Piracetam is a small synthetic molecule, a cyclic derivative of the neurotransmitter GABA, developed by the Belgian drug company UCB and best known as Nootropil. It is the parent of the “racetams,” a family of piracetam-like drugs that share its 2-oxopyrrolidine ring, and it is sold online as a “smart drug” for memory and focus.

Its medical standing is narrow. In the UK, the current Nootropil label covers only one use: add-on treatment of cortical myoclonus (involuntary muscle jerks that start in the brain’s cortex), at doses of 7.2–24 g a day. In the US it has no FDA-approved use, and FDA has taken the position that it may not be sold as a dietary supplement. Evidence that it improves memory, in people with dementia or in healthy adults, is weak.

This page summarizes what the UK label, Cochrane reviews and clinical trials report. It is for education only and is not medical advice.

Property	Detail
Drug class	Nootropic (ATC N06BX03); pyrrolidone derivative of GABA
Brand	Nootropil 800 mg and 1200 mg film-coated tablets (UK)
UK licensed use	Cortical myoclonus in adults, added to other anti-myoclonic drugs
Labeled dose (UK)	Start 7.2 g/day, raised by 4.8 g every 3–4 days to a maximum of 24 g/day, in 2–3 doses
Half-life	5.0 h in young adult men (UK SmPC)
Elimination	Kidneys; about 90% excreted unchanged in urine, no known metabolites
Key safety point	Reduces platelet aggregation and prolongs bleeding time
US status	No FDA-approved use; FDA has said it is not permitted as a dietary supplement
WADA status	Not named on the 2026 Prohibited List (its relative phenylpiracetam is)

What it is

Piracetam’s chemical name is 2-(2-oxopyrrolidin-1-yl)acetamide: formula C₆H₁₀N₂O₂, molecular weight 142.16 g/mol (PubChem). It is a five-membered lactam ring (2-pyrrolidinone) with an acetamide side chain, and it is described as a cyclic derivative of GABA (Winblad, CNS Drug Rev 2005).

Early research papers used the UCB code UCB 6215 and the name Nootropyl (Dimond et al., Psychopharmacology 1979). The pharmacologist Corneliu Giurgea set out the “nootropic” concept, a class of drugs meant to act on the brain’s integrative functions such as learning and memory, in 1972 (Giurgea, Actual Pharmacol 1972).

Piracetam-like drugs fall into three groups (Malykh & Sadaie, Drugs 2010):

Group	Examples	Notes
Classic nootropic racetams	Piracetam, oxiracetam, aniracetam, pramiracetam, phenylpiracetam	Used in humans; some sold as dietary supplements
Antiepileptic racetams	Levetiracetam, brivaracetam, seletracetam	Act by binding synaptic vesicle protein 2A (SV2A)
Other derivatives	Nefiracetam and others	Unknown clinical efficacy; mostly preclinical

Levetiracetam is structurally close to piracetam but has a different pharmacology and clinical use (Genton & Van Vleymen, Epileptic Disord 2000). Phenylpiracetam, piracetam with an added phenyl ring, has its own page at Phenylpiracetam. Citicoline, a different kind of compound marketed for cognition, is covered at Citicoline.

Mechanism: still unknown

The UK label states plainly that piracetam’s mode of action in cortical myoclonus “is as yet unknown” (Nootropil SmPC). A 2010 review called the modes of action of piracetam and most of its derivatives “an enigma” (Malykh & Sadaie, Drugs 2010). Several hypotheses have been proposed, none established as the cause of a clinical effect:

Proposed mechanism	Evidence behind it
Restoring cell membrane fluidity	Interaction with phospholipid head groups, stronger in membranes from aged animal and human brains (laboratory work) (Müller et al., Pharmacopsychiatry 1999)
Positive modulation of AMPA glutamate receptors	Crystal structures of the receptor’s binding domain show piracetam at several sites on the dimer interface, with low occupancy (Ahmed & Oswald, J Med Chem 2010)
Effects on blood cells and vessels	Less platelet aggregation, more deformable red cells, lower fibrinogen and von Willebrand factor in human pharmacodynamic studies (Nootropil SmPC)

Unlike levetiracetam, piracetam does not bind with high affinity to levetiracetam’s brain-specific binding site (Genton & Van Vleymen, Epileptic Disord 2000).

