Piracetam

2-(2-oxopyrrolidin-1-yl)acetamide

Overview

Piracetam belongs to Nootropics.

Key safety note: Piracetam has an exceptionally favourable safety and tolerability profile: acute toxicity is very low, it is not sedating or respiratory-depressant, and it is not associated with dependence, addictive tolerance or a withdrawal syndrome: a sharp contrast to the sedative-hypnotics.[4][5][6]
Effects
Subjective effects vary. What a substance feels like depends on dose, individual physiology, mindset, and setting. The points below describe commonly reported effects, not guaranteed, uniform, or desirable outcomes.
  • Piracetam produces subtle effects and is generally non-intoxicating: trials and users report modest improvements in aspects of memory, attention and processing, most consistently in people with age-related decline, dementia or post-hypoxic states rather than in healthy young adults, where the evidence is weak and inconsistent.
  • It is neither sedating nor stimulating and does not produce euphoria. There is no recognised recreational 'high'. When unwanted psychological effects occur they are usually over-activation, nervousness, agitation, irritability, anxiety or insomnia, rather than intoxication.
  • Any subjective effect has a slow, mild onset. Because piracetam is low-potency, very large single doses mainly add side effects rather than proportionally greater benefit.
Dosing & duration
Harm-reduction note: These are commonly cited reference ranges, not a recommendation or a “safe” dose. Potency, purity, body chemistry, tolerance, and drug combinations vary widely. Start low, go slow, wait for full effects before redosing, and never assume an unknown product matches these figures. Missing data is not evidence of safety.

Oral (tablets, capsules or oral solution). Parenteral formulations exist for hospital use. Piracetam is used essentially only orally.. Piracetam is not a recreational drug. It is not meaningfully euphoric and has no accepted 'recreational' dose. The figures below are therapeutic/clinical reference ranges from the medical literature, not a recommendation. Clinical doses are high (grams, not milligrams) because piracetam is low-potency, and are divided across the day. Doses must be reduced in renal impairment, because piracetam is cleared unchanged by the kidneys.

Dose ranges

Nootropic (off-label)

1.2–2.4 g/day

Cognitive / geriatric (typical clinical)

2.4–4.8 g/day, divided

Cortical myoclonus (high)

7.2–24 g/day

Duration

onset

≈30–60 minutes (oral)

total

Plasma half-life ≈4–5 h, clinical benefit is assessed over days to weeks, not per dose

after effects

No recognised comedown or withdrawal syndrome. Not associated with dependence

Chemical & Physical Properties
FormulaC6H10N2O2
Molar mass142.16 g/mol
StateSolid (crystalline)
Melting point151.5–152.5 °C
Boiling pointDecomposes
DensityNot reported
Vapor pressureNot reported
pKaNot reported
LogP-1.54 (log Kow, experimental)
SolubilityNot reported
Refractive indexNot reported
Identifiers & Synonyms
CAS7491-74-9
CAS (enantiomer)
PubChem CID4843
InChIKeyGMZVRMREEHBGGF-UHFFFAOYSA-N
InChIInChI=1S/C6H10N2O2/c7-5(9)4-8-3-1-2-6(8)10/h1-4H2,(H2,7,9)
SMILESC1CC(=O)N(C1)CC(=O)N

