Piracetam is a nootropic cyclic GABA derivative used in myoclonus, sickle cell disease, alcohol dependence, and as a general cognitive enhancer.

Generic Name
DrugBank Accession Number

Piracetam is a nootropic drug in the racetams group, with chemical name 2-oxo-1-pyrrolidine acetamide. It shares the same 2-oxo-pyrrolidone base structure with pyroglutamic acid and is a cyclic derivative of the neurotransmitter γ-aminobutyric acid (GABA). However its mechanism of action differ from that of endogenous GABA. Piracetam has neuroprotective and anticonvulsant properties and is reported to improve neural plasticity 1. Its efficacy is documented in cognitive disorders and dementia, vertigo, cortical myoclonus, dyslexia, and sickle cell anemia although the clinical application in these conditions is not yet established. Piracetam has effects on the vascular system by reducing erythrocyte adhesion to the vascular endothelium, hindering vasospasms and facilitating microcirculation 1.

Originally marketed by UCB Pharma in 1971, piracetam was the first nootropic drug to modulate cognitive function without causing sedation or stimulation 1. It is not approved for any medical or dietary use by the FDA. In the UK, piracetam is prescribed mainly for myoclonus, but is used off-label for other conditions such as learning difficulties in children, memory loss or other cognitive defects in the elderly, and sickle-cell vaso-occlusive crises 4. Evidence to support its use for many conditions is unclear.

Small Molecule
Approved, Investigational
Average: 142.1558
Monoisotopic: 142.074227574
Chemical Formula
  • Piracetam
  • Piracetamum
External IDs
  • CL-871
  • KT-801
  • UCB 6215



Indicated in adult patients suffering from myoclonus of cortical origin, irrespective of aetiology, and should be used in combination with other anti-myoclonic therapies 5.

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Associated Conditions
Indication TypeIndicationCombined Product DetailsApproval LevelAge GroupPatient CharacteristicsDose Form
Treatment ofAlcohol dependence••••••••••••
Treatment ofAlcohol withdrawl••••••••••••••••••••
Treatment ofCognitive deficits caused by injuries, craniocerebral••••••••••••••••••••
Treatment ofCognitive dysfunctions••••••••••••
Treatment ofCognitive impairments•••••••••••••••••••••••••••
Contraindications & Blackbox Warnings
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Piracetam is known to mediate various pharmacodynamic actions:

Neuronal effects:

Piracetam modulates the cholinergic, serotonergic, noradrenergic, and glutamatergic neurotransmission although the drug does not display high affinity to any of the associated receptors (Ki >10μM). Instead, piracetam increases the density of postsynaptic receptors and/or restore the function of these receptors through stabilizing the membrane fluidity 1. In the forebrain of aging mice, the density of NMDA receptors was increased by approximately 20% following 14 days of piracetam treatment. Based on the findings of various animal and human studies, the cognitive processses including learning, memory, attention and consciousness were enhanced from piracetam therapy without inducing sedation and psychostimulant effects 5. Piracetam mediate neuroprotective effects against hypoxia-induced damage, intoxication, and electroconvulsive therapy 5.

In two studies involving alcohol-treated rats with evidences of withdrawal-related neuronal loss, piracetam was shown to reduce the extent of neuronal loss and increase the numbers of synapses in the hippocampus by up to 20% relative to alcohol-treated or alcohol-withdrawn rats 1. This suggests that piracetam is capable in promoting neuroplasticity when recoverable neural circuits are present 1. Although the mechanism of action is not fully understood, administration of piracetam prior to a convulsant stimulus reduces the seizure severity and enhances the anticonvulsant effectiveness of conventional antiepileptics such as carbamazepine and diazepam 3.

Vascular effects:

Piracetam is shown to increase the deformability of erythrocytes, reduce platelet aggregation in a dose-dependent manner, reduce the adhesion of erythrocytes to vascular endothelium and capillary vasospasm. In healthy volunteers, piracetam mediated a direct stimulant effect on prostacycline synthesis and reduced the plasma levels of fibrinogen and von Willebrand’s factors (VIII: C; VIII R: AG; VIII R: vW) by 30 to 40% 5. Potentiated microcirculation is thought to arise from a combination of effects on erythrocytes, blood vessels and blood coagulation 1.

