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Serotonin transporter-ibogaine complexes illuminate mechanisms of inhibition and transport.
2019
|
structural study (cryo-electron microscopy) |
|
↑Supports
|
Cryo-electron microscopy structures of SERT-ibogaine complexes in multiple conformations define the structural rearrangements during transport and show ibogaine is a non-competitive transport inhibitor that binds competitively with SSRIs. |
|
Noncompetitive Functional Inhibition at Diverse, Human Nicotinic Acetylcholine Receptor Subtypes by Bupropion, Phencyclidine, and Ibogaine
1999
|
in vitro study |
|
↑Supports
|
Ibogaine produced noncompetitive, insurmountable blockade of human muscle-type and ganglionic nicotinic acetylcholine receptors in the low to intermediate micromolar range. |
|
Degeneration of Purkinje cells in parasagittal zones of the cerebellar vermis after treatment with ibogaine or harmaline.
1993
|
experimental animal study |
|
↓Opposes
|
Ibogaine and harmaline caused selective degeneration of a subset of Purkinje cells in parasagittal stripes of the cerebellar vermis, indicating neurotoxic effects. |
|
Treatment of acute opioid withdrawal with ibogaine.
1999
|
case series |
33 |
↑Supports
|
Resolution of opioid withdrawal without further drug seeking occurred within 24 hours in 25 of 33 patients and was sustained over 72 hours, with one fatality possibly involving surreptitious heroin use. |
|
Effects and aftereffects of ibogaine on morphine self-administration in rats.
1991
|
preclinical experimental study |
|
↑Supports
|
Ibogaine dose-dependently reduced morphine self-administration, with a persistent aftereffect lasting days to weeks in some rats that was not attributable to motor impairment or conditioned aversion. |
|
Effects of iboga alkaloids on morphine and cocaine self-administration in rats: relationship to tremorigenic effects and to effects on dopamine release in nucleus accumbens and striatum.
1994
|
experimental study |
|
↑Supports
|
All tested iboga alkaloids and harmaline dose-dependently reduced morphine and cocaine self-administration, with some compounds producing persistent decreases lasting several days. |
|
The ibogaine medical subculture.
2008
|
ethnographic study with systematic quantitative data collection |
3414 |
↑Supports
|
An estimated 3,414 individuals had taken ibogaine as of February 2006, with 68% doing so for a substance-related disorder and 53% specifically for opioid withdrawal, the most common reason. |
|
Glial Cell Line-Derived Neurotrophic Factor Mediates the Desirable Actions of the Anti-Addiction Drug Ibogaine against Alcohol Consumption
2005
|
experimental study |
|
↑Supports
|
Ibogaine reduced ethanol intake in two-bottle choice, operant self-administration, and relapse models, and this effect was mediated by upregulated GDNF signaling in the ventral tegmental area. |
|
Inhibitory effects of ibogaine on cocaine self-administration in rats.
1993
|
experimental study |
|
↑Supports
|
A single 40 mg/kg injection of ibogaine significantly decreased cocaine intake for more than 48 hours, with repeated weekly administration producing a more pronounced reduction. |
|
A preliminary investigation of ibogaine: case reports and recommendations for further study.
1994
|
case series |
7 |
↑Supports
|
After single ibogaine doses of 700-1800 mg, none of seven subjects showed significant opiate withdrawal at the end of the psychoactive period, and three of six taking 1000 mg or more appeared drug-free at 14 weeks or longer. |
|
The Olivocerebellar Projection Mediates Ibogaine-Induced Degeneration of Purkinje Cells: A Model of Indirect, Trans-Synaptic Excitotoxicity
1997
|
experimental study with pharmacological ablation |
|
↓Opposes
|
Pharmacological ablation of the inferior olive almost completely prevented ibogaine-induced Purkinje cell degeneration and glial activation, indicating the neurotoxicity is indirect and dependent on the olivocerebellar projection. |
|
Treatment of opioid use disorder with ibogaine: detoxification and drug use outcomes.
2018
|
observational study |
30 |
↑Supports
|
Subjective opioid withdrawal scores fell from 31.0 to 14.0 about 76 hours after a mean total dose of 1,540 mg ibogaine HCl, 50% reported no opioid use at 1 month, and drug use, legal, and family/social scores improved through 12 months. |
|
Ibogaine treatment outcomes for opioid dependence from a twelve-month follow-up observational study.
2018
|
observational study |
14 |
↑Supports
|
A single ibogaine treatment significantly reduced opioid withdrawal scores acutely and produced significant reductions in addiction severity and depression scores at 12-month follow-up among completers, with one death during treatment. |
|
Ibogaine, a noncompetitive inhibitor of serotonin transport, acts by stabilizing the cytoplasm-facing state of the transporter.
