Quick Navigation


Aniracetam is a fat-soluble molecule in the racetams family, anecdotally touted to be more potent than Piracetam and more catered to creativity and holistic thinking as well as reducing anxiety and depression. Human studies are lacking.

Our evidence-based analysis on aniracetam features 39 unique references to scientific papers.

Research analysis led by Kamal Patel .
Reviewed by
Examine.com Team
Last Updated:

Summary of Aniracetam

Primary Information, Benefits, Effects, and Important Facts

Aniracetam is a compound in the group of racetams due to its common pyrrolidone structure. It is one of the more common Racetamic structures. It is fat-soluble and thus needs to be ingested with fatty acids. Additionally, Aniracetam is cholinergic

Aniracetam acts as a positive modulator of some excitatory receptors known as AMPA receptors and decreases the rate of receptor desensitization. This typically manifests as a controlled and prolonged neurological stimulation effect. Since AMPA receptors differ in structure across the brain, different AMPA modulators affect the brain in different ways.

Anecdotally, Aniracetam has been know to aid in 'collective and holistic thinking', or putting the pieces of the puzzle together. It also increases blood flow and activity in the area of the brain known for this action, the association cortex.

Aniracetam, as an AMPA modulator, is currently being studied for usage in depression and other CNS disorders such as Alzheimer's disease.

Evidence-based information on what works

No fake reviews. No selling you supplements. Just the science.

Our free supplement mini-course teaches you what works, what's a waste, and how to achieve your health goals.

Join the over 200,000 people who have gone through this course (saving themselves time, money, and stress).

Things To Know & Note

Is a Form Of

Other Functions:

Also Known As

1-p-anisoyl-2-pyrrilidinone, Ro 13-5057, CAS 72432-10-1, 1(4-methoxybenzoyl)-2-pyrrolidinone

Do Not Confuse With


Goes Well With

  • Aniracetam is known anecdotally to be stimulatory, however it's effects are unlike caffeine stimulation.

  • Aniracetam is fat-soluble, however it appears to be taken up even in a fasted state. Food does not appear to be needed.

  • Aniracetam has a highly bitter taste to the powder

How to Take Aniracetam

Recommended dosage, active amounts, other details

Doses between 10 mg/kg bodyweight and 100 mg/kg bodyweight have been used in rats with efficacy in laboratory settings. Limited human evidence finds that oral doses in the 1,000-1,500 mg range (over the course of a day) tend to be effective.

Doses as low as 400 mg have been reported to have some efficacy, and it is common to take the above 1,000-1,500 mg aniracetam in two divided doses of 500-750 mg twice daily with meals.

Aniracetam powder has a highly bitter taste, so capsules may be a better purchase for those who wish to avoid that.

Research Breakdown on Aniracetam

Click on any below to expand the corresponding section. Click on to collapse it.

Click here to fully expand all sections or here to fully collapse them.

Aniracetam is a pyrrolidinone compound of the racetam family,[1] and has an additional anisoyl ring with a methoxy group at the lone para position. (replacing the amine group of piracetam) with an O-methoxy group on the furthest binding point. Its structure is dissimilar to that of oxiracetam (which is quite similar to piracetam) and Pramiracetam (fairly unique structure) yet closely related to that of nefiracetam.

Aniracetam is a piracetam molecule in which the amine is replaced by a methylated phenyl group, this modification was made to enhance fat solubility and underlies differences between piracetam and aniracetam

Aniracetam as well as the structurally similar Nefiracetam are able to enhance long-lasting calcium channel currents in neurons at concentrations as low as 1µM.[2]

Aniracetam appears to be greatly taken up from the gut even in a fasted state, but is subject to extensive first pass hepatic metabolism. Due to this, it has an overall bioavailabiliy of around 8.6-11.4%.[3] Bioavailability is presumed higher when taken with fatty acids, but unexplored.

