Aniracetam, ≥99%

Chemical Name: 1-(4-methoxybenzoyl)-2-pyrrolidinone

Synonyms: 1-anisoyl-2-pyrrolidinone; Ro 13-5057; Ampamet; Draganon; Sarpul; 1-(4-methoxybenzoyl)pyrrolidin-2-one

CAS #: 72432-10-1

Cognitive enhancer (Nootropic) that potentiates AMPA receptor mediated ion conductance and potentiates mGluR activity; also demonstrates anxiolytic activity.

Form: White powder
Molecular Formula:  C12H13NO3

Molecular Weight:    219.24 g/mol
Solubility:    Insoluble in water

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This Material is Sold For Research Use Only. Terms of Sale Apply. Not for Human Consumption, nor Medical, Veterinary, or Household Uses.

Chemical Information:

CAS Number:72432-10-1
Molecular Weight:219.24
Melting Point:121-122 °C
Molecular Formula:C12H13NO3
Synonyms:1-(4-methoxybenzoyl)-2-pyrrolidinone; 1-p-anisoyl-2-pyrrolidinone; Ro 13-5057
PubChem CID:2196
PubChem Substance ID:24277955
MDL Number:MFCD00153767

Technical Information:

Application:A nootropic agent with modulatory actions at Glutamate and AMPA receptors demonstrating anxiolytic activity
Appearance:White crystalline powder
Physical State:Solid
Solubility:Soluble to 25 mM in Ethanol, Soluble to 50 mM in Chloroform, Soluble to 100 mM in DMSO, Insoluble in water.
Storage:Store at room temperature, in a sealed airtight container, protected from heat, light and humidity.
Stability:Aniracetam is stable for at least four years when stored as above.

Modes of action:

In rats, post administration plasma levels have been determined by HPLC method. Aniracetam has an overall bioavailability of around 8.6-11.4%, when taken up by the gut. [1] In human studies, plasma levels of Aniracetam were determined using sensitive liquid chromatography-tandem mass spectrometry (LC-MS/MS) method. Cmax was found to be 8.75+/-7.82 and 8.65+/-8.7ng/mL over two testing periods, with corresponding Tmax times of 0.4+/-0.1 hour. [2]

Human studies have shown the key metabolite to be N-Anisoyl-GABA (4,p-Anisaminobutyric acid, ABA), with roughly 70% of ingested Aniracetam being transformed into ABA through the liver. [3] Alternate metabolites include P-Anisic Acid and 2-pyrrolidinone. [4]

Aniracetam is a potent agonist for AMPA receptors in the glutaminergic system. At a concentration range of 1-5mM, Aniracetam binds to AMPA receptors and potentiates receptor activity, especially in the presence of positive stimuli (as indicated in Xenopus oocytes and in human hippocampus pyramidal cells). [5] Tang et al. showed that Aniracetam reversibly and selectively slows the desensitization kinetics of non-NMDA receptors while simultaneously modulating fast EPSC. [6]

Further studies have shown that Aniracetam increases peak amplitude of EPSCs, as well as the amplitude and duration of signals from IPSCs, resulting in a decrease in ESPC/ISPC charge ratio and representing a shift in the excitation-inhibition balance, towards inhibition. D Ling and L Bernardo have postulated that this may be due to Aniracetam’s additional modulation of the GABAergic system. [7]

Studies on hippocampal cells have shown that 100mM of Aniracetam is capable of improving norepinephrine release from NMDA receptors. To further illustrate the point, Pittaluga et al. showed that Aniracetam reduces kynurenic acid antagonism of norepinephrine release by NMDA receptor­s, as well as modulating the inhibitory effects of the AMDA antagonist NBQX. [8]

At an extremely low concentration of 0.1 nM, Aniracetam is capable of potentiating nicotinic α4β2 receptor transmission by 200-300%, through coupling mechanisms with G(s) proteins. [9] Since Aniracetam acts on AMPA receptors, it can be consider an Ampakine. Studies have shown that these kinds of compounds (including Piracetam and Oxiracetam) also have the ability to upregulate Brain-derived Neurotrophic factor (BDNF) expression, for extended periods that exceed the AUC of the Ampakine. [10]

Further scientific research:

Please note that this is not a comprehensive account of the scientific research on Aniracetam to date. We have made a humble attempt to convey some of the most relevant research on the subject to date, in a variety of applications.