Mechanism of action

Piracetam interacts with the polar heads in the phospholipids membrane and the resulting mobile drug-lipid complexes are thought to reorganize the lipids and influence membrane function and fluidity 1. Such interaction has been reported in a study that investigated the effects of neuronal outgrowth induced by beta amyloid peptides; while amyloid peptides cause lipid disorganization within the cell membranes leading to neuronal death, piracetam demonstrated to decrease the destabilizing effects of amyloid peptide 2. The authors suggest that piracetam induces a positive curvature of the membrane by occupying the polar groups in the phospholipids to counteract the negative curvature induced by amyloid peptides , which in turn would decrease the likelihood of membrane fusion 1. This mechanism of action is thought to improve membrane stability, allowing the membrane and transmembrane proteins to maintain and recover the three-dimensional structure or folding for normal function 4 such as membrane transport, chemical secretion, and receptor binding and stimulation 1.

Through restored membrane fluidity, piracetam promotes restored neurotransmission such as glutamatergic and cholinergic systems, enhances neuroplasticity and mediates neuroprotective and anticonvulsant effects at the neuronal level 1. It is also demonstrated that piracetam also improves the fluidity of platelet membranes. At the vascular level, piracetam decreases adhesion of erythrocytes to cell wall and reduces vasospasm which in turn improves microcirculation including cerebral and renal blood flow 1.


Piracetam displays a linear and time-dependent pharmacokinetic properties with low intersubject variability over a large range of doses. Piracetam is rapidly and extensively absorbed following oral administration with the peak plasma concentration is reached within 1 hour after dosing in fasted subjects. Following a single oral dose of 3.2 g piracetam, the peak plasma concentration (Cmax) was 84 µg/mL. Intake of food may decrease the Cmax by 17% and increase the time to reach Cmax (Tmax) from 1 to 1.5 hours. Tmax in the cerebrospinal fluid is achieved approximately 5 hours post-administration 4.

The absolute bioavailability of piracetam oral formulations is close to 100% and the steady state plasma concentrations are achieved within 3 days of dosing 4.

Volume of distribution

Vd is approximately 0.6L/kg. Piracetam may cross the blood-brain barrier as it was measured in the cerebrospinal fluid following intravenous administration 4. Piracetam diffuses to all tissues except adipose tissues, crosses placental barrier and penetrates the membranes of isolated red blood cells 4.

Protein binding

Piracetam is not reported to be bound to plasma proteins 4.


As large proportion of total piracetam administered is excreted as unchanged drug, there is no known major metabolism of piracetam 4.

Route of elimination

Piracetam is predominantly excreted via renal elimination, where about 80-100% of the total dose is recovered in the urine. Approximately 90% of the dose of piracetam is excreted in the urine as unchanged drug 4.


The plasma half life of piracetam is approximately 5 hours following oral or intravenous administration. The half life in the cerebrospinal fluid was 8.5 hours 4.


The apparent total body clearance is 80-90 mL/min 4.

Adverse Effects
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The cases of overdose with piracetam is rare. The highest reported overdose with piracetam was oral intake of 75g which was associated with diarrhea and abdominal pain; the signs were most likely related to the extreme high dose of sorbitol contained in the used formulation. In cases of acute, significant overdosage, stomach emptying by gastric lavage or induced emesis is recommended as there are no known antidotes for piracetam 4. Management for an overdose will most likely be symptomatic treatment and may include hemodialysis, where the extraction efficacy of the dialyser is 50 to 60% for the drug 4.

Oral LD50 in a mouse acute toxicity study was 2000 mg/kg MSDS.

Not Available
Pharmacogenomic Effects/ADRs
Not Available


Drug Interactions
This information should not be interpreted without the help of a healthcare provider. If you believe you are experiencing an interaction, contact a healthcare provider immediately. The absence of an interaction does not necessarily mean no interactions exist.
AbacavirAbacavir may decrease the excretion rate of Piracetam which could result in a higher serum level.
AceclofenacAceclofenac may decrease the excretion rate of Piracetam which could result in a higher serum level.
AcemetacinAcemetacin may decrease the excretion rate of Piracetam which could result in a higher serum level.
AcetaminophenAcetaminophen may decrease the excretion rate of Piracetam which could result in a higher serum level.
AcetazolamideAcetazolamide may increase the excretion rate of Piracetam which could result in a lower serum level and potentially a reduction in efficacy.
Food Interactions
Not Available