Is fat-soluble and logically enhanced when taken with fatty acids, does not appear to need fatty acids to be absorbed

Plasma levels of aniracetam have been noted to peak at 2.3mcg/L (300mg) and 14.1mcg/L (1200mg) with an elimination half life of 35 minutes following ingestion of aniracetam.[1] It appears to have extensive first pass metabolism in the liver[1] with the main metabolites being N-anisoyl-GABA, 2-pyrrolidinone, and anisic acid. 95.8% of the dose is recovered, mostly in the urine, 28 hours post ingestion.[1]

In a study of healthy male volunteers, Aniracetam showed a Cmax (max concentration) of 8.75+/-7.82 and 8.65+/-8.7ng/mL over two testing periods which correspond to a Tmax (time at max) of 0.4+/-0.1 hour each time; in response to 400mg oral Aniracetam.[4] The plasma elimination half-lives were 47+/-0.16 and 49+/-0.24 hours and plasma AUC 4.53+/-6.62 and 4.76+/-6.65ng/h/mL in this study as well. These relatively low peaks of Aniracetam may be due to extensive metabolism after oral administration.[4]

It appears that superloading Aniracetam (50-100mg/kg bodyweight) does not augment the Cmax or Tmax significantly, and tends to only prolong the AUC to 1.7-2.1 hours.[3]

Appears to be rapidly absorbed in under 30 minutes, and rapidly metabolized; higher doses do not change the time it takes to work, but may prolong the AUC (Area-Under-Curve) of Aniracetam, either by delaying excretion or metabolism

The main human metabolite of Aniracetam is a compound known as N-Anisoyl-GABA (aka. 4,p-Anisaminobutyric acid or ABA),[5] which accounts for 70% of orally ingested Aniracetam by weight after hepatic (liver) biotransformation.[4] Alternate pathways lead to production of P-Anisic Acid (which can be conjugated by wither glucuronic acid or glycine) and 2-pyrrolidinone (which then goes on to the Kreb's Cycle to produce energy via the succinate intermediate).[3][6]

One study that confirmed protective effects against amnesia in a choice reaction test with aniracetam (10-100mg/kg) subsequently tested all metabolites, with both P-anisic acid and 2-pyrrolidinone failing to exert anti-amnesiac effects while N-anisoyl-GABA at 30mg/kg was similarly effective.[7]

Aniracetam is heavily metabolized into N-anisoyl-GABA and P-Anisic Acid, which should be considered for bioactivity in the body

AMPA is one of the three subsets of glutamate (excitatory) receptors, of which the other two are kainate and NMDA (N-methyl-D-Aspartate).[8][9] These AMPA receptors mediate fast excitatory amino acid transmission, and are heterogenously expressed in the brain as heteromers with eight possible subunits (GluR1 through R4, each in a flip or flop variant).[10]

Aniracetam is a modulator of the AMPA receptor that works by binding to a non-active site of AMPA receptors and allosterically modifying the binding site, of which the final result is a reduced rate of desensitization[11] in the presence of positive stimuli (such as glutamate, which is intrinsically produced).[12] This occurs in the concentration range of 1-5mM.[11][13]

AMPA receptors appear to be positively modulated by aniracetam, similar to other basic racetam compounds

Aniracetam has been noted to be a positve modulator of kainate receptors.[14][15]

Aniracetam does not directly agonize NDMA receptors, but does not appear to hinder agonism of NMDA receptors either.[16][17]

May have a positive influence on kainate receptors, does not appear to interact with NMDA receptors much if at all

Activation of AMPA receptors is able to release noradrenaline from neurons, and 100µM (but not 10µM) of aniracetam is able to potentiate AMPA's effects on noradrenaline release in these hippocampal cells.[18]

Kyurenic acid is able to attenuate the ability of NDMA to release noradrenaline from cells, and this inhibition is attenuated in the presence of aniracetam (EC50 in the range of 10-100nM and near full inhibition at 1µM) without inherently affecting basal outflow or NMDA induced release of noradrenaline at this dose;[18] blocking the AMPA receptor failed to block this effect, and while kyurenic acid also suppresses AMPA receptor activation aniracetam (1-100µM) does not antagonize this effect (cyclothiazide, however, was effective).[18]

Aniracetam appears to enhance the effects of corticol GABAergic inhibition[19] independent of NMDA.[20]

Aniracetam appears to be able to potentiate signalling via nicotinic α4β2 receptors at 0.1nM via interactions with GS proteins, independent of protein kinases.[21]

Aniracetam has been shown at 50mg/kg oral ingestion (rats) to decrease the turnover rates for dopamine in the striatum and reducing dopamine levels in the hypothalamus and striatum; serotonin levels decreased in the hypothalamus but increased in the cortex and striatum, where it reduced turnover (hypothalamus) and increase turnover (cortex, striatum, brain stem).[22]

Aniracetam seems to be able to alleviate damage done to memory and learning impairment caused by various agents and traumas such as cholinergic antagonists, cerebral ischaemia and electroconvulsive shock.[1] Aniracetam can also protect against scopolamine-induced damage, and does so (at 1.5g) to a greater extent than Piracetam (at 2.4g).[23][1]

