Tabernanthe iboga
Viewing r2 — May 14, 2026 — CURRENT
Back to HistoryInteractions, related substances, and reports reflect the current entry and are not shown for historical revisions.
''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, ibogaine, acts on multiple brain systems simultaneously — including glutamate, opioid, nicotinic, and serotonin pathways.[1] This broad multi-system action produces prolonged visionary and dissociative states unlike any other known plant.
Psychedex is in open beta. We are still fine-tuning the generation and review process. Please double-check sources.
Iboga is the sacramental plant of the Bwiti religion in Gabon, where it has been used in initiation and healing ceremonies for generations.[2] Western interest shifted toward addiction medicine in 1962, when Howard Lotsof reported that a single ibogaine dose ended his opioid withdrawal.[3] A landmark 2024 clinical trial showed large reductions in PTSD and depression in combat veterans, and a 2026 US executive order directed accelerated regulatory review.[4][5]
Subjective effects include vivid autobiographical visions, contact with perceived entities, intense body sensitivity, profound dissociation, and severe loss of coordination.[6] 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 nausea, physical incapacitation, and confrontation with difficult personal memories are characteristic unsought effects.[7]
Ibogaine does not produce physical dependence or compulsive redosing,[8] but the primary acute risk is cardiac — ibogaine slows heart repolarization in a way that can trigger fatal arrhythmias, particularly without continuous cardiac monitoring.[9] Co-administration with other heart-affecting drugs or certain 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.[10]
History[edit]
Traditional and historical use
Tabernanthe iboga was formally described by botanist Henri Ernest Baillon in 1888.[11] The plant is the sacramental core of the Bwiti religion, practiced by the Mitsogho, Fang, and Babongo peoples of Gabon and neighboring countries.[2] 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.[12][2]
Sub-visionary doses have also been used to reduce fatigue during extended hunting, to treat fever and pain, and as an aphrodisiac.[12] No controlled ethnopharmacological studies with quantified alkaloid dosing have been conducted in the traditional Bwiti setting.
Modern era
In the 1930s–1950s, ibogaine was marketed in France as "Lambarene" (5 mg tablets) as a fatigue remedy.citation needed In 1962, Howard Lotsof self-administered ibogaine and reported it ended his opioid craving and withdrawal;[3] the DEA classified ibogaine as Schedule I in 1967.citation needed The 2024 MISTIC trial at Stanford reported large reductions in PTSD, depression, and anxiety in veterans with traumatic brain injury,[4] and a 2026 US executive order directed accelerated regulatory review.[5] Gabon declared T. iboga a national cultural heritage strategic reserve in 2000 and banned wild-harvest exports in 2019.[13]
Botanical Overview[edit]
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.[13]
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.
Alkaloid Profile[edit]
Dominant alkaloid: ibogaine
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[10] — making dose prediction from uncharacterized plant material unreliable. Ibogaine acts on serotonin, glutamate, kappa opioid, and nicotinic systems simultaneously,[1][14] a profile described as "matrix pharmacology"[1] — no single target explains the full experience.
Noribogaine: the sustained metabolite
The liver converts ibogaine into noribogaine, its primary active metabolite. Noribogaine shares ibogaine's activity at serotonin and kappa opioid targets,[1][15] but its half-life of 28–48 hours far exceeds ibogaine's 7–10 hours.[16] 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 channel-blocking mechanism.[17] 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.[10]
Neuroscience[edit]
Where it acts
Ibogaine acts on multiple brain systems at once. It blocks glutamate receptors,[18] activates kappa opioid receptors,[15] blocks nicotinic receptors,[14] and inhibits serotonin reuptake through two separate pathways simultaneously.[1] Evidence from knockout mouse studies also points to 5-HT₂A involvement.[19] Noribogaine sustains much of this activity over its 28–48-hour half-life.[16]
What it changes
Ibogaine's anti-addictive potential appears to arise from several overlapping mechanisms[15][20]: it acutely suppresses dopamine in the brain's reward center, and it triggers release of a growth factor in a region linked to drug-seeking behavior, reducing alcohol self-administration in animal models.[21] 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.[22]
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 neurons in humans at therapeutic doses have not been established, and a proposed remyelination mechanism[20] awaits direct human evidence.
