2-FMA

Uncontrolled hypertension, Coronary artery disease, Recent myocardial infarction, Cerebrovascular disease, Aortic stenosis, Heart failure

2-FMA, as an amphetamine-type sympathomimetic, produces dose-dependent hypertension, tachycardia, and vasoconstriction. In individuals with pre-existing cardiovascular disease, these effects impose additional cardiac workload that may precipitate acute coronary syndrome, arrhythmia, cerebral hemorrhage, or sudden cardiac death. Anchondo et al. (2025) note the fluorinated amphetamine class is associated with heart failure, cerebral hemorrhage, and death. No 2-FMA-specific cardiovascular case reports exist.

Epilepsy, History of seizures, Conditions lowering seizure threshold

Amphetamine-type stimulants can lower seizure threshold. Individuals with epilepsy or other conditions predisposing to seizures face elevated risk. No 2-FMA-specific seizure data exist; this is a class-level inference.

History of psychosis, Schizophrenia, Schizoaffective disorder

Amphetamine-induced psychosis is well-documented (Srisurapanont et al. 2001, Cochrane review). 2-FMA fully substitutes for methamphetamine in discriminative stimulus assays (Anchondo et al. 2025), indicating methamphetamine-like interoceptive effects. Individuals with a history of psychotic disorders are at elevated risk of psychotic episode precipitation. No 2-FMA-specific psychosis data exist.

Hyperthyroidism, Thyrotoxicosis

Hyperthyroidism produces a state of elevated sympathetic tone. Adding an amphetamine-type sympathomimetic may produce additive cardiovascular stress (tachycardia, hypertension, tremor). Class-level inference from amphetamine prescribing contraindications.

Pregnancy, Lactation, Planning conception

Amphetamine-class compounds cross the placental barrier and are excreted in breast milk. No reproductive toxicity data exist for 2-FMA specifically. By class inference, risks include fetal growth restriction, premature birth, and neonatal withdrawal symptoms. The absence of any safety data for 2-FMA in pregnancy makes risk assessment impossible.

Concurrent use of any MAO-A or non-selective MAO inhibitor (phenelzine, tranylcypromine, isocarboxazid, moclobemide, selegiline at systemic doses)

Concurrent MAOI use with any amphetamine-type releasing agent risks severe hypertensive crisis and serotonin toxicity. MAO-A inhibition prevents the intraneuronal degradation of dopamine, norepinephrine, and serotonin released by 2-FMA, producing dangerous accumulation. This is a well-established class-level absolute contraindication for all amphetamine-type stimulants. No 2-FMA-specific case data exist, but the mechanism is identical to that of methamphetamine + MAOI.

Narrow-angle glaucoma, Anatomically narrow anterior chamber angle

Sympathomimetic-induced pupil dilation (mydriasis) can precipitate acute angle-closure glaucoma in anatomically predisposed individuals. This is a standard contraindication for all amphetamine-class drugs. No 2-FMA-specific data exist.

Concurrent tramadol use

Tramadol acts as a serotonin-norepinephrine reuptake inhibitor and weak μ-opioid agonist. Combined with 2-FMA (a monoamine releasing agent), there is dual risk: serotonin syndrome from additive serotonergic effects, and cardiovascular instability from additive noradrenergic stimulation. This combination is classified as potentially lethal in community harm-reduction interaction databases (e.g., TripSit). No published case report of a 2-FMA + tramadol fatality was identified, but the pharmacological mechanism is well-established.