Synonyms

  • Nootropil
Pharmacodynamics & Biochemistry

Piracetam is the prototypical 'racetam' nootropic, a cyclic derivative of the neurotransmitter GABA, but it has essentially no direct GABAergic, sedative or stimulant activity and is not appreciably intoxicating. Its cellular mechanism is still only partly understood and is generally described as modulatory rather than acting through a single high-affinity receptor. The best-characterised molecular action is positive allosteric modulation of AMPA-type ionotropic glutamate receptors: the IUPHAR/BPS Guide to PHARMACOLOGY lists piracetam as a positive allosteric modulator at all four human AMPA-receptor subunits (GluA1–GluA4). By slowing receptor desensitisation it is thought to enhance AMPA-mediated excitatory (glutamatergic) neurotransmission: the 'ampakine'-like action it shares with aniracetam. This modulation is weak and no quantitative affinity or potency values are reported, so no binding table is shown below. Piracetam also has membrane-level effects: it interacts with the polar head groups of membrane phospholipids and is proposed to restore membrane fluidity, which may improve neuronal signalling, mitochondrial function and the mobility of receptors and neurotransmitters: an effect invoked to explain its broad, non-specific actions in ageing and hypoxic tissue. A separate, clinically important action is haemorheological: piracetam reduces platelet aggregation and red-blood-cell adhesion to vascular endothelium and improves erythrocyte deformability and microcirculation. This antithrombotic/rheological effect underlies its use in cortical myoclonus and vascular indications, and is also the reason for its bleeding-related cautions.

Biological targets

  • AMPA
Pharmacokinetics
BioavailabilityOral ≈100% (rapid, complete absorption), not bound to plasma proteins
Tmax≈0.5–1 h (fasting)
Half-life≈4–5 h (plasma), ≈8.5 h in CSF
VdNot reported
Protein bindingNot reported
MetabolismNot metabolised (no known metabolites)
ExcretionRenal, excreted unchanged (~80–100% recovered in urine). Crosses the blood–brain barrier and placenta
Toxicology & Safety
Harm-reduction note: Toxicity and risk depend on dose, route, purity, combinations, setting, and individual health factors. Missing harms should never be interpreted as evidence of safety.

Not reported

Piracetam has an exceptionally favourable safety and tolerability profile: acute toxicity is very low, it is not sedating or respiratory-depressant, and it is not associated with dependence, addictive tolerance or a withdrawal syndrome: a sharp contrast to the sedative-hypnotics. Adverse effects are uncommon and are usually mild over-stimulation: nervousness, agitation, irritability, anxiety, insomnia, and occasionally headache, weight gain, somnolence or gastrointestinal upset. Its main practical cautions come from its antiplatelet action (bleeding risk: cerebral haemorrhage, surgery, anticoagulant co-use) and its renal clearance (dose reduction in renal impairment). Note that in the United States piracetam is neither an approved drug nor a lawful dietary-supplement ingredient, yet it is sold in unregulated 'nootropic' products of uncertain dose and purity.[4][5][6]

Legal Status
Legal note: Legal status can change over time and may vary by country, region, formulation, analogue status, prescription context, and enforcement practice. Always confirm with current official sources before relying on this section.
Interactions & Contraindications

Drug interactions

Anticoagulant and antiplatelet drugs (warfarin, aspirin) Piracetam has its own antiplatelet/antithrombotic action, and high doses (~9.6 g/day) have been reported to potentiate anticoagulation (reduced platelet aggregation, fibrinogen and blood viscosity): an additive bleeding risk.[4]

Contraindications

Bleeding disorder, active haemorrhage or antithrombotic therapy cerebral haemorrhage (contraindicated), bleeding disorders, before surgery, or with antithrombotic therapy, given its antiplatelet action.[4]
Kidney or liver impairment severe renal impairment or end-stage renal disease (contraindicated or dose-reduced, as it is renally cleared unchanged).[4][5]
Huntington's disease or chorea may worsen, generally avoided.[4]
Known hypersensitivity to the drug hypersensitivity to piracetam or other pyrrolidone derivatives.[4]
Usage & Context
  • The prototypical racetam nootropic and a licensed medicine across much of Europe (Nootropil and others), used for age-related cognitive decline, dementia, vertigo and, at high doses, cortical myoclonus. The evidence of benefit is strongest in older people and in post-hypoxic or vascular states.
  • One of the most widely used 'smart drugs' sold online for off-label cognitive enhancement, despite weak and inconsistent evidence in healthy people. In the United States it is sold in unapproved supplements rather than as a medicine.
Sources & Evidence

Further Information