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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 medicine
    Psychoactive Class Depressant / Dissociative / Psychedelic
    Half-Life Ibogaine: ~4–7 h; noribogaine: ~28–49 h (human plasma)

    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

    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.

    Effect Profile

    Curated + 63 Reports
    Psychedelic 8.5

    Strong visuals, headspace, body load, and auditory effects

    Visual Intensity×3
    10104.2
    Headspace Depth×3
    10103.8
    Auditory Effects×1
    8105.3
    Body Load / Somatic Effects×1
    10105.9
    Catalog Erowid BlueLight
    Dissociative 4.3

    Strong motor impairment and mania with moderate insight, mild dissociative depth

    Dissociative Depth×3
    55.13.5
    Mania / Compulsion×1
    93.53.5
    Insight / Novel Thought×2
    71.61.2
    Motor / Sensory Impairment×1
    109.72.4
    Catalog Erowid BlueLight
    Opioid 4.7

    Strong itching/nausea and euphoria with low pain relief and sedation

    Euphoria / Warmth×3
    910
    Analgesia×2
    22.9
    Sedation / Relaxation×1
    22.4
    Itching / Nausea×1
    1010
    Catalog Erowid

    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

    Full tolerance 0h 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)
    30% ●○○

    Experience Report Analysis

    Erowid BlueLight
    46 Reports
    1997–2023 Date Range
    27 With Age Data
    29 Effects Detected

    Demographics

    Gender Distribution

    Age Distribution

    Reports Over Time

    Effect Analysis

    Erowid + Bluelight

    Effects aggregated from 63 experience reports (46 Erowid + 17 Bluelight)

    63 Reports
    88 Effects Detected
    34 Positive
    37 Adverse
    17 Neutral

    Effect Sentiment Distribution

    Confidence Distribution

    Positive Effects 34

    Stimulation 58.7% 70%
    Anxiety Suppression 54.0% 82%
    Color Enhancement 52.2% 70%
    Empathy 42.8% 85%
    Introspection 41.3% 78%
    Tactile Enhancement 36.5% 70%
    Music Enhancement 33.4% 81%
    Euphoria 33.3% 90%
    Focus Enhancement 31.7% 75%
    Body High 30.1% 70%
    Insight 23.5% 86%
    Mystical Quality 17.6% 83%
    Awe 17.6% 77%
    Out-Of-Body Experience 17.6% 87%
    Sedation 12.7% 75%
    Emotional Release 11.8% 82%
    Empathogenic Connection 11.8% 78%
    Geometric Imagery 11.8% 82%
    Contentment 11.8% 80%
    Mood Elevation 11.8% 85%

    Adverse Effects 37

    Body Load 52.9% 84%
    Nausea 50.8% 85%
    Fear 47.1% 84%
    Dizziness 35.3% 85%
    Confusion 35.0% 80%
    Motor Impairment 33.3% 79%
    Insomnia 29.4% 86%
    Increased Heart Rate 19.6% 70%
    Visual Trails 17.6% 83%
    Heaviness 17.6% 78%
    Depersonalization 17.6% 72%
    Vomiting 17.6% 88%
    Restlessness 17.6% 80%
    Vertigo 11.8% 88%
    Thought Loops 11.8% 72%
    Depression 11.8% 82%
    Emotional Blunting 11.8% 78%
    Ataxia 11.8% 85%
    Pain Enhancement 11.8% 80%
    Visual Vibration 11.8% 85%

    Dosage Distribution

    Dose distribution from experience reports

    Median: 860.0 mg IQR: 200.0–1000.0 mg n=19

    Real-World Dose Distribution

    62K Doses

    From 67 individual dose entries

    Oral (n=58)

    Median: 477.0mg 25th: 258.0mg 75th: 1000.0mg 90th: 1330.0mg
    mg/kg median: 6.854 mg/kg 75th: 13.087

    Form / Preparation

    Most common forms and preparations reported

    Body-Weight Dosing

    Dose relative to body weight from reports with weight data

    Median: 7.353 mg/kg IQR: 1.695–12.5 mg/kg n=15

    Redose Patterns

    Redosing behavior across 27 reports

    33.3% 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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