Subjective Effects[edit]
The ibogaine experience is qualitatively unlike either classical psychedelics or dissociative anesthetics, though it shares features with both. It is predominantly internal — narrative autobiographical visions, encounters with perceived entities, and intense body load dominate the acute phase.[6] The physical intensity — severe loss of coordination, nausea, and sensitivity to sound and light — is largely constant above threshold doses, regardless of set or setting.[7]
No commonly used psychedelic plant shares ibogaine's overall profile. Its closest pharmacological parallels are 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.
Effect Grid
The therapeutic anti-addictive range at 10–20 mg/kg ibogaine HCl produces the full ibogaine experience. Internal hallucinations dominate: extended autobiographical narrative sequences, memory replays, entity contact, and transpersonal visions unfold over hours. Introspection enhancement is intense, with deep self-examination and catharsis frequently reported. Anxiety and dysphoria co-occur alongside cognitive euphoria and emotional enhancement. Reality testing impairment is significant — subjects are largely immobilized and non-communicative during the peak.
Severe motor control impairment (ataxia) occurs in nearly all subjects. Nausea and vomiting are near-universal. Bodily heaviness, proprioceptive distortion, sound sensitivity, and spontaneous body sensations are prominent. Abnormal heartbeat from QTc prolongation (mean max 95 ms) requires continuous cardiac monitoring. Appetite suppression is pronounced.
Acute duration is 12–24 hours. Insomnia, physical fatigue, and heightened sensory sensitivity persist 24–72 hours. Mandatory cardiac monitoring with defibrillation access is required throughout.
Modeled from the effect's dose-dependence curve — not per-substance measurements.
Vestibular distortion · Depth perception distortion · Light sensitivity · Proprioceptive distortion · Sound sensitivity · Brightness alteration · Color alteration · Auditory distortion · Visual drifting · Visual haze / noise · Visual morphing · Synesthesia · Tracers · Internal hallucinations · External hallucinations · Perspective hallucinations · Auditory hallucinations · Shadow people
Sound sensitivity · Brightness alteration · Color alteration · Auditory distortion · Visual drifting · Visual haze / noise · Visual morphing · Synesthesia · Tracers · Internal hallucinations · External hallucinations · Perspective hallucinations · Auditory hallucinations · Shadow people
Dizziness · Physical fatigue · Nystagmus (eye wobbles) · Trembling · Vomiting · Involuntary body movements · Appetite suppression · Bodily heaviness · Body schema distortion · Excessive sweating · Heart rate perception changes · Restlessness · Spontaneous body sensations · Stimulation · Bodily pressures · Dry mouth · Headache · Muscle tension · Salivation · Tingling / electric sensations · Vibrations / buzzing · Pain suppression · Bodily dissociation
Vomiting · Involuntary body movements · Appetite suppression · Bodily heaviness · Body schema distortion · Excessive sweating · Heart rate perception changes · Restlessness · Spontaneous body sensations · Stimulation · Bodily pressures · Dry mouth · Headache · Muscle tension · Salivation · Tingling / electric sensations · Vibrations / buzzing · Pain suppression · Bodily dissociation
Cognitive fatigue · Confusion · Immersion enhancement · Focus suppression · Information processing suppression · Thought disorganization · Cognitive dysphoria · Memory fragmentation · Openness enhancement · Thought connectivity · Multiple thought streams · Thought loops · Delirium · Amnesia · Delusions
Focus suppression · Information processing suppression · Thought disorganization · Cognitive dysphoria · Memory fragmentation · Openness enhancement · Thought connectivity · Multiple thought streams · Thought loops · Amnesia · Delusions
Emotional lability · Simultaneous emotions · Empathy enhancement · Irritability · Euphoria
Euphoria
Emotional susceptibility · Sociability suppression · Disinhibition · Cognitive disconnection · Boundary dissolution · Ego dissolution · Identity alteration
Boundary dissolution · Ego dissolution · Identity alteration
Transpersonal feelings · Transpersonal memory access · Entity contact · Near-death experience · Non-dual awareness
Non-dual awareness
Timeline · by preparation
Safety[edit]
- Acute toxicity
- High
- Chronic toxicity
- Moderate
- Withdrawal
- None
- Tolerance buildup
- none
- Tolerance reset
- —
- Physical
- None
- Psychological
- Negligible
- Compulsive redosing
- Negligible
- Dose escalation
- Negligible
- Cross-tol.
