(–)-Benzofuranylpropylaminopentane (BPAP; developmental code name FPFS-1169) is an experimental drug related to selegiline which acts as a monoaminergic activity enhancer (MAE).

[3] BPAP is a highly potent MAE and enhances the nerve impulse propagation-mediated release of serotonin, norepinephrine, and dopamine.

[4][7][5][6] At much higher concentrations, BPAP is also a monoamine reuptake inhibitor, specifically of dopamine and norepinephrine and to a much lesser extent of serotonin.

[11] It stimulates the impulse propagation mediated release of the monoamine neurotransmitters serotonin, dopamine, and norepinephrine in the brain.

[5][12][20] Recent findings have suggested that known synthetic MAEs like BPAP may exert their effects via trace amine-associated receptor 1 (TAAR1) agonism.

[16] The MAE effects of BPAP, for instance on dopamine, can be blocked by monoamine reuptake inhibitors, like nomifensine.

[17] Other compounds which produce MAE effects are the endogenous trace amines phenethylamine and tryptamine, the MAO-B inhibitor selegiline (L-deprenyl), and phenylpropylaminopentane (PPAP).

[12] Following a peak in adolescence, monoamine release in the brain declines with age in rodents and this is associated with reduced behavioral activity.

[15][6][21] Rodent studies have found that MAEs like BPAP and selegiline augment brain monoamine release, slow age-related monoaminergic neurodegeneration, help to preserve behavioral activity with age, and prolong lifespan.

[5][11] It has been said that the monoamine reuptake inhibition of BPAP is not of pharmacological significance at the much lower concentrations that have MAE activity.

[17][14][2] Indolylpropylaminopentane (IPAP), an analogue of BPAP, is a MAE for serotonin, norepinephrine, and dopamine that was derived from tryptamine.

[15][17][25] Unlike BPAP, it shows some selectivity for serotonin, with its maximal impact on this neurotransmitter occurring at 10-fold lower concentrations than for norepinephrine or dopamine.

[7][27] These findings suggest that 3-F-BPAP interacts with the same receptor or biological target as BPAP and acts as a MAE antagonist.

[4][3] An effective dosage of BPAP of 0.1 mg/day, one-tenth of that of the less-potent compound selegiline (1 mg/day), has been suggested for study and use in humans.