Pharmacokinetics

From section 5.2 of the UK SmPC (Nootropil SmPC):

Parameter	Value
Oral bioavailability	Close to 100% (capsules, tablets and solution)
Time to peak plasma level	Within 1.5 h
Dose proportionality	Peak level and AUC proportional to dose
Volume of distribution	0.7 L/kg
Metabolism	No metabolite has been found
Plasma half-life	5.0 h in young adult men
Excretion	Almost completely in urine; about 90% of a dose as unchanged drug
Dialysis	Dialyzer extraction 50–60%

Piracetam crosses the blood-brain barrier and the placenta; levels in newborns are about 70–90% of maternal levels. It also passes into breast milk.

Because the kidneys clear it, clearance falls as kidney function falls. The label cuts the dose by creatinine clearance (CLcr, an estimate of kidney filtering capacity):

Kidney function	CLcr (mL/min)	UK labeled adjustment
Normal	Over 80	Usual daily dose in 2–3 doses
Mild impairment	50–79	Two-thirds of the usual dose
Moderate impairment	30–49	One-third of the usual dose, in 2 doses
Severe impairment	Under 30	One-sixth of the usual dose, once daily
End-stage renal disease	—	Contraindicated

One bioavailability study in 16 healthy men recovered only about two-thirds of a 1,600 mg dose in the urine over 24 hours. The authors argued that a non-renal elimination route may exist (Rameis et al., Int J Clin Pharmacol Ther 1994). The label still treats piracetam as a renally eliminated drug.

Regulatory status

United Kingdom and Europe

The UK SmPC for Nootropil 800 mg and 1200 mg tablets (text revised July 2025) has a single indication: adults with myoclonus of cortical origin, whatever the cause, used together with other anti-myoclonic drugs (Nootropil SmPC). Key labeled points:

Dose: start at 7.2 g/day and increase by 4.8 g every 3–4 days, up to 24 g/day in 2–3 divided doses.
Duration: continue while the underlying brain disease persists; in acute cases, try to reduce or stop every 6 months.
Stopping: taper by 1.2 g every 2 days (every 3–4 days in Lance-Adams syndrome, a post-hypoxic myoclonus), because abrupt withdrawal may trigger myoclonic or generalized seizures.

Indications differ by country. In many European countries piracetam has been prescribed for cognitive impairment, dementia and other disorders (Cohen et al., JAMA Intern Med 2020). The UK label does not include any cognitive indication.

United States

Piracetam has no FDA-approved use; the only drug in its class approved by FDA is levetiracetam (Cohen et al., JAMA Intern Med 2020). According to the same report:

FDA rejected a 2004 new dietary ingredient notification for piracetam (NDI 215);
FDA has determined that piracetam may not be sold as a dietary supplement, and has issued warning letters;
enforcement has been limited, and products labeled as dietary supplements remained on sale.

The investigators bought 5 brands of “dietary supplement” piracetam in 2018 and found it in 4 of them. Measured amounts were 85–118% of the labeled amount, 831–1,542 mg per serving. Following the label directions, a buyer could take up to 11,283 mg a day.

What the research shows

Cortical myoclonus (the licensed use)

The evidence for myoclonus comes from small crossover trials, mostly in patients already taking other anti-myoclonic drugs:

Trial	Design and n	Doses	Main result
Brown et al., Mov Disord 1993	Double-blind crossover, 21 patients with cortical myoclonus who had already responded	2.4–16.8 g/day, 14 days each	Total rating score improved by a median of 22%; 10 of 21 patients had to be rescued from the placebo phase because myoclonus worsened, none from the piracetam phase
Koskiniemi et al., J Neurol Neurosurg Psychiatry 1998	Randomized double-blind crossover, 20 patients with Unverricht-Lundborg disease (a progressive myoclonus epilepsy)	9.6, 16.8 or 24 g/day vs placebo, 2 weeks each	24 g/day improved the primary sum score (p = 0.005); functional disability also improved at 9.6 and 16.8 g; linear dose-effect relation

Both trials were small and short, and the Brown trial enrolled only patients who had already appeared to respond to piracetam.

