Dr. Corneliu Giurgea, the originator of the prototypical nootropic piracetam, and the term “nootropic” itself developed aniracetam in the 70’s. Piracetam is a cyclic derivative of GABA, the primary inhibitory neurotransmitter though it has no GABAergic effect itself.
Three primary metabolites of aniracetam are responsible for the primary differences in aniracetam’s pharmacokinetics. Aniracetam has 3 primary metabolites which all seem to play some part in it’s effect. Aniracetam breaks down and metabolizes into N-anisoyl-GABA seems to be the primary metabolite in humans. These metabolites may be responsible for aniracetam’s multiphasic effect. Rather than the one parent compound (aniracetam) being solely responsible for the effect, it’s quite possible that various metabolites may be influencing the efficacy of this nootropic that has been anecdotally described to have positive effects raning from increased executive function, anxiety relief, improved memory, mild psychostimulatory effect and upmodulation of acetylcholine (the learning and memory neurotransmitter).
In addition to it’s swift metabolism, aniracetam has a short half life of 4-6 hours. In human trials plasma is reached in about 2 hours and return to baseline in approximately 6.
Aniracetam is shown to “preferentially increase extracellular levels of dopamine (DA) and serotonin (5-HT) in the prefrontal cortex (PFC), basolateral amygdala and dorsal hippocampus of the mesocorticolimbic system in stroke-prone spontaneously hypertensive rats.” This may be responsible for anecdotal claims of mood boost.
Despite having some apparent GABAergic effect on cognitive improvement, it is actually also a stronger AMPAkine (AMPA are a subreceptor of the excitatory glutamergic system) than it’s parent compound piracetam. Like all racetam drugs, it has a 2-pyrrolidinone backbone (chemical structure/skeleton).
1000 – 1500mg per day (divided in 2 or 3 doses) is considered optimum. Always remember that cholinergics require choline supplements to be most effective.
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