25B-NBOMe

25B-NBOMe produces clinically significant sympathomimetic cardiovascular activation via α₁-adrenergic receptor binding. Ventricular fibrillation was the documented cause of death in a published fatality. Pre-existing arrhythmias of any type represent absolute contraindication.

Congenital or acquired long QT syndrome is an absolute contraindication given documented cardiac arrhythmia fatalities and the sympathomimetic cardiovascular profile.

Hypertension was documented in all 10 patients in the Gee et al. 2016 case series. Uncontrolled pre-existing hypertension combined with acute vasoconstriction creates risk of hypertensive emergency.

The combination of α₁-adrenergic vasoconstriction, tachycardia, and hypertension creates acute cardiovascular stress risking coronary events.

Seizures documented in NBOMe intoxication case reports (Zawilska et al. 2020). Epilepsy or any seizure disorder constitutes an absolute contraindication.

As a potent 5-HT₂A agonist, 25B-NBOMe is contraindicated in individuals with schizophrenia, schizoaffective disorder, or other psychotic disorders. Class-level contraindication for serotonergic psychedelics.

Bipolar disorder represents a relative contraindication. Documented dopaminergic rewarding effects (Custodio et al. 2020) combined with 5-HT₂A agonism create risk of mood destabilization.

25B-NBOMe undergoes extensive hepatic metabolism via four CYP enzymes. Hepatic impairment could reduce clearance and increase plasma concentrations of a compound with critical acute toxicity.

Acute kidney injury documented in the Gee et al. 2016 case series, secondary to rhabdomyolysis and hyperthermia. Pre-existing renal impairment reduces capacity to handle metabolic stress.

Contraindicated in pregnancy and breastfeeding. Genotoxic signal in rat studies (Wojtas et al. 2021), combined with potent serotonergic activity and cardiovascular stress, creates unacceptable risk to fetal development. No teratogenicity data exist.