Dementia and cognitive impairment

This is the use piracetam is best known for, and the evidence is weak:

Cochrane review. It pooled placebo-controlled randomized trials in dementia or cognitive impairment, including unpublished UCB studies (Flicker & Grimley Evans, Cochrane 2001). Many trials were crossovers whose first-phase data could not be extracted. The only outcome with enough pooled data was the clinician’s global impression of change:

Analysis of global impression of change	Odds ratio for improvement (95% CI)
Fixed-effects model	3.55 (2.45–5.16)
Random-effects model	3.47 (1.29–9.30)
Random effects, excluding one single-blind study	2.89 (1.01–8.24)

The results were heterogeneous, and effects on cognition and other specific measures were inconclusive. The reviewers concluded that the published evidence does not support using piracetam for dementia or cognitive impairment.

Manufacturer meta-analysis. A meta-analysis of 19 double-blind, placebo-controlled trials, led by UCB researchers, reported a significant benefit on global impression of change (Waegemans et al., Dement Geriatr Cogn Disord 2002). It also relied on a global rating rather than specific cognitive tests.
2024 meta-analysis on memory. Eighteen studies with 886 patients with memory impairment found no significant effect on memory: standardized mean difference 0.75 (95% CI −0.19 to 1.69; p = 0.12), with very high heterogeneity (I² = 96%) (Gouhie et al., Clin Neurol Neurosurg 2024).

Healthy adults

There are very few controlled studies of piracetam in people without cognitive problems, and they are old and small:

A double-blind study in normal volunteers gave 4.8 g/day (12 capsules of 400 mg). No effect was seen at 7 days; verbal learning was higher at 14 days (Dimond & Brouwers, Psychopharmacology 1976).
In 26 healthy volunteers whose memory was temporarily impaired with scopolamine, only aniracetam 1,500 mg clearly reversed the deficits. The other treatments, including a single 2,400 mg oral dose of piracetam, produced about as many significant results as chance would predict, and the authors called them questionable (Wesnes et al., J Psychopharmacol 1990).

A 2022 review of “smart drugs” in healthy people, which included piracetam, concluded that their efficacy in healthy individuals is uncertain and any reported improvement temporary (Schifano et al., Drugs 2022).

Other uses tested

Use	Evidence	Conclusion
Acute ischemic stroke	Cochrane review, 3 trials, 1,002 patients (Ricci et al., Cochrane 2012)	Non-significant trend toward more deaths at 1 month (about 31% increase; 95% CI from a 5% reduction to an 81% increase), possibly explained by baseline stroke severity; no difference in function
Sickle cell pain crises	Cochrane review, 3 trials, 169 participants (Al Hajeri & Fedorowicz, Cochrane 2016)	Too few, poor-quality trials to support routine use

Side effects and risks

Bleeding and antiplatelet effects

Piracetam acts on platelets and clotting factors, which matters most for people at risk of bleeding. The UK SmPC reports that (Nootropil SmPC):

in healthy volunteers and people with Raynaud’s phenomenon, doses up to 12 g caused a dose-dependent reduction in platelet function and prolonged bleeding time, without changing the platelet count;
in healthy volunteers, up to 9.6 g lowered fibrinogen and von Willebrand factor by 30–40% and increased bleeding time; 8 g/day for 6 months did the same in Raynaud’s patients;
“haemorrhagic disorder” is listed as a post-marketing adverse reaction of unknown frequency.

A small pharmacodynamic study in 5 healthy subjects found antiplatelet and blood-flow effects after single doses of 4.8 g and 9.6 g. The effects peaked 1–4 hours after the dose and faded by 8–12 hours (Moriau et al., Arzneimittelforschung 1993).

The label therefore advises caution in people with:

severe bleeding, or a risk of bleeding such as a gastrointestinal ulcer;
underlying clotting disorders;
a history of hemorrhagic stroke;
major surgery, including dental surgery;
treatment with anticoagulants or antiplatelet drugs, including low-dose aspirin.

