Tabernanthe iboga

QT prolongation, cardiac arrhythmia, structural heart disease, heart failure, coronary artery disease

Any history of QT prolongation, cardiac arrhythmia, structural heart disease, or heart failure precludes ibogaine administration. hERG IC₅₀ values are in the low-micromolar range for ibogaine (3.53 μM), noribogaine (2.86 μM), and voacangine (2.25 μM). Mean maximum QTc prolongation of 95 ms was observed at 10 mg/kg, with cardiac risk extending up to 72 hours post-dose due to noribogaine's 28–48 hour half-life.

methadone, tricyclic antidepressants, antipsychotics, certain SSRIs, macrolide antibiotics, fluoroquinolone antibiotics, certain antihistamines

Co-administration of ibogaine with any QT-prolonging agent creates additive hERG blockade, compounding the already significant QTc prolongation. All QT-prolonging medications must be discontinued with appropriate washout periods before ibogaine treatment.

schizophrenia, schizoaffective disorder, family history of psychotic spectrum disorders

Personal or family history of psychotic spectrum disorders constitutes a relative contraindication due to risk of precipitated psychosis. No prevalence estimates for ibogaine-associated acute psychosis have been published, but the extended duration (12–24 h) and intensity of hallucinations and dissociation elevate the risk window.

cirrhosis, severe hepatic insufficiency, acute liver failure

CYP2D6 and CYP3A4 are the primary enzymes metabolizing ibogaine. Severe hepatic impairment compromises this metabolism, resulting in unpredictable drug exposure that cannot be reliably managed even with dose reduction.

CYP2D6 poor metabolizer phenotype, CYP2D6 intermediate metabolizer phenotype (relative)

CYP2D6 is the primary metabolic enzyme for ibogaine O-demethylation to noribogaine. In a controlled PK study, CYP2D6 activity correlated strongly with ibogaine exposure (r = 0.82). Poor metabolizers demonstrate ~2× combined active moiety exposure, substantially elevating cardiac risk. CYP2D6 genotyping is recommended before any ibogaine administration.

hypokalemia, hypomagnesemia

Uncorrected electrolyte abnormalities — particularly low potassium and low magnesium — potentiate QT prolongation and increase the risk of torsades de pointes. These must be corrected and verified before ibogaine administration in any setting.

pregnancy, breastfeeding

Pregnancy is an absolute contraindication. No published reproductive safety data exist for ibogaine in any preparation form. The substance's broad receptor activity, significant cardiac toxicity, and extended active metabolite half-life (28–48 h) make risk assessment impossible without dedicated studies.

pediatric patients (under 18)

No safety or efficacy data have been published for ibogaine use in pediatric populations. All clinical studies have enrolled adults only. The established cardiac risk profile precludes use in minors without specific pediatric safety data.

active methadone maintenance, active buprenorphine maintenance, active MOUD without supervised taper

Discontinuation of medications for opioid use disorder (methadone, buprenorphine) for ibogaine treatment creates a dangerous scenario. Incomplete tapering risks precipitated withdrawal, while loss of opioid tolerance after ibogaine treatment increases post-session overdose risk. Supervised tapering under medical guidance is required before ibogaine administration.