Supplements

Aniracetam

Updated · 19 sources

Aniracetam is a synthetic “racetam” nootropic, a poorly water-soluble relative of piracetam known in early research as Ro 13-5057, that boosts signaling through AMPA-type glutamate receptors in laboratory studies. It has been approved to treat dementia in some countries, including Italy, Argentina and China, but it is not approved in the US, where it is sold online in “cognitive enhancement” supplements.

The most important facts are these. When swallowed, aniracetam is broken down so quickly that only about 0.2% of an oral dose is reported to reach the bloodstream unchanged, so its metabolites may account for much of any effect. The dementia trials are small and old, with mixed results: a 6-month, 109-patient trial was positive, while a 3-month, 44-patient trial found no difference from placebo. In healthy adults, evidence is limited to a single scopolamine-challenge study. The FDA has sent warning letters to companies selling aniracetam supplements, and lab testing has found products with undeclared aniracetam and inaccurate labels.

This page summarizes what the clinical trials, pharmacology studies and regulators report. It is for education only and is not medical advice.

Property Detail
Class Racetam (pyrrolidinone) nootropic; positive allosteric modulator of AMPA receptors
Chemical name 1-(4-methoxybenzoyl)pyrrolidin-2-one; C₁₂H₁₃NO₃, 219.24 g/mol
Research code Ro 13-5057
Route Oral
Doses in trials 1,000–1,500 mg/day in dementia trials; single 1,500 mg dose in healthy volunteers
Oral bioavailability About 0.2% as unchanged drug (extensive first-pass metabolism)
Main metabolites N-anisoyl-GABA (4-p-anisamidobutyric acid), p-anisic acid, 2-pyrrolidinone
Approved use Dementia in several countries, including Italy, Argentina and China
US status Not FDA-approved; FDA has issued warning letters to companies selling it in supplements
WADA status Not named on the 2026 Prohibited List

What it is

Aniracetam (1-p-anisoyl-2-pyrrolidinone) shares the 2-oxopyrrolidine ring that defines the racetams, the family that began with piracetam (PubChem; Ito et al., J Physiol 1990). Aniracetam carries a methoxybenzoyl (anisoyl) group and is poorly soluble in water: about 0.14–0.15 mg/mL (Goldsmith and McDowell, Pharmaceutics 2018).

It was studied in the 1980s and early 1990s for “senile cognitive disorders,” mainly mild to moderate Alzheimer-type dementia and cognitive impairment of vascular origin (Lee and Benfield, Drugs Aging 1994). A 2002 review described it as clinically used for behavioral and psychological symptoms of dementia after stroke and in Alzheimer’s disease (Nakamura, CNS Drug Rev 2002).

Other racetams and cognitive compounds in this library include phenylpiracetam, Noopept, citicoline and alpha-GPC.

Mechanism: AMPA receptor modulation

Aniracetam was one of the first drugs shown to boost AMPA receptors, glutamate receptors that carry fast excitatory signals between neurons:

  • Selective potentiation. In frog eggs expressing rat brain receptors and in rat hippocampal slices, aniracetam reversibly potentiated responses at quisqualate/AMPA receptors, but not at kainate, NMDA or GABA receptors. The effect appeared only at concentrations above about 0.1 mM (Ito et al., J Physiol 1990).
  • Slower desensitization. In hippocampal slices, aniracetam strongly reduced glutamate receptor desensitization (the rapid shut-off of the receptor during continued glutamate exposure) and prolonged fast excitatory synaptic currents (Isaacson and Nicoll, PNAS 1991).

A 1994 review added that it may also modulate metabotropic glutamate receptors and facilitate cholinergic transmission (Lee and Benfield 1994). Its main metabolites also affected learning and memory in animal studies, which suggests they contribute to its effects (Nakamura 2002).

The concentrations needed in the laboratory (around 0.1 mM and above) are a problem given how little intact aniracetam reaches the blood after an oral dose, discussed next.

