generation run 2026-04-26
70 min completedmodel pipeline-v5plan not recordedrun/3c1f9300…Selection
Verification
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The model's own caveats
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Reproduce
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- 42 source keys (listed under Sources)
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- none — agent transcripts are persisted from 2026-09 onward
24 searches — query, source, results, what was kept and why
| # | source | query | seen | kept | rationale |
|---|---|---|---|---|---|
| 1 | OpenAlex | ibogaine pharmacology addiction treatment | 10 | 1 | Landmark clinical paper on ibogaine opioid withdrawal treatment |
| 2 | PubMed | ibogaine cerebellar neurotoxicity Purkinje cell rat | 8 | 4 | Critical neurotoxicity data |
| 3 | PubMed | ibogaine pharmacokinetics metabolism noribogaine human | 12 | 9 | PK/PD and metabolism data essential |
| 4 | PubMed | ibogaine PTSD traumatic brain injury veterans treatment | 3 | 3 | High-impact recent clinical data |
| 5 | PubChem | ibogaine | 1 | 1 | Primary chemical identity verification |
| 6 | PubMed | ibogaine pharmacology receptor binding mechanism action | 11 | 9 | Core pharmacology papers |
| 7 | PubMed | ibogaine GDNF neurotrophic factor glial neuroplasticity | 1 | 1 | GDNF mechanism review |
| 8 | ClinicalTrials.gov | ibogaine | 8 | 5 | All ibogaine-specific trials selected |
| 9 | PubMed | ibogaine Tabernanthe iboga root bark alkaloid isolation synthesis total | 1 | 1 | Synthesis and extraction chemistry |
| 10 | PubMed | ibogaine 18-methoxycoronaridine analog safer derivative development | 2 | 2 | 18-MC development and receptor binding overview |
| 11 | OpenAlex | ibogaine pharmacology clinical review fatalities alkaloid Alper | 10 | 6 | High-citation cardiac safety and systematic review papers |
| 12 | PubMed | ibogaine alcohol dependence treatment ethanol self-administration | 4 | 2 | Primary GDNF mechanism papers |
| 13 | web | ibogaine legal status Schedule I DEA US UK scheduling history Howard Lotsof | 10 | 3 | Legal status and historical data not in PubMed |
| 14 | web | ibogaine legal status by country | 1 | 1 | Comprehensive legal status by jurisdiction |
| 15 | DOI verification | DOI verification for key papers | 2 | 2 | API verification of key papers |
| 16 | PubChem web · absence | ibogaine CAS melting point logP LD50 | 0 | 0 | Attempted physical property lookup; failed |
| 17 | OpenAlex | ibogaine cardiac safety deaths arrhythmia hERG QT prolongation | 8 | 2 | Key cardiac safety primary research papers |
| 18 | PubMed · absence | ibogaine LD50 lethal dose toxicity animal study mouse rat | 0 | 0 | LD50 data gap noted |
| 19 | PubMed | ibogaine cocaine stimulant withdrawal self-administration dopamine accumbens | 1 | 1 | Key dopamine/serotonin nucleus accumbens data; 18-MC comparison |
| 20 | OpenAlex | ibogaine observational naturalistic opioid outcome long-term abstinence | 8 | 0 | Searched for naturalistic outcome data; not found in top results |
| 21 | web · absence | ibogaine physical properties CAS LD50 | 0 | 0 | Gap documented - CAS, SMILES, melting point not API-verified |
| 22 | PubMed and OpenAlex combined | Research output compilation | 52 | 1 | All selected items relevant to ibogaine research output |
| 23 | PubMed · absence | ibogaine LD50 lethal dose toxicity animal | 0 | 0 | Gap documented |
| 24 | PubMed | ibogaine noribogaine serotonin reuptake transporter SERT dopamine DAT | 1 | 0 | Not directly relevant enough to ibogaine pharmacology for citation |
98 claims by section — every cited sentence, checked against its source
safety32 · 24 ok