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International/Other Brands
Myocalm (Taiho Pharmaceuticals)


ATC Codes
N06BX03 — Piracetam
Drug Categories
Chemical TaxonomyProvided by Classyfire
This compound belongs to the class of organic compounds known as alpha amino acids and derivatives. These are amino acids in which the amino group is attached to the carbon atom immediately adjacent to the carboxylate group (alpha carbon), or a derivative thereof.
Organic compounds
Super Class
Organic acids and derivatives
Carboxylic acids and derivatives
Sub Class
Amino acids, peptides, and analogues
Direct Parent
Alpha amino acids and derivatives
Alternative Parents
Pyrrolidine-2-ones / N-alkylpyrrolidines / Tertiary carboxylic acid amides / Primary carboxylic acid amides / Lactams / Azacyclic compounds / Organopnictogen compounds / Organonitrogen compounds / Organic oxides / Hydrocarbon derivatives
show 1 more
2-pyrrolidone / Aliphatic heteromonocyclic compound / Alpha-amino acid or derivatives / Azacycle / Carbonyl group / Carboxamide group / Hydrocarbon derivative / Lactam / N-alkylpyrrolidine / Organic nitrogen compound
show 10 more
Molecular Framework
Aliphatic heteromonocyclic compounds
External Descriptors
Not Available
Affected organisms
Not Available

Chemical Identifiers

CAS number
InChI Key


General References
  1. Winblad B: Piracetam: a review of pharmacological properties and clinical uses. CNS Drug Rev. 2005 Summer;11(2):169-82. [Article]
  2. Kurz C, Ungerer I, Lipka U, Kirr S, Schutt T, Eckert A, Leuner K, Muller WE: The metabolic enhancer piracetam ameliorates the impairment of mitochondrial function and neurite outgrowth induced by beta-amyloid peptide. Br J Pharmacol. 2010 May;160(2):246-57. doi: 10.1111/j.1476-5381.2010.00656.x. Epub 2010 Mar 9. [Article]
  3. Fischer W, Kittner H, Regenthal R, Russo E, De Sarro G: Effects of piracetam alone and in combination with antiepileptic drugs in rodent seizure models. J Neural Transm (Vienna). 2004 Sep;111(9):1121-39. doi: 10.1007/s00702-004-0155-6. Epub 2004 May 14. [Article]
  4. Nootropil tablets Drug Summary [Link]
  5. electronic Medicines Compendium (eMC): Nootripil Summary of Product Characteristics [Link]
PDBe Ligand
Download (47.2 KB)

Clinical Trials

Clinical Trials
4CompletedTreatmentVertigo, Peripheral1
4Enrolling by InvitationTreatmentStatus Epilepticus1
4Not Yet RecruitingOtherDrug Adherence Marker1
4TerminatedTreatmentAcute Ischemic Stroke of the Middle Cerebral Artery1
3CompletedTreatmentTardive Dyskinesia (TD)1


Not Available
Not Available
Dosage Forms
SolutionIntravenous1 gr/5ml
SyrupOral200 mg/ml
SolutionOral20 %
Solution / dropsOral
InjectionIntravenous200 MG/ML
TabletOral800.000 mg
Tablet, film coatedOral
Powder, for solutionOral
Solution200 mg/1ml
SolutionOral20 g
SyrupOral8 g
TabletOral1200 MG
TabletOral800 MG
Injection, solutionParenteral3 G
SolutionParenteral12 g/60ml
Injection, solution12 G/60ML
SolutionIntravenous; Oral
SolutionIntravenous; Oral3 G/15ML
SolutionOral20.000 g
Solution / dropsOral33.33 %
InjectionIntramuscular; Intravenous1 gr
SyrupOral200 ml
Injection, solutionParenteral3 g/15ml
SolutionConjunctival; Ophthalmic0.2 g
InjectionParenteral3 g
SyrupOral20 g
SolutionOral20 g/100ml
PowderOral48 g
Tablet, film coatedOral1200.00 mg
Tablet, film coatedOral800.00 mg
Tablet, coatedOral1200 mg
InjectionParenteral1 g/5ml
Injection, solutionIntravenous1 mg/5ml
InjectionIntramuscular; Intravenous1 gr/5ml
Injection, solutionIntramuscular; Intravenous
Tablet, extended releaseOral
Tablet, film coatedOral800000 MG
TabletOral80000000 mg
Injection, solution
Injection, solution3 G/15ML
SolutionOral333.3 mg/ml
SolutionParenteral1 g/5ml
SolutionOral33 %
GranuleOral2.4 G
Injection, solution1 g/5ml
Injection, solutionIntravenous1 g/5ml
TabletOral0.8 g
Granule, for solutionOral
Granule, for suspensionOral
Injection, solutionIntravenous
InjectionIntramuscular; Intravenous
Tablet, coatedOral800 mg
CapsuleOral400 mg
Tablet, film coatedOral1200 mg
Tablet, film coatedOral800 mg
Not Available
Not Available


