1-Phenyl-2-propylaminopentane (PPAP), also known as α,N-dipropylphenethylamine (DPPEA) and by the developmental code name MK-306, is an experimental drug related to selegiline which acts as a catecholaminergic activity enhancer (CAE).

PPAP is a CAE and enhances the nerve impulse propagation-mediated release of norepinephrine and dopamine. It produces psychostimulant-like effects in animals. In 2025, it was discovered that PPAP is a potent catecholamine reuptake inhibitor, including of dopamine and to a lesser extent of norepinephrine. The drug is a phenethylamine and amphetamine derivative and was derived via structural modification of selegiline.

PPAP was first described in the literature in 1988 and in the first major paper in 1992. It led to the development of the improved monoaminergic activity enhancer (MAE) benzofuranylpropylaminopentane (BPAP) in 1999. PPAP was a reference compound for studying the MAE system for many years. However, it was superseded by BPAP, which is more potent, selective, and also enhances serotonin. There has been interest in PPAP for potential clinical use in humans, including in the treatment of depression, attention deficit hyperactivity disorder (ADHD), and Alzheimer's disease. It was encountered as a novel designer drug in 2020.

PPAP is classified as a catecholaminergic activity enhancer (CAE), a drug that stimulates the impulse propagation-mediated release of the catecholamine neurotransmitters norepinephrine and dopamine in the brain.

Unlike stimulants such as amphetamine, which release a flood of monoamine neurotransmitters in an uncontrolled manner, (–)-PPAP instead only increases the amount of neurotransmitters that get released when a neuron is stimulated by receiving an impulse from a neighboring neuron. Both amphetamine and (–)-PPAP promote the release of monoamines; however, while amphetamine causes neurons to release neurotransmitter stores into the synapse regardless of external input, (–)-PPAP does not influence the pattern of neurotransmitter release and instead releases a larger amount of neurotransmitters than normal.

Recent findings have suggested that known synthetic monoaminergic activity enhancers (MAEs) like PPAP, BPAP, and selegiline may exert their effects via trace amine-associated receptor 1 (TAAR1) agonism. This was evidenced by the TAAR1 antagonist EPPTB reversing the MAE effects of BPAP and selegiline, 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 therapeutic index for PPAP in animal models is greater than that of amphetamine while producing comparable improvements in learning, retention, and antidepressant effects. It has been found to reduce deficits induced by the dopamine depleting agent tetrabenazine in the shuttle box learning test in rats.

PPAP and selegiline are much less potent than BPAP as MAEs. Whereas PPAP and selegiline are active at doses of 1 to 5 mg/kg in vivo in rats, BPAP is active at doses of 0.05 to 10 mg/kg. BPAP is 130 times as potent as selegiline in the shuttle box test. In contrast to BPAP however, the MAE effects of PPAP and selegiline are not reversed by the BPAP antagonist 3-F-BPAP. In addition, whereas PPAP and selegiline are selective as MAEs of norepinephrine and dopamine, BPAP is a MAE of not only norepinephrine and dopamine but also of serotonin.