Aniracetam has been shown to reduce measures of anxiety in rats, and has anecdotally reported to do the same in humans. It is suspected to do so via a mix of serotonergic, dopaminergic, and cholinergic interactions. Improvements as measured by social interactions were seen in doses ranging from 10mg/kg body weight to 100mg/kg bodyweight.[24]

It has demonstrated efficacy in reducing depression in aged rats at 100mg/kg bodyweight, but was ineffective at exerting anti-depressive effects in younger mice.[25] These effects were mimicked with Aniracetam metabolites, and were abolished with haloperidol and mecamylamine, and thus the mechanism was theorized to be enhancing dopaminergic signalling via the nicotinic acetylcholinergic receptors.[25]

There may also be interactions with depression and downstream effects of Aniracetam's main mechanism of action, AMPA receptor modulation.[26]

Aniracetam has been found to specifically decrease the rate of receptor desensitization in lab animal hippocampus (specifically quisqualate receptors)[27], suggesting a potential benefit to memory formation. It does not seem affect choline uptake into hippocampal cells in any way,[28] and actually encourages acetylcholine release.[29]

Aniracetam also increases the release of dopamine and serotonin via cholinergic mechanisms in the prefrontal cortex[30], with implications in improving judgement. This may also in part explain it's involvement as an anti-depressant.[31] Via either the same or alternate mechanisms (positive AMPA modulation) Aniracetam has also been shown to reduce impulsiveness in the rat.

Through the general mechanism of AMPA modulation (and thus applicable to Piracetam and Oxiracetam), Ampakines can upregulate Brain-derived Neurotrophic factor (BDNF)[32] for, although the effects can attentuate rapidly via reduced AMPA receptor levels. One study perfomed on rat hippocampus slices in vitro suggested that that AMPA receptor attenutaion can be avoided by stimulating the cultures for 24 hrs, followed by a 24 hr washout period. The 24 hrs on/ 24 hrs off stimulation protocol was able to maintain increased levels of BDNF expression over a 5 day period.[33][34]

Further studies on rat hippocampus slices cultured in vitro suggest that AMPA receptor attenuation can similarly be circumvented with a daily dosing protocol of 3 hrs.[35] More research is needed to determine whehter such attenuation can be avoided in vivo with a similar intermittent dosing protocol. Since BDNF is implicated in increasing adult neural plasticity, such studies would be of great interest in the neurology field.[36][37]

It is also being studied in other cognitive deficits such as Alzheimer's disease[38] or other cognitive ailments[26] as either a mechanism to biologically reverse neurological changes or to alleviate symptoms of said disorders.

Aniracetam has also been implicated in rats to alleviate some cognitive deficits in the hippocampus onset by Fetal Alcohol Syndrome (FAS) in a dosage of 50mg/kg bodyweight.[39]