Paroxetine pretreatment approximately doubles active moiety AUCsupported
Paroxetine doubles active moiety exposure. jcph.471
hERG IC50 values are 3.53 µM (extracted ibogaine), 4.09 µM (semi-synthetic ibogaine), and 2.86 µM (noribogaine)supported
hERG IC50: ibogaine (semisynthesis) 4.09 µM, ibogaine (extraction) 3.53 µM, noribogaine 2.86 µM. s12012-015-9311-5
Therapeutic concentrations of both compounds retard action potential repolarization in human iPSC-derived ventricular-like cardiomyocytes — the first experimental demonstration of cardiac risk in human cardiac cellssupported
First experimental proof that therapeutic concentrations of ibogaine and noribogaine significantly retard action potential repolarization in human ventricular-like cardiomyocytes (iPSC-derived). s12012-016-9366-y
Noribogaine's longer half-life means cardiac risk persists days after ibogaine ingestion, explaining reported delayed fatalities.supported
Explains delayed incidence of cardiac adverse events several days after ibogaine intake. s12012-016-9366-y
Claim in safety — inconclusiveinconclusiveworking →
Clinical observations confirm the risk: reversible QTc prolongation and bradycardia were documented in a Dutch OUD detoxification study, noribogaine produced dose-dependent QTcI prolongation of 0.17 ms/ng/mL (mean increases of 16–42 ms across 60–180 mg dose groups), and a case report documented prolonged multiple cardiac arrhythmias following internet-purchased ibogaine.supported
Ibogaine treatment of OUD patients induces clinically relevant but reversible QTc prolongation, bradycardia, and severe ataxia. add.15448
Clinical observations confirm the risk: reversible QTc prolongation and bradycardia were documented in a Dutch OUD detoxification study, noribogaine produced dose-dependent QTcI prolongation of 0.17 ms/ng/mL (mean increases of 16–42 ms across 60–180 mg dose groups), and a case report documented prolonged multiple cardiac arrhythmias following internet-purchased ibogaine.supported
Concentration-dependent QTcI increase 0.17 ms/ng/mL; mean 16-42 ms across 60-180 mg dose groups. cpdd.254
Clinical observations confirm the risk: reversible QTc prolongation and bradycardia were documented in a Dutch OUD detoxification study, noribogaine produced dose-dependent QTcI prolongation of 0.17 ms/ng/mL (mean increases of 16–42 ms across 60–180 mg dose groups), and a case report documented prolonged multiple cardiac arrhythmias following internet-purchased ibogaine.supported
Case of prolonged cardiac arrhythmias following internet-purchased ibogaine. 15563650.2017.1287372
Multiple fatalities temporally associated with ibogaine have been reported in the literaturesupported
Life-threatening complications and sudden death cases accumulating. molecules20022208
Claim in safety — inconclusiveinconclusiveworking →
Consolidated case reviews are contained in dedicated toxicology reviews.supported
Review of ibogaine cardiac effects: life-threatening complications and sudden death cases accumulating. molecules20022208
Consolidated case reviews are contained in dedicated toxicology reviews.supported
Review of ibogaine toxicity. Reports of toxicity are cause for concern. 15563650.2016.1138226
The Stanford MISTIC protocol co-administers magnesium with ibogaine as a QTc-stabilizing measure; no unexpected serious adverse events occurred in 30 participants.supported
MISTIC: 30 male SOF veterans with TBI. No SAEs. Magnesium co-administration. s41591-023-02705-w
In rats, ibogaine causes dose-dependent Purkinje cell degeneration via a trans-synaptic excitotoxic mechanism: activation of inferior olivary neurons produces excessive glutamate release at climbing fiber synapses, causing Purkinje cell deathsupported
