Fenethylline

Case reports document reversible type 1B Brugada ECG pattern in fenethylline users without prior Brugada diagnosis (Gul et al. 2023). In persons with established Brugada syndrome, the arrhythmogenic risk is substantially elevated, with potential for ventricular fibrillation and sudden cardiac death.

Fenethylline's amphetamine metabolite causes coronary vasospasm and platelet activation. In persons with recent MI or unstable angina, these effects act on compromised vasculature with high risk of reinfarction or fatal arrhythmia. A case of acute inferior MI in a 23-year-old following captagon ingestion is documented (Gokdemir & Giden 2019).

Rat models demonstrate QT prolongation and ST elevation with captagon exposure (Shehata et al. 2025). Persons with baseline conduction abnormalities or prolonged QT are at elevated risk of torsades de pointes and other ventricular arrhythmias, particularly when combined with QT-prolonging medications.

Systematic review links amphetamine-type stimulants to acute coronary syndrome via coronary vasospasm, accelerated atherosclerosis, platelet activation, and direct cardiotoxicity (Gresnigt et al. 2023). Fenethylline's amphetamine metabolite acts via these same mechanisms. Existing coronary artery disease amplifies risk.

Captagon-induced psychosis is well-documented in clinical populations. In a series of 101 male inpatients, psychosis emerged at regular daily doses of 1-15 tablets, with 25.7% developing morbid jealousy delusions (Shalaby et al. 2023). Persons with pre-existing psychotic disorders or first-degree family history of schizophrenia are at substantially elevated risk.

Fenethylline is metabolized via CYP2D6 (amphetamine moiety) and CYP1A2 (theophylline). Hepatic impairment affecting these enzymes alters the ratio of parent compound to metabolites, producing unpredictable pharmacokinetic profiles and potentially toxic metabolite accumulation.

No fenethylline-specific reproductive or developmental toxicity data have been published. Amphetamine-class compounds cross the placental barrier and are present in breast milk. Use during pregnancy or lactation is contraindicated based on class-level extrapolation from amphetamine reproductive safety data.

Concurrent use of fenethylline with any monoamine oxidase inhibitor (or within 14 days of MAOI discontinuation) risks catastrophic hypertensive crisis and serotonin syndrome via uncontrolled monoamine accumulation from amphetamine-driven reverse transport combined with blocked enzymatic degradation.

The amphetamine metabolite competitively inhibits CYP2D6 (Wu et al. 2019). Co-administration with narrow-therapeutic-index drugs metabolized by CYP2D6 — including certain antidepressants, antipsychotics, opioids (codeine, tramadol), and beta-blockers (metoprolol) — may produce dangerously elevated plasma levels of the co-administered drug.