Clinical reviews:

In 1994, Lee and Benfield published a review of trials on Aniracetam showing that it was an effective positive modulator of metabotropic glutamate receptors and AMPA-sensitive glutamate receptors, with possible actions on cholinergic transmission. Results from Lee and Benfield’s review showed possible benefits on patients with Alzheimer’s, including long-term studies of Aniracetam at 1500mg/day for 4-6 months. The authors also suggested that there was preliminary evidence of benefits in patients with cognitive impairment, and that Aniracetam is well tolerated. [11]

O’Neill and Witkin published a review in 2007 on the downstream effects of Aniracetam’s interactions with AMPA receptors, postulating that these effects may have utility in certain CNS disorders, some of which have been elucidated in rodent models of Alzheimer’s and depression. [12]

In 2002, Nakamura published a review of the potential clinical efficiency of Aniracetam. He found that, although Aniracetam had been successful in numerous animal models of human cognitive disorders, there was not sufficient evidence to guarantee its clinical efficiency in humans. He did, however, recommend clinical trials in humans to further develop the above concept. [13]

Human studies:

Human studies on Aniracetam are scarce.

There is some evidence of potential effects in Alzheimer’s and a few authors have suggested Aniracetam as a research chemical for development in this field. Specifically, O’Neill et al. report that clinical studies have indicated that AMPA receptor modulators (including Aniracetam) improve cognitive performance in elderly people, as well as in patients suffering from neurological and psychological disorders.

O’Neill et al. therefore recommend further research into the potential of AMPA for development of agents to be used for the treatment of:

-       Cognitive impairment associated with Alzheimer’s disease and schizophrenia

-       Depression

-       Slowing progression and enhancing recovery from Parkinson’s [14]

In 2012, Koliaki et al. presented a study that evaluated the efficiency of Aniracetam – both as a monotherapy and in combination with ChEIs – in 276 elderly patients suffering from dementia. The treatment lasted 12 months in total, with patients in the Aniracetam group showing adequately maintained parameters after 12 months, and significant emotional state improvements after 3 months. [15]

Toxicity reviews:

There is currently a lack of data on Aniracetam’s potential toxicity, both in human and animal studies. However, PubChem database shows a H361 warning (100%) for Aniracetam: Suspected of damaging fertility or the unborn child. [16]

Animal studies:

In 1984, Petkov et al. showed that Aniracetam may have effects on the dopaminergic system. They found that rats treated with 50mg/kg Aniracetam showed reduced dopamine in the hypothalamus and striatum, and increased 5-HT in the cortex and striatum. [17]

In 2001, Shirane and Nakamura reported that Aniracetam was found to increase both dopamine and serotonin in the prefrontal cortex, amygdala, and dorsal hippocampus in stroke-prone rats. The authors found that these results were due to Aniracetam’s effects on the cholinergic system – through mediating the action of N-anisoyl-GABA on somatodendritic nACh, presynaptic nACh, and NMDA receptors alike. [18]

In 1982, Cumin et al. published results of their studies on the effects of Aniracetam on rodents. Their publication indicated that Aniracetam was able to:

-       Reduce rats’ incapacity to learn escape routes after exposure to sublethal hypercapnia (in a highly effective manner)

-       Prevent scopolamine-induced short-term amnesia

-       Protect against short-term memory-loss after electroconvulsive shock treatment

-       Prevent the long-term memory-loss associated with chloramphenicol or cycloheximide poisoning

-       Reverse the deficit in attention in a passive avoidance task associated with cycloheximide treatment 2 days prior

-       Prevent the deficit in memory retrival in an active avoidance task associated with subconvulsant electroshock or hypercapnia [19]