Inferior olive ablation prevents ibogaine-induced Purkinje cell degeneration. Ibogaine activates inferior olivary neurons causing glutamate release at climbing fibers — indirect excitotoxic mechanism. pmid:9348351
Sigma-2 receptor activation mediates this pathwaysupported
Sigma-2 action mediates neurotoxicity. pmid:9668680
The NOAEL in rats is 25 mg/kg (i.p.); degeneration appears at 75–100 mg/kgsupported
Purkinje cell degeneration at 75-100 mg/kg (rats). NOAEL 25 mg/kg. pmid:10966515
The standard anti-addictive dose in rat models (40 mg/kg) does not cause Purkinje cell loss above saline controls.supported
40 mg/kg ibogaine (anti-addictive dose) produced no Purkinje cell degeneration. pmid:8930373
Severe ataxia renders patients unable to walk during the acute phase; supine positioning is mandatorypartially supported
Ibogaine treatment of OUD patients induces clinically relevant but reversible QTc prolongation, bradycardia, and severe ataxia. add.15448
Dose-dependent bradycardia is consistently reported; 18-MC lacks this effectsupported
Only ibogaine causes cerebellar damage (>=100 mg/kg), tremors, bradycardia. pmid:11085336
Ibogaine does not support self-administration in animal modelssupported
No effect on CPP. Meta-analysis of 27 studies. tp.2016.71
CYP2D6 poor metabolizers (genetic or drug-induced) face substantially increased cardiac risk unless the ibogaine dose is reduced.supported
Paroxetine doubles active moiety exposure. Genotyping recommended before ibogaine treatment. jcph.471
One fatality in the foundational clinical case series was attributed to possible surreptitious heroin use during ibogaine treatmentpartially supported
33 cases of opioid detoxification. One fatality. First systematic case series. pmid:10506904
ABCB1 inhibitors (verapamil, cyclosporine) may increase ibogaine oral bioavailability and CNS penetrationsupported
ABCB1+ABCG2 limit oral availability and brain penetration. fphar.2022.855000
CYP3A4 is not a significant interaction pathway for ibogaine or noribogaine.supported
CYP3A4 not significant. fphar.2022.855000
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Cardiac arrhythmia or structural heart disease — increased vulnerability to ibogaine-induced conduction abnormalitiessupported
Ibogaine propensity to induce cardiac arrhythmias. Life-threatening complications and sudden death cases accumulating. molecules20022208
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
Claim in safety — inconclusiveinconclusiveworking →
CYP2D6 inhibitor use without dose adjustment — approximately doubles ibogaine exposuresupported
Paroxetine doubles active moiety exposure. jcph.471
pharmacology24 · 19 ok
Kappa-opioid receptor (KOR) agonism (Ki ~2.0–2.1 µM) and NMDA receptor open-channel antagonism (IC50 3.1 µM in rat hippocampal neurons; [³H]dizocilpine binding IC50 3.2 µM) together account for ibogaine's effects on morphine and cocaine self-administrationpartially supported
Ki values for ibogaine at kappa-opioid receptors 2.08 µM. pmid:1377086
Kappa-opioid receptor (KOR) agonism (Ki ~2.0–2.1 µM) and NMDA receptor open-channel antagonism (IC50 3.1 µM in rat hippocampal neurons; [³H]dizocilpine binding IC50 3.2 µM) together account for ibogaine's effects on morphine and cocaine self-administrationpartially supported
IC50 3.1 µM at -60 mV for NMDA current block in rat hippocampal neurons. [3H]dizocilpine binding IC50 3.2 µM. pmid:8793904
Partial reversal by the kappa antagonist norbinaltorphimine combined with the NMDA agonist confirms both mechanisms operate in vivosupported
Combination of kappa antagonist + NMDA agonist partially prevented ibogaine inhibition of morphine self-administration. Both kappa agonist and NMDA antagonist actions contribute to anti-addictive effects. pmid:9138735
