Loading…
for educational and safety purposes
BPAP and PPAP both come up in the same conversations; they overlap on Dopamine and Norepinephrine. BPAP: BPAP is an experimental laboratory compound created in the late 1990s by the Hungarian and Japanese team behind selegiline; it has never been approved as a medicine in any country. PPAP: PPAP is a laboratory compound derived from selegiline that was designed to stimulate the brain without the uncontrolled neurotransmitter dumping that amphetamines cause.
BPAP is an experimental laboratory compound created in the late 1990s by the Hungarian and Japanese team behind selegiline; it has never been approved as a medicine in any country. It is described as a "monoaminergic activity enhancer", meaning that in animal tissue it makes dopamine, noradrenaline and serotonin neurons release more transmitter when they fire, rather than forcing transmitter out the way amphetamine does; at higher concentrations it also blocks dopamine and noradrenaline reuptake. Essentially all the evidence comes from rats, mice and cell cultures, and almost all of it was produced by the two groups with a stake in the compound, namely Knoll's Semmelweis University laboratory and Fujimoto Pharmaceutical Corporation. No clinical trial in humans has ever been run or even registered, so claims about memory, mood, longevity or anti-aging benefit in people rest on no human evidence at all.
PPAP is a laboratory compound derived from selegiline that was designed to stimulate the brain without the uncontrolled neurotransmitter dumping that amphetamines cause. In rats it increases the dopamine and noradrenaline released when a nerve cell actually fires, an effect its developers named a catecholaminergic activity enhancer effect; unlike selegiline it does not block the enzyme MAO-B. A 2026 screening study also found it blocks dopamine reuptake, slightly more strongly than amphetamine did in the same assay. Almost the entire evidence base is rat and cell work from one Hungarian laboratory; PPAP has never been given to a human in any published study, so no human dose or safety information exists, and it has since appeared as an unregulated substance on the European drug market.
both fingerprints on one instrument; where the marks line up the two compounds work the same lever, where a slot goes dark only one of them touches it. read straight from each entry's affinity table; nothing here is invented.
Uptake inhibitor
Uptake inhibition
Uptake inhibitor
Uptake inhibition
Weak uptake inhibitor
Weak uptake inhibition
enhances (not releases)
NOT an inhibitor (explicit negative)
Weak ligand; neuroprotection blocked by sigma antagonist BD1063
agonist
Proposed agonist
Proposed interaction at a distinct site; enhances vesicular monoamine accumulation and release
enhances (impulse coupled release)
Enhances impulse-propagation-mediated release of dopamine and noradrenaline
Absent
inhibits (newer finding)
No inhibition; this is the defining negative property
supports
Enhanced at low concentration, inhibited at high concentration
strengths are the entries' qualitative ratings (strong / moderate / weak); Ki and EC50 figures appear where an entry records them.