A 2001 study by Nakamura and Kurasawa showed the potential anxiolytic effects of Aniracetam in rats. Aniracetam, at a dosage of 10-100mg/kg, increased total social interaction scores as well as social interaction time. It also showed anxiolytic effects for two other models – the elevated plus-maze test, and conditioned fear stress test. Aniracetam metabolites mimicked the anxiolytic effects in vivo. [20] The same authors tested the potential antidepressant effects of Aniracetam in a study published in Psychopharmacology, 2001. Aniracetam showed significant positive results in aged rats, but not in young rats. The results were again mimicked by Aniracetam metabolites. [21]

Ito et al. showed that Aniracetam potentiates ionotropic quisqualate (iQA) receptors in a reversible manner – as shown in Xenopus oocytes and rat hippocampal cells. It was found to increase conductace range of iQA and AMPA responses without influencing selectivity of ion-gated channels. [22]

Wijayawardhane et al. show that Aniracetam has the capacity to restore synaptic transmission in rat pups with laboratory-induced fetal alcohol syndrome (characterized by impaired impaired hippocampal AMPAR-mediated neurotransmission). Postnatal treatment with Aniracetam restored synptic transmission and ameliorated the cognitive defects associated with in-womb ethanol exposure. [23]

A 2014 study found that Aniracetam did not alter cognitive or affective behavior in healthy mice. The authors found that Aniracetam did not improve scores for elevated plus maze, locomotion, or repetitive behaviors in the population of C57BL/6J mice. However, they found that it did improve the pharmacological profile associated with learning and memory by increasing hippocampal acetylcholine, serotonin, glutamate, and dopamine levels. Additionally, the authors stated that Aniracetam has been shown to significantly facilitate long-term potentiation (LTP), reverse memory loss, reduce anxiety, and reverse ethanol-induced brain damage. [24]