NMDA blockade is use- and voltage-dependent, consistent with an open-channel mechanismsupported
Use- and voltage-dependent open-channel block. pmid:8793904
In vivo anticonvulsant activity (ED50 31 mg/kg i.p. for maximal electroshock protection in mice) provides further evidence of functional NMDA antagonism.supported
ED50 31 mg/kg for maximal electroshock protection in mice. pmid:8793904
Intra-VTA GDNF microinjection mimics ibogaine's anti-alcohol effect, while anti-GDNF antibodies block it; GDNF receptor (Ret) and ERK1 phosphorylation are increasedsupported
Microinjection into VTA reduced ethanol self-administration. GDNF receptor (Ret) and ERK1 phosphorylation increased. Anti-GDNF antibodies blocked ibogaine's anti-alcohol effect. pmid:15659598
Noribogaine, but not 18-methoxycoronaridine (18-MC), also induces GDNF in SH-SY5Y cells and reduces alcohol self-administration when infused into the VTAsupported
Noribogaine (but not 18-MC) induces GDNF mRNA increase in SH-SY5Y cells. Intra-VTA noribogaine decreases alcohol self-administration. j.1369-1600.2010.00251.x
Ibogaine inhibits the serotonin transporter (SERT) at low micromolar concentrations, acutely increasing extracellular serotonin in the nucleus accumbens — an effect not shared by noribogaine or 18-MCpartially supported
Only ibogaine increases serotonin in accumbens. 18-MC has lower NMDA, sigma-2, sodium channel, and 5-HT transporter affinity. pmid:11085336
Claim in pharmacology — inconclusiveinconclusiveworking →
Claim in pharmacology — inconclusiveinconclusiveworking →
Ibogaine acutely decreases extracellular dopamine in the nucleus accumbens and blocks morphine-induced and nicotine-induced dopamine releasepartially supported
Ibogaine and noribogaine decrease dopamine in nucleus accumbens, block morphine-induced dopamine release. Binds kappa-opioid, NMDA, serotonin uptake; ibogaine also sigma-2 and nicotinic. pmid:9668680
Ibogaine acutely decreases extracellular dopamine in the nucleus accumbens and blocks morphine-induced and nicotine-induced dopamine releasepartially supported
18-MC vs ibogaine: both decrease dopamine in nucleus accumbens. pmid:11085336
Claim in pharmacology — inconclusiveinconclusiveworking →
Claim in pharmacology — inconclusiveinconclusiveworking →
Ibogaine binds nicotinic acetylcholine receptors (nAChRs) as an antagonist; this action is implicated in reduction of nicotine intake in rats. 18-MC shares this property.partially supported
Binds kappa-opioid, NMDA, serotonin uptake; ibogaine also sigma-2 and nicotinic. pmid:9668680
Claim in pharmacology — not_supportednot supportedworking →
An emerging hypothesis proposes that ibogaine reopens critical periods for reward learning through GDNF-mediated and extracellular matrix mechanisms, analogous to critical-period reopening described for other psychedelics.supported
GDNF induction, glutamate/dopamine modulation, neuroplasticity reopening as unified mechanism across addiction, OCD, PTSD, eating disorders. fphar.2025.1744383
In mice, brain-to-plasma ratio reaches 3.4, indicating substantial CNS penetration; ABCB1 knockout increases brain penetration 1.5-foldpartially supported
ABCB1+ABCG2 limit oral availability and brain penetration. Brain-to-plasma ratio 3.4 in mice. fphar.2022.855000
The compound distributes extensively into tissues, with sequestration in adipose tissue providing a reservoir for slow release and prolonged pharmacological effects.supported
Ibogaine/noribogaine sequestered in fat. pmid:10911925
CYP3A4 does not significantly affect ibogaine or noribogaine pharmacokinetics.supported
CYP3A4 not significant. fphar.2022.855000