2007
|
laboratory study |
|
↑Supports
|
Ibogaine inhibited serotonin transport noncompetitively by decreasing transport rate and stabilized the cytoplasm-facing state of the transporter, in contrast with cocaine. |
|
Ibogaine: complex pharmacokinetics, concerns for safety, and preliminary efficacy measures.
2000
|
observational study |
|
↑Supports
|
A single oral ibogaine dose significantly decreased craving for cocaine and heroin during inpatient detoxification and reduced depressive symptoms that remained lower 30 days after discharge. |
|
Ibogaine for Substance Use Disorders.
2026
|
review |
|
↕Mixed
|
Argues that ibogaine is a promising candidate for substance use disorders with potential to rapidly reduce withdrawal and cravings after a single dose, but that evidence rests on small observational studies and case reports and carries significant cardiotoxicity, neurological, and fatality risks. |
|
A Harm-Reduction–Oriented Clinical Framework for Ibogaine Administration and Risk Management
2026
|
theoretical |
|
?Unclear
|
Argues that most serious adverse events from ibogaine arise from preventable factors in patient selection, preparation, dosing, monitoring, and post-treatment care, and proposes a harm-reduction clinical framework emphasizing dynamic risk assessment, cardiac electrophysiology, and metabolic variability. |
|
Extracellular flux analysis and proteomic profiling indicate ibogaine promotes synaptic plasticity and neural repair by a metabolic preconditioning mechanism
2026
|
preclinical experimental study |
|
↑Supports
|
Ibogaine produced rapid concentration-dependent metabolic suppression followed by a delayed energy rebound in neurons, and oral ibogaine in mice caused transient spinal cord protein changes consistent with metabolic stress that resolved by 72 hours, which the authors propose may reflect metabolic preconditioning that enhances plasticity and repair. |
|
Adverse Health Outcomes of Psilocybin, LSD, MDMA, Ibogaine, and 5-MeO-DMT
2026
|
cross-sectional survey |
|
?Unclear
|
Describes self-reported health outcomes attributed to recent use of ibogaine and other psychedelics in a nationally representative survey, with no specific outcomes or effect sizes reported in the available text. |
|
QT Prolongation With Methadone, Donepezil, and Ibogaine
2026
|
commentary |
|
↓Opposes
|
States that ibogaine carries a high risk of QT prolongation and torsades de pointes, and that a magnesium pre-dosing protocol was developed to reduce this risk. |
|
Implications of Potential US FDA Approval of Psychedelics or Psychedelic-Adjacents Such as Ibogaine for Pharmacy in Japan.
2026
|
narrative review |
|
?Unclear
|
Argues that FDA approval of a psychedelic or psychedelic-adjacent agent would not automatically change Japanese regulation but would create pressure, and contends ibogaine would pose the greatest pharmacy challenge, requiring CYP2D6 phenotype assessment, QT drug-interaction screening, and cardiac monitoring. |
|
Ibogaine as a Double-Edged Sword: Developmental Cardiotoxicity and Neurobehavioral Alterations in Zebrafish
2026
|
observational study using a zebrafish model |
|
↓Opposes
|
Ibogaine induced early-onset bradycardia at 100 ng/mL and pericardial edema at 500 ng/mL, and disrupted neurobehavioral endpoints at concentrations lower than those causing morphological toxicity. |
|
Dynamic Substates of the Default Mode Network Are Associated with Mystical Experiences and Clinical Outcomes after Magnesium-Ibogaine Treatment in Veterans with Traumatic Brain Injury
2026
|
observational trial |
30 |
↑Supports
|
Magnesium-ibogaine did not alter static default mode network connectivity but produced sustained decreases in the switching rate of a dynamic DMN substate, correlated with mystical experience scores and clinical improvements at one month. |
|
Sustained abstinence in severe ketamine use disorder following ibogaine treatment case report
2026
|
case report |
1 |
↑Supports
|
After an 800 mg ibogaine HCl flood dose plus two 300 mg boosters, the patient reported immediate cessation of cravings and serial toxicology and psychometrics were consistent with abstinence from ketamine, cocaine, and alcohol over about 17 months, with improved depression and quality of life. |
|
Toward a nuanced framework for the medical development of ibogaine and its analogues and derivatives: implications for psychopharmacology
2026
|
review |
|
?Unclear
|
Argues that two development strategies exist for ibogaine-based therapies, broad polypharmacological compounds and selective bespoke analogs, each with distinct translational trade-offs, and that the field should resist oversimplified narratives about derivative superiority. |