- —
Toxicity
Cardiac toxicity is the primary acute risk across all ibogaine-containing preparations. Ibogaine and noribogaine block the cardiac channel that governs heart repolarization.[17] In a 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.[7] In 6 of 14 subjects, elevated QT prolongation persisted beyond 24 hours.[7]
Fatal cardiac arrhythmias have occurred, predominantly in unsupervised settings without cardiac monitoring.[9][23] Sudden death has been reported up to 72 hours after ingestion[9][17] — the cardiac risk window extends far beyond the visionary phase. The UK National Poisons Information Service documents real-world ibogaine toxicity presentations over a 10-year case series.[24]
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.[10] No jurisdiction mandates certified laboratory testing or Certificate of Analysis requirements for iboga products. Independent analytical verification is the only available risk mitigation.[10]safety citation needed
In rats, ibogaine causes degeneration of cerebellar neurons at high doses.[25][26] At 40 mg/kg — within the anti-addictive dose range in rodents — this effect was not observed.[27] In humans, severe transient loss of coordination was observed in all 14 patients in the clinical safety study.[7] The MISTIC cohort showed structural brain improvements rather than deterioration at one month;[22] long-term effects at therapeutic doses have not been established.
Psychological Risks
Anxiety, fear, and confrontation with difficult autobiographical material are commonly reported during the acute phase.[28] These experiences form a documented factor in the Ibogaine Experience Scale (N=499).[6] Individuals with pre-existing psychotic spectrum disorders face risk of acute psychological decompensation. Delirium-like states may occur at high doses, and an exaggerated startle response has been reported during the residual phase. Long-term psychological risks in the general population remain uncharacterized beyond case reports and observational cohorts.safety citation needed
Tolerance & Dependence
Ibogaine does not produce classical tolerance or physical dependence. No withdrawal has been documented in humans.[29][15] Traditional Bwiti use is intermittent — not daily. Animal studies do not show self-administration, and no compulsive redosing patterns have been observed.[8] 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.[16]
QT-prolonging drugs (methadone, tricyclic antidepressants, antipsychotics, certain SSRIs, some antihistamines) compound ibogaine's cardiac effect and elevate risk of a dangerous arrhythmia called torsades de pointes.[9][23]
Opioids interact in a timing-dependent and complex way. Ibogaine may precipitate or attenuate opioid withdrawal depending on timing relative to last opioid dose.[15][30] Post-ibogaine loss of opioid tolerance increases overdose risk on resumption.[31]
Serotonergic agents: Ibogaine's serotonin reuptake inhibitor creates a theoretical risk of a dangerous overheating and seizure response when combined with MAOIs or serotonin releasers.[1] safety citation needed No published clinical case report of ibogaine-induced serotonin syndrome was identified.
Contraindications
Pre-existing cardiac conditions — QT prolongation, arrhythmia, structural heart disease, or heart failure — are absolute contraindications.[17][7] CYP2D6 poor metabolizers face approximately double the active compound exposure, substantially increasing cardiac and neurological risk.[16][23] Severe liver impairment, uncorrected electrolyte abnormalities (particularly low potassium or magnesium),[32] personal or family history of psychotic spectrum disorders,[32] pregnancy, and active opioid maintenance therapy without supervised tapering[31] are additional contraindications. Concurrent QT-prolonging medications must be discontinued with appropriate washout periods before any ibogaine administration.
Preparations[edit]
Raw root bark, total alkaloid extract, and purified ibogaine HCl are pharmacologically distinct products with non-overlapping 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[10] — dose prediction from uncharacterized bark is impossible. Traditional Bwiti initiation doses involve consumption over 1–3 days in quantities reported as several hundred grams.[12] Onset is gradual (1–3 hours); acute visionary phase lasts 12–24 hours; residual effects persist up to 72 hours. Nausea and 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 potency remains. Onset, duration, and effect character resemble raw bark. Gastrointestinal 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 pharmaceutical-grade preparation used in clinical settings. Clinical studies have used doses of 10–20 mg/kg.[7][16] Onset occurs approximately 1.5–4 hours after ingestion,[16][33] with an acute phase lasting 12–24 hours. Cardiac risk (QTc prolongation) requires continuous monitoring.[7] The experience tends to be described as "cleaner" than raw bark — less gastrointestinal distress, equivalent visionary intensity at equivalent ibogaine doses.