CYP2D6 genotype robustly correlates with ibogaine AUC (r = 0.82) and Cmax (r = 0.77)partially supported
CYP2D6 phenotype correlated with ibogaine AUC r=0.82. jcph.471
CYP2D6 poor metabolizers — whether genetic or drug-induced (e.g., by paroxetine pretreatment) — exhibit approximately 2-fold higher active moiety exposure, necessitating dose reduction and pre-treatment genotyping.supported
Paroxetine doubles active moiety exposure. Genotyping recommended before ibogaine treatment. jcph.471
The primary active metabolite noribogaine has a substantially longer half-life of 28–49 hours, accounting for both the prolonged therapeutic effects and the extended cardiac risk window following a single dose.supported
Noribogaine 3-60 mg: Tmax 2-3h, dose-linear AUC/Cmax, mean t1/2 28-49h, Vd 1417-3086L. jcph.404
Human PK/PD relationships in opioid use disorder patients — correlating ibogaine and metabolite concentrations with side effects and withdrawal severity — have been characterized in a Dutch OUD detoxification cohort.supported
PK/PD relationships of ibogaine and metabolites in OUD patients during ibogaine-supported detoxification. 02698811241237873
neuroscience10 · 9 ok
Noribogaine also induces GDNF in neuroblastoma cells (SH-SY5Y), suggesting that neurotrophic signaling persists into the noribogaine-dominant pharmacological phase.supported
Noribogaine (but not 18-MC) induces GDNF mRNA increase in SH-SY5Y cells. j.1369-1600.2010.00251.x
Sigma-2 receptor activation mediates this effectsupported
Sigma-2 action mediates neurotoxicity. pmid:9668680
The anti-addictive dose in rats (40 mg/kg) does not produce Purkinje cell loss above saline controls, and the NOAEL is 25 mg/kg.partially supported
40 mg/kg ibogaine (anti-addictive dose) produced no Purkinje cell degeneration. High doses (100 mg/kg) caused degeneration in lateral/intermediate cerebellum. pmid:8930373
The anti-addictive dose in rats (40 mg/kg) does not produce Purkinje cell loss above saline controls, and the NOAEL is 25 mg/kg.partially supported
Purkinje cell degeneration at 75-100 mg/kg (rats). NOAEL 25 mg/kg. 50 mg/kg borderline (2/6 affected). pmid:10966515
Does cerebellar neurotoxicity occur in humans at therapeutic doses? Rat data show a dose-dependent threshold (NOAEL 25 mg/kg i.p.), but interspecies extrapolation to human oral doses (~10–25 mg/kg) is uncertain. No controlled neuroimaging studies of cerebellar integrity following clinical ibogaine use have been published.supported
Purkinje cell degeneration at 75-100 mg/kg (rats). NOAEL 25 mg/kg. pmid:10966515
Ibogaine acutely reduces dopamine release in the nucleus accumbens (NAc), the terminal field of the mesolimbic reward pathway originating in the VTAsupported
Ibogaine and noribogaine decrease dopamine in nucleus accumbens. pmid:9668680
Ibogaine acutely reduces dopamine release in the nucleus accumbens (NAc), the terminal field of the mesolimbic reward pathway originating in the VTAsupported
18-MC vs ibogaine: both decrease dopamine in nucleus accumbens. pmid:11085336
Claim in neuroscience — inconclusiveinconclusiveworking →
Intra-VTA GDNF microinjection reproduces ibogaine's anti-alcohol effect; anti-GDNF antibodies block itsupported
Microinjection into VTA reduced ethanol self-administration. Anti-GDNF antibodies blocked ibogaine's anti-alcohol effect. pmid:15659598
Ibogaine may reopen critical periods for reward learning through GDNF-mediated neuroplasticity and extracellular matrix reorganization in the VTAsupported
GDNF induction, glutamate/dopamine modulation, neuroplasticity reopening as unified mechanism across addiction, OCD, PTSD, eating disorders. fphar.2025.1744383
summary8 · 7 ok
Claim in summary — inconclusiveinconclusiveworking →
