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

BPAP is a highly potent MAE and enhances the nerve impulse propagation-mediated release of serotonin, norepinephrine, and dopamine. At much higher concentrations, BPAP is also a monoamine reuptake inhibitor, specifically of dopamine and norepinephrine and to a much lesser extent of serotonin. BPAP produces psychostimulant-like effects in animals, with these effects mediated by its MAE actions. The drug is a substituted benzofuran derivative and tryptamine relative structurally related to phenylpropylaminopentane (PPAP).

BPAP was first described in 1999. There has been interest in BPAP for potential clinical use in humans, including in the treatment of Parkinson's disease, Alzheimer's disease, and depression. There has also been interest in BPAP to help slow aging.

BPAP is a monoaminergic activity enhancer (MAE). It stimulates the impulse propagation mediated release of the monoamine neurotransmitters serotonin, dopamine, and norepinephrine in the brain. However, whereas the related MAE phenylpropylaminopentane (PPAP) is only a catecholaminergic activity enhancer (CAE), BPAP enhances both serotonin and the catecholamines. In addition, BPAP is a more potent MAE than PPAP.

Unlike psychostimulants like amphetamine, which are monoamine releasing agents that induce release of a flood of monoamine neurotransmitters in an uncontrolled manner, BPAP instead only increases the amount of neurotransmitter that is released when a neuron is stimulated by receiving an impulse from a neighbouring neuron. As such, while both amphetamine and BPAP increase the amount of neurotransmitters that are released, amphetamine causes neurons to dump neurotransmitter stores into the synapse regardless of external input, while with BPAP the pattern of neurotransmitter release is not changed. Instead, when the neuron would normally release neurotransmitter, a larger amount than normal is released with BPAP.

In an in vivo rodent study, BPAP was found to maximally increase dopamine levels in the striatum by 44%, in the substantia nigra by 118%, and in the olfactory tubercle by 57%; norepinephrine levels in the locus coeruleus by 228%; and serotonin levels in the raphe nucleus by 166%. MAEs, including BPAP, have a peculiar and characteristic bimodal concentration–response relationship, with two bell-shaped curves of MAE activity across tested concentration ranges. Hence, there is a narrow concentration range for optimal pharmacodynamic activity.

The actions of BPAP and other MAEs are distinct from those of monoamine reuptake inhibitors and monoamine oxidase inhibitors. Whereas BPAP enhances the nerve stimulation-induced release of serotonin, norepinephrine, and dopamine in the rat brain stem in vitro, the selective norepinephrine reuptake inhibitor desipramine (desmethylimipramine), the selective serotonin reuptake inhibitor fluoxetine, the selective MAO-A inhibitor clorgyline, the selective MAO-B inhibitor lazabemide, and the potent dopamine receptor agonists bromocriptine and pergolide were all ineffective.

Recent findings have suggested that known synthetic MAEs like BPAP may exert their effects via trace amine-associated receptor 1 (TAAR1) agonism. This was evidenced by the TAAR1 antagonist EPPTB reversing its MAE effects, among other findings. Another compound, rasagiline, has likewise been found to reverse the effects of MAEs, and has been proposed as a possible TAAR1 antagonist. The MAE effects of BPAP, for instance on dopamine, can be blocked by monoamine reuptake inhibitors, like nomifensine. This is thought to be because BPAP uses the monoamine transporters, like the dopamine transporter, to enter monoaminergic neurons and then mediates its MAE effects via intracellular TAAR1 activation whilst inside of pre-synaptic nerve terminals.