Magnesium-ibogaine combination
The MISTIC trial co-administered magnesium with ibogaine.[4] Magnesium may modulate the same cardiac 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 bioavailability data are in the Dose · by preparation card on this page.
Harm Reduction[edit]
Forms & Identification
Iboga preparations vary enormously in potency and purity. Raw root bark, total alkaloid extracts, and purified ibogaine HCl are pharmacologically distinct products with non-overlapping dose ranges. GC/MS analysis of commercial products found unknown adulterants in almost all samples tested, and one product labeled "iboga" contained no iboga alkaloids at all.[10]
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.
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 arrhythmia, or structural heart disease should not proceed.[17][7]
- CYP2D6 genotyping should be completed before administration. Poor metabolizers face approximately double the active compound exposure.[16]
- Discontinue all CYP2D6 inhibitors and QT-prolonging medications with appropriate washout periods before any session. This includes paroxetine, fluoxetine, bupropion, methadone, tricyclic antidepressants, and many antipsychotics.
- Correct electrolyte imbalances — particularly potassium and magnesium — before administration.[32]
- 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 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. Nausea and vomiting are near-universal; anti-emetics should be available.
- Opioid tapering: Complete any taper from opioid maintenance therapy under medical supervision before the session. Post-ibogaine loss of opioid tolerance increases overdose risk on resumption.[31]
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 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 loss of coordination.[7]
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 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 therapist or experienced facilitator — beginning 1–3 days after the session and continuing over subsequent weeks — help translate insights into sustained behavioral change.
Recovery & Support
Ibogaine does not produce dependence or a withdrawal. Recovery support in the ibogaine context typically addresses the underlying condition that motivated treatment — most commonly 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 pre-treatment opioid doses can be fatal.[31] Ongoing 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 resources, crisis lines, and support pathways → View all
Emergency Response
Recognizing an emergency:
- Irregular heartbeat, chest pain, or palpitations during or after a session
- Loss of consciousness or unresponsiveness
- Seizure activity
- Breathing difficulty or cessation
- Severe confusion or 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 recovery position.
- 3. Do not leave the person alone — cardiac events can occur up to 72 hours post-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: 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.
Legal Status[edit]
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 Schedule I controlled substance at the federal level, though a 2026 executive order directed the FDA and DEA to accelerate research and create Right to Try access pathways.[5] Nine US states have enacted ibogaine-related legislation as of May 2026, including Texas, Kentucky, Oregon, and Louisiana.[34] 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.[35] In Gabon, the plant itself is protected as a national cultural heritage strategic reserve, with wild-harvest exports banned since 2019.[13] 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.
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.
references
- [1]
- [2] ^abcQuiroz D, van Andel T (2018) The Cultural Importance of Plants in Western African Religions — Economic Botany doi:10.1007/s12231-018-9410-x
- [3] ^abRodríguez-Cano BJ et al., Bouso JC (2023) Underground ibogaine use for the treatment of substance use disorders: A qualitative analysis of subjective experiences — Drug and alcohol review doi:10.1111/dar.13587
- [4] ^abcCherian KN, Keynan JN, Anker L, et al. (2024) Magnesium-ibogaine therapy in veterans with traumatic brain injuries — Nature medicine doi:10.1038/s41591-023-02705-w
- [5] ^abcKozlov M (2026) US speeds up research into mind-altering drugs - including mysterious 'ibogaine' — Nature doi:10.1038/d41586-026-01286-1
- [6] ^abcGonzález Espejito F et al., Bouso JC (2025) The Ibogaine Experience Scale (IES): Development and psychometric properties of a multidimensional measure of ibogaine's subjective effects — PloS one doi:10.1371/journal.pone.0333296