Ibogaine acts simultaneously on multiple receptor systems: kappa-opioid receptor agonism (Ki ~2.0 µM), NMDA receptor open-channel antagonism (IC50 3.1 µM), serotonin transporter inhibition, sigma-2 receptor binding, and nicotinic acetylcholine receptor antagonismpartially supported
Ki values for ibogaine at kappa-opioid receptors 2.08 µM. pmid:1377086
Ibogaine acts simultaneously on multiple receptor systems: kappa-opioid receptor agonism (Ki ~2.0 µM), NMDA receptor open-channel antagonism (IC50 3.1 µM), serotonin transporter inhibition, sigma-2 receptor binding, and nicotinic acetylcholine receptor antagonismsupported
IC50 3.1 µM at -60 mV for NMDA current block in rat hippocampal neurons. Use- and voltage-dependent open-channel block. pmid:8793904
Ibogaine acts simultaneously on multiple receptor systems: kappa-opioid receptor agonism (Ki ~2.0 µM), NMDA receptor open-channel antagonism (IC50 3.1 µM), serotonin transporter inhibition, sigma-2 receptor binding, and nicotinic acetylcholine receptor antagonismsupported
Radioligand binding assays targeting over 50 distinct neurotransmitter receptors. Ibogaine interacted with mu, delta, kappa opioid, 5HT2, 5HT3, muscarinic 1/2, dopamine/NE/5HT uptake sites, NMDA ion channels, sodium ion channels. pmid:7568622
A key downstream mechanism is upregulation of glial cell line-derived neurotrophic factor (GDNF) in the ventral tegmental areasupported
Ibogaine increased GDNF expression in VTA midbrain. GDNF receptor (Ret) and ERK1 phosphorylation increased. Anti-GDNF antibodies blocked ibogaine's anti-alcohol effect. pmid:15659598
Greater mystical experience intensity (MEQ30) predicts larger therapeutic outcomessupported
Greater mystical experiences during ibogaine associated with larger PTSD reductions immediately and 1 month post-treatment. MEQ30 by time interaction significant. j.jad.2025.120722
Ibogaine's primary acute risk is cardiac arrhythmia. hERG channel blockade by ibogaine (IC50 3.53–4.09 µM) and noribogaine (IC50 2.86 µM) prolongs QT interval, with documented torsades de pointes and sudden cardiac death at therapeutic dosespartially supported
hERG IC50: ibogaine (semisynthesis) 4.09 µM, ibogaine (extraction) 3.53 µM, noribogaine 2.86 µM. Voltage-dependent low-affinity blockade. s12012-015-9311-5
Ibogaine does not support self-administration in animal models and shows no dependence liabilitysupported
Meta-analysis of 27 studies: ibogaine reduced drug self-administration (especially first 24h). No effect on CPP. tp.2016.71
comparative-pharmacology7 · 6 ok
Data compiled from , , , and .supported
hERG IC50: ibogaine (semisynthesis) 4.09 µM, ibogaine (extraction) 3.53 µM, noribogaine 2.86 µM, voacangine 2.25 µM. 18-MC IC50 >50 µM. s12012-015-9311-5
Data compiled from , , , and .supported
18-MC vs ibogaine: both decrease dopamine in nucleus accumbens. Only ibogaine increases serotonin in accumbens. Ibogaine/noribogaine sequestered in fat. pmid:11085336
Data compiled from , , , and .supported
Ibogaine/noribogaine have low microM affinities for kappa/mu opioid, NMDA, 5HT-3, sigma-2, sodium channels, serotonin transporter. pmid:11705115
Noribogaine is a more potent hERG blocker (IC50 2.86 µM vs 3.53–4.09 µM for ibogaine) and induces GDNF in the VTApartially supported
hERG IC50: ibogaine (semisynthesis) 4.09 µM, ibogaine (extraction) 3.53 µM, noribogaine 2.86 µM. s12012-015-9311-5
Noribogaine is a more potent hERG blocker (IC50 2.86 µM vs 3.53–4.09 µM for ibogaine) and induces GDNF in the VTApartially supported
Noribogaine (but not 18-MC) induces GDNF mRNA increase in SH-SY5Y cells. Intra-VTA noribogaine decreases alcohol self-administration. j.1369-1600.2010.00251.x
Claim in comparative-pharmacology — inconclusiveinconclusiveworking →