In a study of patients with recurrent venous thrombosis, adding 9.6 g/day piracetam to acenocoumarol (a warfarin-like anticoagulant) did not change the anticoagulant dose needed, but it further reduced platelet aggregation, fibrinogen and von Willebrand factor.

Contraindications

Per the UK SmPC, piracetam must not be used in people with:

hypersensitivity to piracetam or other pyrrolidone derivatives;
severe renal impairment (creatinine clearance under 20 mL/min) or end-stage renal disease;
cerebral hemorrhage;
Huntington’s chorea.

Common side effects

The UK label draws on placebo-controlled trials with more than 3,000 people taking piracetam:

Frequency	Adverse reactions
Common (1–10%)	Nervousness, hyperkinesia (excess movement), weight gain
Uncommon (0.1–1%)	Depression, somnolence, asthenia (weakness)
Frequency not known (post-marketing)	Bleeding disorder, allergic reactions including angioedema, agitation, anxiety, confusion, hallucinations, ataxia, balance problems, worsening epilepsy, headache, insomnia, vertigo, nausea, vomiting, diarrhea, abdominal pain, dermatitis, itching and hives

At 1.6–15 g/day in clinical studies, hyperkinesia, somnolence, nervousness and depression were more frequent than with placebo, and the label advises caution with driving.

Interactions

Drug metabolism: interactions through liver enzymes are unlikely, since about 90% is excreted unchanged and piracetam did not meaningfully inhibit major CYP450 enzymes in vitro.
Thyroid hormones: confusion, irritability and sleep disturbance have been reported with thyroid extract (T3 + T4).
Antiepileptic drugs: 20 g/day for 4 weeks did not change blood levels of carbamazepine, phenytoin, phenobarbital or valproate.
Anticoagulants and antiplatelets: see the bleeding section above.

Pregnancy, breastfeeding and older adults

There are no adequate human pregnancy data, and piracetam reaches the fetus at 70–90% of maternal levels; the label says not to use it in pregnancy unless clearly necessary. It is excreted in breast milk, so the label advises against use while breastfeeding. In older adults on long-term treatment, the label calls for regular checks of creatinine clearance.

Unregulated supplements

Products sold online as supplements are not made under drug-quality controls. The doses in the products tested by Cohen and colleagues reached over 11 g a day if taken as labeled. Their risks at these doses, especially in older people with reduced kidney function, are unknown (Cohen et al., JAMA Intern Med 2020).

Sports

Piracetam is not named on the WADA 2026 Prohibited List. Its derivative phenylpiracetam (fonturacetam, also called carphedon) is named as a non-specified stimulant, prohibited in competition (S6.A). The list’s S0 catch-all covers only substances with no current approval by any health authority, and piracetam holds a current UK marketing authorization.

Key takeaways

The original racetam. Piracetam is a cyclic GABA derivative developed by UCB and the parent of the piracetam-like drugs, from aniracetam to levetiracetam. How it works is still unknown.
Licensed for myoclonus, not memory, in the UK. The current UK label covers only add-on treatment of cortical myoclonus, at high doses of 7.2–24 g/day.
Not approved in the US. Piracetam has no FDA-approved use, and FDA has said it may not be sold as a dietary supplement, though such products have stayed on sale.
Weak cognitive evidence. A Cochrane review found benefit only on global impressions, not on specific cognitive measures, and did not support its use in dementia; data in healthy adults are sparse and old.
Short half-life, cleared by the kidneys. The half-life is about 5 hours, and doses must be cut in kidney impairment.
Bleeding risk. Piracetam reduces platelet aggregation and prolongs bleeding time, so the label urges caution with anticoagulants, antiplatelet drugs (including low-dose aspirin) and surgery.