  1. ^ a b c d e f Lee CR, Benfield P. Aniracetam. An overview of its pharmacodynamic and pharmacokinetic properties, and a review of its therapeutic potential in senile cognitive disorders. Drugs Aging. (1994)
  2. ^ Yoshii M, Watabe S. Enhancement of neuronal calcium channel currents by the nootropic agent, nefiracetam (DM-9384), in NG108-15 cells. Brain Res. (1994)
  3. ^ a b c Ogiso T, et al. Pharmacokinetics of aniracetam and its metabolites in rats. J Pharm Sci. (1998)
  4. ^ a b c Pharmacokinetics and bioequivalence study of aniracetam after single-dose administration in healthy Chinese male volunteers.
  5. ^ 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)
  6. ^ Zhang J, et al. 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. (2007)
  7. ^ Nakamura K, Kurasawa M. Serotonergic mechanisms involved in the attentional and vigilance task performance of rats and the palliative action of aniracetam. Naunyn Schmiedebergs Arch Pharmacol. (2000)
  8. ^ Eleore L, et al. Modulation of the glutamatergic receptors (AMPA and NMDA) and of glutamate vesicular transporter 2 in the rat facial nucleus after axotomy. Neuroscience. (2005)
  9. ^ Bowie D. Redefining the Classification of AMPA-selectiveIonotropic Glutamate Receptors. J Physiol. (2011)
  10. ^ Ozawa S, Kamiya H, Tsuzuki K. Glutamate receptors in the mammalian central nervous system. Prog Neurobiol. (1998)
  11. ^ a b Isaacson JS, Nicoll RA. Aniracetam reduces glutamate receptor desensitization and slows the decay of fast excitatory synaptic currents in the hippocampus. Proc Natl Acad Sci U S A. (1991)
  12. ^ Francotte P, et al. In search of novel AMPA potentiators. Recent Pat CNS Drug Discov. (2006)
  13. ^ Tang CM, et al. Modulation of the time course of fast EPSCs and glutamate channel kinetics by aniracetam. Science. (1991)
  14. ^ Modulation of the time course of fast EPSCs and glutamate channel kinetics by aniracetam.
  15. ^ Aniracetam reduces glutamate receptor desensitization and slows the decay of fast excitatory synaptic currents in the hippocampus.
  16. ^ Kaneko S, et al. Effects of several cerebroprotective drugs on NMDA channel function: evaluation using Xenopus oocytes and {3H}MK-801 binding. Eur J Pharmacol. (1991)
  17. ^ Allosteric potentiation of quisqualate receptors by a nootropic drug aniracetam.
  18. ^ a b c Pittaluga A, et al. 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. (1999)
  19. ^ Nootropic Agents Enhance the Recruitment of Fast GABAA Inhibition in Rat Neocortex.
  20. ^ Recruitment of GABAA inhibition in rat neocortex is limited and not NMDA dependent.
  21. ^ Zhao X, et al. Nootropic drug modulation of neuronal nicotinic acetylcholine receptors in rat cortical neurons. Mol Pharmacol. (2001)
  22. ^ Petkov VD, et al. Changes in the brain biogenic monoamines of rats, induced by piracetam and aniracetam. Acta Physiol Pharmacol Bulg. (1984)
  23. ^ Cumin R, et al. Effects of the novel compound aniracetam (Ro 13-5057) upon impaired learning and memory in rodents. Psychopharmacology (Berl). (1982)
  24. ^ Nakamura K, Kurasawa M. Anxiolytic effects of aniracetam in three different mouse models of anxiety and the underlying mechanism. Eur J Pharmacol. (2001)
  25. ^ a b Nakamura K, Tanaka Y. Antidepressant-like effects of aniracetam in aged rats and its mode of action. Psychopharmacology (Berl). (2001)
  26. ^ a b O'Neill MJ, Witkin JM. AMPA receptor potentiators: application for depression and Parkinson's disease. Curr Drug Targets. (2007)
  27. ^ Ito I, et al. Allosteric potentiation of quisqualate receptors by a nootropic drug aniracetam. J Physiol. (1990)
  28. ^ Shih YH, Pugsley TA. The effects of various cognition-enhancing drugs on in vitro rat hippocampal synaptosomal sodium dependent high affinity choline uptake. Life Sci. (1985)
  29. ^ Ouchi Y, et al. The effect of aniracetam on cerebral glucose metabolism in rats after lesioning of the basal forebrain measured by PET. J Neurol Sci. (1999)
  30. ^ Shirane M, Nakamura K. Aniracetam enhances cortical dopamine and serotonin release via cholinergic and glutamatergic mechanisms in SHRSP. Brain Res. (2001)
  31. ^ Knapp RJ, et al. Antidepressant activity of memory-enhancing drugs in the reduction of submissive behavior model. Eur J Pharmacol. (2002)
  32. ^ Lauterborn JC, et al. Positive modulation of AMPA receptors increases neurotrophin expression by hippocampal and cortical neurons. J Neurosci. (2000)
  33. ^ Lauterborn JC, et al. Chronic elevation of brain-derived neurotrophic factor by ampakines. J Pharmacol Exp Ther. (2003)
  34. ^ Simmons DA, et al. Up-regulating BDNF with an ampakine rescues synaptic plasticity and memory in Huntington's disease knockin mice. Proc Natl Acad Sci U S A. (2009)
  35. ^ Lauterborn JC, et al. Ampakines cause sustained increases in brain-derived neurotrophic factor signaling at excitatory synapses without changes in AMPA receptor subunit expression. Neuroscience. (2009)
  36. ^ Brain-derived neurotrophic factor mechanisms and function in adult synaptic plasticity: new insights and implications for therapy.
  37. ^ Kramár EA, et al. A novel mechanism for the facilitation of theta-induced long-term potentiation by brain-derived neurotrophic factor. J Neurosci. (2004)
  38. ^ O'Neill MJ, et al. AMPA receptor potentiators for the treatment of CNS disorders. Curr Drug Targets CNS Neurol Disord. (2004)
  39. ^ Vaglenova J, et al. Aniracetam reversed learning and memory deficits following prenatal ethanol exposure by modulating functions of synaptic AMPA receptors. Neuropsychopharmacology. (2008)