Pharmacokinetics

Aniracetam is cleared before it can circulate in meaningful amounts:

Finding Source
Low oral bioavailability of 0.2% in humans; extensive first-pass metabolism in the liver and hydrolysis in the gut Goldsmith and McDowell 2018, citing a 1993 human pharmacokinetic study
In rats, bioavailability of the parent drug was 11.4% and 8.6% after 50 and 100 mg/kg oral doses; it was largely converted to 4-p-anisamidobutyric acid (N-anisoyl-GABA), p-anisic acid and 2-pyrrolidinone, with 2-pyrrolidinone persisting longest Ogiso et al., J Pharm Sci 1998
In 6 hospitalized women (mean age 84.5) with cerebrovascular disease given 200 mg, the metabolites anisic acid and p-methoxyhippuric acid peaked at 2 h and returned to baseline by 6 h; metabolite half-lives were 4–7 times longer than in young volunteers, and no side effects were observed Endo et al., Behav Brain Res 1997

Goldsmith and McDowell wrote that because systemic aniracetam concentrations are difficult to detect, “large gaps in the pharmacology of aniracetam exist” (Goldsmith and McDowell 2018). Their cyclodextrin formulation was designed for intravenous research use, not for consumers.

The practical points are that the parent drug disappears quickly, older adults with reduced kidney function clear the metabolites much more slowly, and the amounts of unchanged aniracetam reaching the brain in people are not well characterized.

Regulatory status

  • Approved abroad. Aniracetam is “approved for use to treat dementia in several countries including Italy, Argentina, and China” (Cohen et al., Neurol Clin Pract 2021). In the 2025 European and Australian surveillance study, it was classified as a prescription medicine in the participating EU countries and Australia, with a therapeutic range of 200–750 mg/day (Vanhee et al., J Xenobiot 2025).
  • United States. Aniracetam is not approved for human use in the US (Cohen et al. 2021), and a Drugs@FDA search returned no aniracetam product (openFDA, accessed November 2026). According to Cohen and colleagues, “The FDA has issued a series of warning letters to companies selling picamilon, phenibut, omberacetam, and aniracetam” supplements, but FDA had not issued a consumer warning about aniracetam in supplements or required recalls, and these drugs remained listed as ingredients in supplement databases.
  • Controlled substances. Aniracetam is not listed in the DEA schedules (21 CFR 1308).

What the research shows

Dementia and cognitive impairment

Study Design, participants Dose, duration Result
Sourander et al., Psychopharmacology 1987 Double-blind RCT; 44 patients with Alzheimer-type dementia 1 g/day for 3 months Several cognitive tests improved, but also in the placebo group; no difference in clinical efficacy. Confusion led to stopping treatment in 4 patients on aniracetam vs 1 on placebo
Senin et al., Eur Neuropsychopharmacol 1991 Double-blind multicenter RCT; 109 patients with mild to moderate probable Alzheimer’s disease 6 months Aniracetam group differed significantly from placebo by the end, improving from baseline while the placebo group steadily declined; tolerability described as excellent
Koliaki et al., CNS Neurosci Ther 2012 Open-label, not randomized by computer; 276 patients with cognitive disorders in four groups 1,500 mg/day; up to 12 months Aniracetam patients maintained test scores at 6 and 12 months; in mild dementia (MMSE 15–25), better cognition than cholinesterase inhibitors at 6 months. The authors stated that “no safe conclusions can be drawn”

A 1994 review summarized the trial program as showing that 1,500 mg/day was more effective than placebo on all tests at 4 and 6 months in one trial, and more effective than piracetam 2,400 mg/day on 8 of 18 tests in a 6-month comparison. The reviewers concluded that further trials were needed to confirm efficacy (Lee and Benfield 1994).

Important limits:

  • The randomized trials are small (44 and 109 patients), date from 1987–1991, and used diagnostic criteria and outcome scales that predate modern dementia trials.
  • The two placebo-controlled trials point in opposite directions.
  • The largest study, Koliaki 2012, was open label with an untreated comparison group made up of patients who had chosen not to take medication, and the aniracetam group had better baseline scores (Koliaki et al. 2012).
  • No large modern trial or systematic review was found.