Noribogaine's substantially longer half-life (28–49 hours vs ~1–10 hours for ibogaine) means that following oral ibogaine administration, pharmacological activity transitions from an ibogaine-dominant phase to a noribogaine-dominant phase within hourssupported
Noribogaine 3-60 mg: Tmax 2-3h, dose-linear AUC/Cmax, mean t1/2 28-49h, Vd 1417-3086L. jcph.404
pharmacokinetic-detail5 · 5 ok
In a single 20 mg dose study in healthy volunteers, CYP2D6 genotype correlated with ibogaine AUC at r = 0.82 and Cmax at r = 0.77partially supported
CYP2D6 phenotype correlated with ibogaine AUC r=0.82. Influence of CYP2D6 activity on the pharmacokinetics and pharmacodynamics of a single 20 mg dose. jcph.471
These parameters were established in ascending-dose healthy volunteer and opioid-dependent patient studiessupported
Noribogaine 3-60 mg: Tmax 2-3h, dose-linear AUC/Cmax, mean t1/2 28-49h, Vd 1417-3086L. No safety issues. jcph.404
These parameters were established in ascending-dose healthy volunteer and opioid-dependent patient studiessupported
Ascending Single-Dose, Double-Blind, Placebo-Controlled Safety Study of Noribogaine in Opioid-Dependent Patients. Dose-linear PK. cpdd.254
In ABCB1-knockout mice, brain-to-plasma ratios increase ~1.5-fold, indicating that efflux transporters actively restrict CNS penetration despite ibogaine's lipophilicitypartially supported
ABCB1+ABCG2 limit oral availability and brain penetration. Brain-to-plasma ratio 3.4 in mice. fphar.2022.855000
ABCB1 inhibitors (verapamil, cyclosporine) may therefore increase both oral bioavailability and brain exposure, though this interaction has not been characterized in humans.supported
ABCB1+ABCG2 limit oral availability and brain penetration. fphar.2022.855000
clinical-evidence3 · 1 ok
No unexpected serious adverse events occurred.supported
No SAEs. s41591-023-02705-w
Claim in clinical-evidence — inconclusiveinconclusiveworking →
Claim in clinical-evidence — inconclusiveinconclusiveworking →
history3 · 2 ok
Claim in history — inconclusiveinconclusiveworking →
The root bark has been used for centuries in Bwiti religious practices among the Fang people for initiation rites, spiritual ceremonies, and as a stimulant at sub-hallucinogenic dosessupported
Root bark from Tabernanthe iboga used traditionally in West Africa in religious rituals. In smaller doses reported anecdotally to have stimulant properties. j.jep.2016.05.022
During the late 1980s and 1990s, Lotsof organized informal treatment sessions in the Netherlands, producing the first published clinical case series.supported
33 cases of opioid detoxification. First systematic case series. pmid:10506904
chemistry2 · 1 ok
Claim in chemistry — inconclusiveinconclusiveworking →
Published physicochemical data:supported
Review of physicochemical properties, bioanalytical methods, and pharmacology of ibogaine as anti-addictive agent. 0960327107087802
effects-overview2 · 0 ok
receptor-pharmacology2 · 2 ok
Several binding constants remain imprecisely reported — specific Ki values for ibogaine at SERT and sigma-2 receptors were not extracted from available abstracts, although both interactions are qualitatively confirmed.partially supported
Ibogaine interacted with mu, delta, kappa opioid, 5HT2, 5HT3, muscarinic 1/2, dopamine/NE/5HT uptake sites, NMDA ion channels, sodium ion channels. pmid:7568622
Several binding constants remain imprecisely reported — specific Ki values for ibogaine at SERT and sigma-2 receptors were not extracted from available abstracts, although both interactions are qualitatively confirmed.supported
Binds kappa-opioid, NMDA, serotonin uptake; ibogaine also sigma-2 and nicotinic. pmid:9668680