5-MeO-DiBF

severe heart failure, uncontrolled hypertension, recent myocardial infarction, unstable angina

No cardiovascular data exist for 5-MeO-DiBF. By class effect, serotonergic psychedelics acting at 5-HT2A receptors can produce sympathomimetic cardiovascular responses. Individuals with severe cardiovascular disease are at elevated risk from these effects.

schizophrenia, schizoaffective disorder, bipolar I disorder with psychotic features

Personal or family history of psychotic-spectrum disorders is an absolute contraindication for all serotonergic psychedelics. 5-HT2A receptor agonism can trigger acute psychotic episodes or worsen existing psychotic illness. No substance-specific data exist for 5-MeO-DiBF; this is a class-level contraindication.

Pregnancy and lactation are absolute contraindications due to complete absence of reproductive toxicity data. No animal or human studies have assessed teratogenicity, embryotoxicity, or breast milk transfer for 5-MeO-DiBF.

phenelzine use, tranylcypromine use, moclobemide use, isocarboxazid use

Concurrent use of any monoamine oxidase inhibitor (irreversible or reversible MAO-A) with 5-MeO-DiBF poses substantial risk of severe serotonin syndrome and hypertensive crisis. This is a class-level absolute contraindication for all serotonergic tryptamine psychedelics.

tramadol use

Tramadol has been implicated in fatal serotonin toxicity reactions when combined with other serotonergic drugs (Gillman 2005). The combination with 5-MeO-DiBF could produce serotonin syndrome via dual mechanisms (direct receptor agonism plus reuptake inhibition). No case report exists for 5-MeO-DiBF specifically, but the mechanistic basis is well-supported.

fluoxetine use, sertraline use, paroxetine use, escitalopram use, venlafaxine use, duloxetine use

Concurrent SSRI or SNRI use with 5-MeO-DiBF carries risk of additive serotonergic effects and unpredictable modulation of psychedelic intensity. No substance-specific interaction data exist. This is a class-level relative contraindication.

fluoxetine use, paroxetine use, bupropion use, quinidine use

Potent CYP2D6 inhibitors could theoretically increase 5-MeO-DiBF plasma concentrations if the compound is a CYP2D6 substrate as predicted from indolealkylamine class metabolism. This represents a plausible mechanism for unexpectedly potentiated effects. The CYP2D6 metabolism assumption is itself inferred, not confirmed.