Healthy adults

The main human study in healthy people used scopolamine, a drug that blocks acetylcholine and temporarily impairs memory. Twenty-six volunteers received scopolamine on seven occasions, followed by various doses of aniracetam or piracetam in a double-blind crossover design (Wesnes et al., J Psychopharmacol 1990):

  • Aniracetam 1,500 mg by mouth significantly reversed the scopolamine-induced deficits in memory and information processing.
  • Intravenous aniracetam (2, 100 and 200 mg) and oral piracetam 2,400 mg produced only about as many significant results as chance would predict.

This shows an effect in an artificially impaired state, not an improvement over normal function. In mice without cognitive impairment, two studies found that oral aniracetam did not change learning, memory, anxiety or repetitive behavior (Elston et al., PLoS One 2014; Reynolds et al., F1000Res 2017). The first of these noted the “growing community of individuals who self-administer” aniracetam for its purported effects.

Other uses

A 2002 review listed many animal models in which aniracetam had effects, including models of attention, anxiety, depression and sleep disturbance, but stated that “there is no convincing evidence that promising effects of aniracetam in the animal models will guarantee its clinical efficacy” (Nakamura 2002).

Side effects and risks

  • Generally well tolerated in trials. Reviews and trials describe good tolerability, with no apparent rise in liver enzymes (Lee and Benfield 1994; Senin et al. 1991). Incidence rates of adverse effects were not available when the main review was written.
  • Confusion. In the 1987 trial, 4 patients on aniracetam vs 1 on placebo stopped because of confusion (Sourander et al. 1987).
  • Anxiety, irritability, insomnia. The 2012 open-label study reported mild, transient anxiety, irritability and insomnia, with no discontinuations for drug-related side effects (Koliaki et al. 2012).
  • Older adults and kidney function. Metabolite half-lives were 4–7 times longer in very old patients with low creatinine clearance (Endo et al. 1997).
  • Interactions, pregnancy, long-term use. No interaction studies, pregnancy data or long-term safety data in healthy people were found in the sources reviewed here.

Unregulated supplements

Products sold as supplements carry risks that do not come from the drug itself:

  • US supplements, 2019. Cohen and colleagues bought 10 cognitive enhancement supplements online in September 2019. They detected five unapproved drugs, including aniracetam, at amounts up to 502 mg per serving. Aniracetam was among the drugs found in products that did not declare it on the label, and 75% (9/12) of declared drug quantities were inaccurate. A single product could expose consumers to as many as four unapproved drugs (Cohen et al., Neurol Clin Pract 2021).
  • Europe and Australia, 2020–2024. Official medicines control laboratories found aniracetam in illicit nootropic samples at 0.2–735 mg per unit, the top value close to the maximum pharmacological dose of 750 mg/day (Vanhee et al. 2025).

Sports

Aniracetam is not named on the WADA 2026 Prohibited List. Its relative fonturacetam (4-phenylpiracetam, phenylpiracetam) is named as a non-specified stimulant prohibited in competition (S6.A) (WADA 2026 Prohibited List). Because cognitive supplements have been found to contain undeclared drugs (Cohen et al. 2021), athletes face a contamination risk.

Key takeaways

  • A racetam that boosts AMPA receptors. In lab studies aniracetam slows AMPA receptor desensitization, but only at concentrations around 0.1 mM and above.
  • Very poor oral bioavailability. About 0.2% of an oral dose is reported to reach the blood unchanged; it is rapidly converted to N-anisoyl-GABA, anisic acid and 2-pyrrolidinone, which may carry much of its activity.
  • Mixed, dated dementia evidence. A 109-patient 1991 trial was positive and a 44-patient 1987 trial was not; the largest later study was open label and inconclusive.
  • Little evidence in healthy people. A single 1,500 mg dose reversed scopolamine-induced memory deficits, and studies in unimpaired mice found no benefit.
  • Approved abroad, not in the US. It is a dementia drug in some countries, but FDA has not approved it and has sent warning letters to supplement sellers.
  • Supplement quality is poor. US and European testing found undeclared aniracetam, doses up to 502–735 mg per unit and inaccurate labels.

