Aniracetam is a powerful nootropic based off the racetam structure. These molecules were first created in the 1960's when piracetam was created.
Aniracetam is a slight improvement to this original molecule allowing for greater potency. It's most commonly used to improve memory, concentration, cognitive fatigue, and to delay the onset of Alzheimer's.
It works through the neurotransmitter acetylcholine, increasing its production in the brain. This popular nootropic substance is one of the safest, and most effective on the market. Recommended to take with a choline donor such as Alpha-GPC for best results.
Where Does It Come From?
- Improves memory
- Improves congcentration
- Delays onset of Alzheimer's
- Glutamatergic modulator
- Cholinergic modulator
- Serotonergic (mild)
- Dopaminergic (mild)
- Post stroke depression 
- To prolong the onset of Alzheimer's
- For mild-strong cognitive enhancement
- To improve memory
- Sleepi disturbances
- Parkinson's disease
600 - 3000 mg/day
Dose usually broken into segments four hours apart.
Best used in combination with a choline donor like Alpha-GPC.
The IUPAC name for aniracetam is (1-(4-methoxybenzoyl)-2-pyrrolidinone, CAS
As with all racetams, aniracetam has a 2-pyrrolidone nucleus made up of oxygen, nitrogen, and hydrogen.
The bioavailability of aniracetam is fairly high. From there, it is metabolised into 2 main species. 70% N-anisoyl-γ-amino-butyric acid, and 30% p-anisic acid and 2-pyrrolidinone [3-6].
Aniracetam has been shown to increase the release of acetylcholine from the hippocampus .
The antidepressant effects of aniracetam was shown in mice during a forced swim test. The results of this study showed a significantly enhanced effect on aged mice than healthy adult mice. The effects were suggested to be due to the combined effects of 2-pyrrolidinone and N-anisoyl-GABA (not individually however). The mechanism involves the facilitation of dopamineergic transmission (D2 receptor activation) through nicotinic acetylcholine receptor stimulation . The dosage range in this study was 30 and 100 mg/kg. No significant difference was noted between these doses.
Aniracetam was also shown to selectively enhance 5-HT release in mesocorticolimbic .serotonergic terminals (prefrontal cortex, basolateral amygdala and dorsal hippocampus) . These are well known sites of stress response and emotional memory.
Aniracetam was found to increase glutamatergic transmission via the quisqualate
or α-amino-3-hydroxy-5-methyl-4-isoxazolepropionate (AMPA) receptor .
The toxicity of aniracetam is very low. Still compiling research.
Aniracetam, as with all racetams are synergistic with choline donors. Due to the stimulation of acetylcholine production, having an excess of choline donor support improves the synthesis of acetylcholine.
Aniracetam is also synergystic with acetylcholinesterase inhibiters due to combined effect on acetylcholine levels. Combining the two in formula allows both substances to be taken in smaller doses.
Recent Blog Posts:
- Nakamura, K., & Tanaka, Y. (2001). Antidepressant-like effects of aniracetam in aged rats and its mode of action. Psychopharmacology, 158(2), 205-212. doi:10.1007/s00213010084
- Yasuomi O, Takeharu K, Hiroyuki O, Shingo N, Hideo T. The effect of aniracetam on cerebral glucose metabolism in rats after lesioning of the basal forebrain measured by PET. J Neuro Sci.1999;164:7–12.
- Tian Y., Zhang J.-J., Feng S.-D., Zhang Z.-J., & Chen Y. (2008). Pharmacokinetics and bioequivalence study of aniracetam after single-dose administration in healthy Chinese male volunteers. Arzneimittel-Forschung/Drug Research, 58(10), 497-500.
- Guenzi A, Zanetti M. Determination of aniracetam and its main metabolite, N-anisoyl-GABA, in human plasma by high-performance liquid chromatography. J Chromatogr. 1990;530:397–406.
- Masatoshi S, Kazuo N. Aniracetam enhances cortical dopamine and serotonin release via cholinergic and glutamatergic mechanisms in SHRSP. Brain Res. 2001;916:211–221.
- Oqiso T, Iwaki M, Tanino T, Ikede K, Paku T, Horibe Y, et al. Pharmacokinetics of aniracetam and its metabolites in rats. J Pharm Sci. 1998;87(5):594–598
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