripheral Imagery 1 of 17
    Pupil Dilation 1 of 17
    Temporal Disorientation 1 of 17
    Pareidolia 1 of 17
    Environmental Transfiguration 1 of 17
    Tingling 1 of 17

    Also reported in combinations. In the 13 Ibogaine reports where another drug was taken too, 3 mention hospital, emergency services or an overdose, 1 a seizure and 1 psychosis (too few reports for percentages). In the 33 single-substance reports: 15.2%, 0.0% and 6.1%. These are not in the figures above: they cannot be put down to Ibogaine alone, and a mention is not always something that happened to the writer.

    Dosage Distribution

    Dose distribution from experience reports, one dose per report (the first listed). Doses above Q3 + 3×IQR, far above what people typically take, are left out of the median and range and listed under each route: most are real heavy doses or overdoses, not mistakes.

    Median: 830.0 mg IQR: 237.5–1000.0 mg n=18

    1 report gave a dose above the typical range (30,000 mg), so it is not in the figures above. Listing a dose here does not mean it is safe.

    Show the report

    Real-World Dose Distribution

    Erowid

    From 61 of 67 recorded dose entries: those that state a weight (mg, g or µg), in routes with at least five of them. Values above Q3 + 3×IQR, far above what people typically take, are left out; they can include real heavy doses and overdoses, not only mistakes.

    Oral (n=58)

    Median: 477.0mg 25th: 258.0mg 75th: 1000.0mg 90th: 1330.0mg

    Common Combinations

    Most co-occurring substances, as a share of all 46 reports filed under Ibogaine; whiskers are 95% intervals

    Form / Preparation

    Most common forms and preparations, as a share of the 22 reports that give one; whiskers are 95% intervals

    Body-Weight Dosing

    Dose per kg of body weight, one dose per report (the first listed), from reports giving a weight of 30–250 kg. Doses above Q3 + 3×IQR, far above what people typically take, are left out of the median and range and listed under each route.

    Median: 6.179 mg/kg IQR: 2.009–11.695 mg/kg n=14

    1 dose more than 50 times the median may be a typing or unit error and is not in the figures either: check the report.

    Show the report

    Possibly a typing or unit error:

    Redose Patterns

    Redosing behavior across 27 reports

    33.3% (95% interval 19 to 52 percent) Redosed
    1.8 Avg Doses
    110m Median Interval

    Legal Status

    Country Status Notes
    Gabon National Treasure (Protected) Declared a national treasure by the Council of Ministers of the Republic of Gabon in 2000. Iboga is fundamental to the Bwiti religion and is used legally for ceremonial purposes including rites of passage, spiritual communion, and communication with ancestors. Traditional and religious use is protected under national recognition.

    Harm Reduction

    drugs.wiki

    Ibogaine and its active metabolite noribogaine inhibit cardiac hERG channels at clinically relevant concentrations, prolonging ventricular repolarization (QT interval) and predisposing to torsades de pointes; adverse cardiac events can appear days after a single dose due to noribogaine’s long half-life. Pre-dose screening (12-lead ECG, QTc, heart history) and correction of electrolytes (potassium, magnesium) materially reduce arrhythmia risk. High-variability plant products (root bark/TA) complicate dosing; ibogaine HCl allows weight-based calculations (typical ‘flood’ 15–25 mg/kg) but still requires continuous monitoring and ready access to advanced cardiac care. Significant ataxia, vertigo, bradycardia, and vomiting are common during peaks; patients should remain supine with assistance to minimize falls and aspiration. Because noribogaine is a strong SERT inhibitor and ibogaine/noribogaine are metabolized by polymorphic CYP2D6, poor metabolizers or those taking CYP2D6 inhibitors can experience prolonged exposure and QT risk; dose reduction and extended monitoring are prudent. Combining ibogaine with methadone and other potent QT-prolongers is a well-documented hazard; most clinical protocols require opioid transitions/washouts and continuous telemetry. Stimulants (including cocaine/amphetamines) amplify cardiac risk during and for several days post-dose; strict abstinence is recommended pre/post. Anti-emetics like ondansetron also prolong QT; if anti-nausea medication is clinically necessary, it should be selected and monitored by medical staff. Post-ibogaine, opioid tolerance often drops; relapse can therefore be more lethal—harm-reduction planning (naloxone, support, follow-up) is essential. Legal status varies widely; in many countries ibogaine is controlled or unapproved for treatment—unregulated settings may lack the monitoring capacity required for safe administration.

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