Sources

Mercury Pharmaceuticals (ADVANZ Pharma). Nootropil 800 mg film-coated tablets: Summary of Product Characteristics. Text revised July 2025. emc.
National Center for Biotechnology Information. PubChem Compound Summary for CID 4843, Piracetam. PubChem.
Winblad B. Piracetam: a review of pharmacological properties and clinical uses. CNS Drug Rev. 2005;11(2):169–182. PubMed.
Giurgea C. Pharmacology of integrative activity of the brain. Attempt at nootropic concept in psychopharmacology [in French]. Actual Pharmacol (Paris). 1972;25:115–156. PubMed.
Dimond SJ, Scammell RE, Pryce IG, et al. Some effects of piracetam (UCB 6215, Nootropyl) on chronic schizophrenia. Psychopharmacology (Berl). 1979;64(3):341–348. PubMed.
Malykh AG, Sadaie MR. Piracetam and piracetam-like drugs: from basic science to novel clinical applications to CNS disorders. Drugs. 2010;70(3):287–312. PubMed.
Genton P, Van Vleymen B. Piracetam and levetiracetam: close structural similarities but different pharmacological and clinical profiles. Epileptic Disord. 2000;2(2):99–105. PubMed.
Müller WE, Eckert GP, Eckert A. Piracetam: novelty in a unique mode of action. Pharmacopsychiatry. 1999;32(Suppl 1):2–9. PubMed.
Ahmed AH, Oswald RE. Piracetam defines a new binding site for allosteric modulators of alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) receptors. J Med Chem. 2010;53(5):2197–2203. PubMed.
Rameis H, Hitzenberger G, Kutscher R, et al. Pharmacokinetics of piracetam: a study on the bioavailability with special regard to renal and non-renal elimination. Int J Clin Pharmacol Ther. 1994;32(9):458–465. PubMed.
Cohen PA, Zakharevich I, Gerona R. Presence of piracetam in cognitive enhancement dietary supplements. JAMA Intern Med. 2020;180(3):458–459. PubMed; PMC.
Brown P, Steiger MJ, Thompson PD, et al. Effectiveness of piracetam in cortical myoclonus. Mov Disord. 1993;8(1):63–68. PubMed.
Koskiniemi M, Van Vleymen B, Hakamies L, et al. Piracetam relieves symptoms in progressive myoclonus epilepsy: a multicentre, randomised, double blind, crossover study comparing the efficacy and safety of three dosages of oral piracetam with placebo. J Neurol Neurosurg Psychiatry. 1998;64(3):344–348. PubMed.
Flicker L, Grimley Evans J. Piracetam for dementia or cognitive impairment. Cochrane Database Syst Rev. 2001;(2):CD001011. PubMed.
Waegemans T, Wilsher CR, Danniau A, et al. Clinical efficacy of piracetam in cognitive impairment: a meta-analysis. Dement Geriatr Cogn Disord. 2002;13(4):217–224. PubMed.
Gouhie FA, Barbosa KO, Cruz ABR, et al. Cognitive effects of piracetam in adults with memory impairment: a systematic review and meta-analysis. Clin Neurol Neurosurg. 2024;243:108358. PubMed.
Dimond SJ, Brouwers EM. Increase in the power of human memory in normal man through the use of drugs. Psychopharmacology (Berl). 1976;49(3):307–309. PubMed.
Wesnes K, Anand R, Simpson P, et al. 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.
Schifano F, Catalani V, Sharif S, et al. Benefits and harms of ‘smart drugs’ (nootropics) in healthy individuals. Drugs. 2022;82(6):633–647. PubMed.
Ricci S, Celani MG, Cantisani TA, et al. Piracetam for acute ischaemic stroke. Cochrane Database Syst Rev. 2012;(9):CD000419. PubMed.
Al Hajeri A, Fedorowicz Z. Piracetam for reducing the incidence of painful sickle cell disease crises. Cochrane Database Syst Rev. 2016;(2):CD006111. PubMed.
Moriau M, Crasborn L, Lavenne-Pardonge E, et al. Platelet anti-aggregant and rheological properties of piracetam. A pharmacodynamic study in normal subjects. Arzneimittelforschung. 1993;43(2):110–118. PubMed.
World Anti-Doping Agency. The 2026 Prohibited List. In effect from January 1, 2026. WADA.

Piracetam