Sources

  1. National Center for Biotechnology Information. Aniracetam (CID 2196). PubChem. PubChem.
  2. Cohen PA, Avula B, Wang YH, Zakharevich I, Khan I. Five unapproved drugs found in cognitive enhancement supplements. Neurol Clin Pract. 2021;11(3):e303–e307. PubMed.
  3. Goldsmith SD, McDowell A. Designing a formulation of the nootropic drug aniracetam using 2-hydroxypropyl-β-cyclodextrin suitable for parenteral administration. Pharmaceutics. 2018;10(4):240. PubMed.
  4. Ogiso T, Iwaki M, Tanino T, et al. Pharmacokinetics of aniracetam and its metabolites in rats. J Pharm Sci. 1998;87(5):594–598. PubMed.
  5. Ito I, Tanabe S, Kohda A, Sugiyama H. Allosteric potentiation of quisqualate receptors by a nootropic drug aniracetam. J Physiol. 1990;424:533–543. PubMed.
  6. 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;4(3):257–273. PubMed.
  7. Nakamura K. Aniracetam: its novel therapeutic potential in cerebral dysfunctional disorders based on recent pharmacological discoveries. CNS Drug Rev. 2002;8(1):70–89. PubMed.
  8. 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;88(23):10936–10940. PubMed.
  9. Endo H, Tajima T, Yamada H, et al. Pharmacokinetic study of aniracetam in elderly patients with cerebrovascular disease. Behav Brain Res. 1997;83(1-2):243–244. PubMed.
  10. Vanhee C, Deconinck E, George M, et al. The occurrence of illicit smart drugs or nootropics in Europe and Australia and their associated dangers: results from a market surveillance study by 12 official medicines control laboratories. J Xenobiot. 2025;15(3):88. PubMed.
  11. US Food and Drug Administration. openFDA Drugs@FDA dataset: search for active ingredient aniracetam (no matching records; accessed November 2026). openFDA.
  12. Drug Enforcement Administration. Schedules of controlled substances. 21 CFR part 1308. eCFR.
  13. Sourander LB, Portin R, Mölsä P, Lahdes A, Rinne UK. Senile dementia of the Alzheimer type treated with aniracetam: a new nootropic agent. Psychopharmacology (Berl). 1987;91(1):90–95. PubMed.
  14. Senin U, Abate G, Fieschi C, et al. Aniracetam (Ro 13-5057) in the treatment of senile dementia of Alzheimer type (SDAT): results of a placebo controlled multicentre clinical study. Eur Neuropsychopharmacol. 1991;1(4):511–517. PubMed.
  15. Koliaki CC, Messini C, Tsolaki M. Clinical efficacy of aniracetam, either as monotherapy or combined with cholinesterase inhibitors, in patients with cognitive impairment: a comparative open study. CNS Neurosci Ther. 2012;18(4):302–312. PubMed.
  16. Wesnes K, Anand R, Simpson P, Christmas L. The use of a scopolamine model to study the potential nootropic effects of aniracetam and piracetam in healthy volunteers. J Psychopharmacol. 1990;4(4):219–232. PubMed.
  17. Elston TW, Pandian A, Smith GD, Holley AJ, Gao N, Lugo JN. Aniracetam does not alter cognitive and affective behavior in adult C57BL/6J mice. PLoS One. 2014;9(8):e104443. PubMed.
  18. Reynolds CD, Jefferson TS, Volquardsen M, et al. Oral aniracetam treatment in C57BL/6J mice without pre-existing cognitive dysfunction reveals no changes in learning, memory, anxiety or stereotypy. F1000Res. 2017;6:1452. PubMed.
  19. World Anti-Doping Agency. The 2026 Prohibited List. In force January 1, 2026. WADA.