  • [1] Ogiso T, Iwaki M, Tanino T, Ikeda K, Paku T, Horibe Y, Suzuki H. (1998). Pharmacokinetics of aniracetam and its metabolites in rats, J Pharm Sci, 87(5):594-8.
  • [2] Yuan T, Zhang JJ, Feng SD, Zhang ZJ, Chen Y. (2008). Pharmacokinetics and bioequivalence study of aniracetam after single-dose administration in healthy Chinese male volunteers, Arzneimittel-Forschung, 58(10) pp. 497-500, ISSN: 0004-4172
  • [3] Guenzi A., Zanetti M. (1990). Determination of aniracetam and its main metabolite, N-anisoyl-GABA, in human plasma by high-performance liquid chromatography, J Chromatogr, 14;530(2):397-406.
  • [4] Zhang J, Liang J, Tian Y, Zhang Z, Chen Y. (2007). Sensitive and selective liquid chromatography-tandem mass spectrometry method for the quantification of aniracetam in human plasma, J Chromatogr B Analyt Technol Biomed Life Sci, 15;858(1-2):129-34.
  • [5] Isaacson JS, Nicoll RA. (1991). Aniracetam reduces glutamate receptor desensitization and slows the decay of fast excitatory synaptic currents in the hippocampus. Proc Natl Acad Sci USA, 1;88(23):10936-40.
  • [6] Tang CM, Shi QY, Katchman A, Lynch G. (1990). Modulation of the time course of fast EPSCs and glutamate channel kinetics by Aniracetam, Science, 254(5029), pp. 288-290.
  • [7] Ling DSF, Benardo LD. (2005). Nootropic Agents Enhance the Recruitment of Fast GABAA Inhibition in Rat Neocortex. Cereb Cortex,15(7):921-928.
  • [8] Pittaluga A, Bonfanti A, Arvigo D, Raiteri M. (1999). Aniracetam, 1-BCP and cyclothiazide differentially modulate the function of NMDA and AMPA receptors mediating enhancement of noradrenaline release in rat hippocampal slices. Naunyn Schmiedebergs Arch Pharmacol, 359(4):272-9.
  • [9] Zhao X,  Kuryatov A, Lindstrom JM, Yeh JZ, Narahashi T. (2001). Nootropic drug modulation of neuronal nicotinic acetylcholine receptors in rat cortical neurons. Mol Pharmacol, 59(4):674-83.
  • [10] Lauterborn JC, Truong GS, Baudry M, Bi X, Lynch G, Gall CM. (2003). Chronic elevation of brain-derived neurotrophic factor by ampakines. J Pharmacol Exp Ther, 307(1):297-305.
  • [11] Lee CR, Benfield P. (1994). Aniracetam. An overview of its pharmacodynamic and pharmacokinetic properties, and a review of its therapeutic potential in senile cognitive disorders. Drugs Aging, 4(3):257-73.
  • [12] O'Neill MJ, Witkin JM. (2007). AMPA receptor potentiators: application for depression and Parkinson's disease. Curr Drug Targets, 8(5):603-20.
  • [13] Nakamura K. (2002). Aniracetam: its novel therapeutic potential in cerebral dysfunctional disorders based on recent pharmacological discoveries. CNS Drug Rev, 8(1):70-89.
  • [14] O'Neill MJ, Bleakman D, Zimmerman DM, Nisenbaum ES. (2004). AMPA receptor potentiators for the treatment of CNS disorders, Curr Drug Targets CNS Neurol Disord, 3(3):181-94.
  • [15] Koliaki CC. (2012). Clinical efficacy of aniracetam, either as monotherapy or combined with cholinesterase inhibitors, in patients with cognitive impairment: a comparative open study. CNS Neurosci Ther, 18(4):302-12.
  • [16] Aniracetam, CID 2196, PubChem, Open Chemistry Database, U.S. National Library of Medicine, Center for Biotechnology Information, available online from [Accessed Jul 19, 2018.
  • [17] Petkov VD, Grahovska T, Petkov VV, Konstantinova E, Stancheva S. (1984). Changes in the brain biogenic monoamines of rats, induced by piracetam and Aniracetam, Acta Physiol Pharmacol Bulg, 10(4):6-15.
  • [18] Shirane M, Nakamura K. (2001). Aniracetam enhances cortical dopamine and serotonin release via cholinergic and glutamatergic mechanisms in SHRSP, Brain Res, 19;916(1-2):211-21.
  • [19] Cumin R, Bandle EF, Gamzu E, Haefely WE. (1982). Effects of the novel compound aniracetam (Ro 13-5057) upon impaired learning and memory in rodents, Psychopharmacology (Berl), 78(2):104-11.
  • [20] Nakamura K, Kurasawa M. (2001). Anxiolytic effects of aniracetam in three different mouse models of anxiety and the underlying mechanism. Eur J Pharmacol, 420(1):33-43.
  • [21] Nakamura K, Tanaka Y. (2001). Antidepressant-like effects of aniracetam in aged rats and its mode of action. Psychopharmacology (Berl), 158(2):205-12.
  • [22] Ito I, Tanabe S, Kohda A, Sugiyama H. (1990). Allosteric potentiation of quisqualate receptors by a nootropic drug Aniracetam. J Physiol, 424:533-43.
  • [23] Wijayawardhane N, Shonesy BC, Vaglenova J, Vaithianathan T, Carpenter M, Breese CR, Dityatev A, Suppiramaniam V. (2007). Postnatal aniracetam treatment improves prenatal ethanol induced attenuation of AMPA receptor-mediated synaptic transmission. Neurobiol Dis, 26(3):696-706.
  • [24] Elston TW, Pandian A, Smith GD, Holley AJ, Gao N, Lugo JN. (2014). Aniracetam Does Not Alter Cognitive and Affective Behavior in Adult C57BL/6J Mice. PLoS One, 9(8): e104443.

Precaution and Disclaimer:

This Material is Sold For Research Use Only. Terms of Sale Apply. Not for Human Consumption, nor Medical, Veterinary, or Household Uses.

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