Experimental Properties
melting point (°C)152MSDS
boiling point (°C)DecomposesMSDS
Predicted Properties
Water Solubility479.0 mg/mLALOGPS
pKa (Strongest Acidic)15.93Chemaxon
pKa (Strongest Basic)-2Chemaxon
Physiological Charge0Chemaxon
Hydrogen Acceptor Count2Chemaxon
Hydrogen Donor Count1Chemaxon
Polar Surface Area63.4 Å2Chemaxon
Rotatable Bond Count2Chemaxon
Refractivity35.06 m3·mol-1Chemaxon
Polarizability13.96 Å3Chemaxon
Number of Rings1Chemaxon
Rule of FiveYesChemaxon
Ghose FilterNoChemaxon
Veber's RuleNoChemaxon
MDDR-like RuleNoChemaxon
Predicted ADMET Features
Not Available


Mass Spec (NIST)
Not Available
SpectrumSpectrum TypeSplash Key
LC-MS/MS Spectrum - LC-ESI-QFT , positiveLC-MS/MSsplash10-002b-9400000000-651dc28016b653b55d23
LC-MS/MS Spectrum - LC-ESI-QFT , positiveLC-MS/MSsplash10-002b-9400000000-9c47f9c6616fbfad2c93
LC-MS/MS Spectrum - LC-ESI-QFT , positiveLC-MS/MSsplash10-0002-9100000000-079c7eb43e2dcfe07d5f
LC-MS/MS Spectrum - LC-ESI-QFT , positiveLC-MS/MSsplash10-0002-9000000000-94d697783ea2c537498f
LC-MS/MS Spectrum - LC-ESI-QFT , positiveLC-MS/MSsplash10-0002-9000000000-5dd797bddeacd8764c16
LC-MS/MS Spectrum - LC-ESI-QFT , positiveLC-MS/MSsplash10-006t-9000000000-e270872ffd02b3d53ab2
Predicted MS/MS Spectrum - 10V, Positive (Annotated)Predicted LC-MS/MSsplash10-0002-9800000000-59d805b361727e0af1e4
Predicted MS/MS Spectrum - 10V, Negative (Annotated)Predicted LC-MS/MSsplash10-0006-9200000000-0afd56bb184f85b5297c
Predicted MS/MS Spectrum - 20V, Positive (Annotated)Predicted LC-MS/MSsplash10-0002-9300000000-2b7b6a91fd06cbd09313
Predicted MS/MS Spectrum - 20V, Negative (Annotated)Predicted LC-MS/MSsplash10-0006-9000000000-658f166270f320ad6c24
Predicted MS/MS Spectrum - 40V, Negative (Annotated)Predicted LC-MS/MSsplash10-0006-9000000000-bb78bef63e060b378ff8
Predicted MS/MS Spectrum - 40V, Positive (Annotated)Predicted LC-MS/MSsplash10-052f-9100000000-62adac0d2c79e1534ad3
Predicted 1H NMR Spectrum1D NMRNot Applicable
Predicted 13C NMR Spectrum1D NMRNot Applicable
Chromatographic Properties
Collision Cross Sections (CCS)
AdductCCS Value (Å2)Source typeSource
DarkChem Lite v0.1.0
DarkChem Lite v0.1.0
DeepCCS 1.0 (2019)
DarkChem Lite v0.1.0
DarkChem Lite v0.1.0
DeepCCS 1.0 (2019)
DarkChem Lite v0.1.0
DarkChem Lite v0.1.0
DeepCCS 1.0 (2019)

Drug created at October 20, 2015 19:46 / Updated at May 07, 2021 21:06