Product Code: CAS:7491-74-9
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Product Summary:

Piracetam is a cyclical derivative of GABA, synthesized by converting 2-pyrrolidinone into an amide. It was discovered in 1964 by Romanian chemist, Corneliu E. Giurgea, who later coined the term “nootropic” to describe the novel effects of this compound. Piracetam is the archetype of the Racetam class of nootropics. It is observed to increase cholinergic neurotransmission without exhibiting stimulant properties. Additional effects observed in research trials include the following:

Product Description

Synonyms:Piracetam (Nootropil)

Formal Name:2-(2-oxopyrrolidin-1-yl)acetamide

Formula   C6H10N2O2

Molecular Weight: 142.16 g/mol

Purity        ≥99%

CAS Number: 7491-74-9

Other names

2-(2-Oxo-pyrrolidin-1-yl)-acetamide, 2-(2-Oxopyrrolidino)acetamide, 5-21-06-00360 (Beilstein Handbook Reference), Avigilen, Axonyl, BRN 1526393, CI-871, Cerebroforte, Ciclofalina, Encetrop, Euvifor, Gabacet, Genogris, KT-801, N-Carbamoylmethyl-2-pyrrolidinone, Naofukang, Nootron, Nootrop, Nootropil, Nootropyl, Normabrain, Norzetam, Piracetamas, Piracetamum, Piracétam, Pirasetaami, Pirasetam, Pirroxil, Pyracetam, Pyramem, Pyrrolidone Acetamide, UCB-6215.

What Is Piracetam?

Piracetam (Nootropil, Breinox, Lucetam, Nootropyl) is also known as 2-(2-oxopyrrolidin-1-yl)acetamide. It was the first nootropic substance discovered by Dr. Corneliu E. Giurgea, who remarked that it exhibited a cognitive enhancement effect without causing stimulation or depression of the central nervous system. His researched showed that Piracetam could increase learning and memory, protect the brain from injury, and that it exhibited few side effects and extremely low toxicity. Giurgea coined the phrased “nootropic” from the Greek words, nous, or “mind”, and trepein, or “to turn”, to describe Piracetam. This Racetam thus became the first in a new class of compounds that could “bend the mind.”


Piracetam absorption occurs rapidly and peak plasma levels are recorded within 1.5 hours following oral administration. Oral bio-availability has been assessed at almost 100% based on Area Under Curve (AUC0-24) analysis. The plasma half-life has been established at 5.0 hours in young adult men with a volume of distribution of 0.7 L/kg. No metabolites of Piracetam have been detected so far.

Initial researchers concluded that Piracetam was almost entirely eliminated via renal pathways and excreted in urine. A recent study suggests that there may be extrarenal elimination pathways as only two-thirds of the oral dosage was detected in urine.

Piracetam USES

Piracetam is used in some countries as a medical agent and is administered for a wide range of purposes. Its primary medical use is as a neuro-protective agent before or after stroke. The substance is believed to reduce the risk of ischemic stroke as well as minimize post-stroke damages to the brain. It is also an anti-coagulant and anti-thrombotic agent which is often used safety in conjunction with other therapies.

There have been many studies on treatment with Piracetam for neurological disorders. Many of these studies have shown positive results but not enough to approve them as treatments in the medical field. For instance, there has been evidence in studies for effectiveness in improving symptoms in Alzheimer’s and Dementia patients. Although, symptoms for these patients were often improved, it is not an approved therapy because it has not been shown to fully reverse the conditions or take the place of other approved drugs and therapies.

For these reasons, Piracetam is used mainly off-label. It has proven to be fairly safe, with low toxicity, side effects and drug interactions. Evidence shows it may have validity in treating symptoms of Dyslexia and a host of learning disabilities and neurological disorders but this should not be relied on as therapy without consultation of a licensed medical practitioner.

Benefits Of Piracetam

Improves general cognition and working memory.

Increases oxygen utilization and glucose metabolism in the brain.

Slows signs of aging and reverses some forms of neuron damage.

Enhances cellular membrane fluidity and exerts a neuroprotective effect.

Preclinical studies (mainly rat models) have shown piracetam to 1) enhance subject performance in a standard, passive-avoidance test (learning and memory), 2) protect against shock/hypoxia-induced amnesia (neuroprotection), and 3) reduce alcohol and alcohol-withdrawal related neuronal loss, when neural circuitry is recoverable (neuroplasticity).

The drug has applications in treating cognitive disorders, vertigo, cortical myoclonus (involuntary, spontaneous muscle movements), dyslexia, and sickle cell anemia.

The magnitude of piracetam’s cognitive-enhancement varies depending on the individual. Studies have shown more noticeable effects/improvements in aged vs. young animals.

Piracetam Chemical Structure

Piracetam (2-oxo-1-pyrrolidine-acetamide) is a cyclical derivative of the neurotransmitter Gamma-Aminobutyric acid (GABA), although it is not observed to interact with GABA receptors. Like other Racetam nootropics, it features a 5-carbon oxopyrrolidone ring structure. Piracetam can be formed by removing a molecule from GABA, resulting in a cyclical shape that retains two nitrogens with one amide containing a side chain with two carbon atoms and the other nitrogen molecule. Piracetam is synthesized by condensing 2-pyrrolidinone with ethyl chloroacetate and a metal hydride. The resulting ester is then converted into an amide with ammonia.

Piracetam Mechanism of Action

Increased Oxygen and Glucose Consumption

Piracetam is observed to increase brain oxygen consumption and reduce the negative effects of oxidative stress. Oxygen utilization is one measure of brain activity with increased consumption linked to increased alertness. Piracetam may have a beneficial effect under conditions of hypoxia (oxygen deficiency) due to activity of adenylate kinase.

In one study, treatments of between 100-500 mg/kg a day resulted in improved mitochondrial function following oxidative stress (deprivation of sufficient oxygen levels). Subjects first underwent a state of mild serum deprivation which is associated with decreased mitochondrial membrane potential and ATP production. Administration of Piracetam resulted in near complete reversal of the negative effects and reduced antioxidant enzyme activities in aged mouse brains. The results were more pronounced in aged animals than in young healthy animals.

Heiss et al. studied the effects of Piracetam on cerebral glucose metabolism in human patients with Alzheimer’s disease and multiinfarct dementia or unclassified dementia. The nootropic was found to increase utilization of glucose in the Alzheimer’s group, but not in the dementia groups. This compound was also found to increase local cerebral glucose utilization in the rat cerebral cortex following induction of hypoxia. The stimulation of metabolic glucose pathways has been suggested as one mechanism for Piracetam’s neuroprotective effect against oxygen insufficiency.

Glutamatergic Receptors

Piracetam is theorized to positively modulate AMPA-sensitive glutamate receptors, but not NMDA or Kainate receptors. Piracetam (as well as Aniracetam and Oxiracetam) lead to increased max density of the binding sites for the [3H]AMPA receptors in synaptic membranes taken from the rat cerebral cortex. This lead to increased efficacy, but not potency, of AMPA action potentials. Both Piracetam and Aniracetam bind to GluA2 and GluA3 AMPA receptor subtypes, however differences have been observed between the specific binding sites of these two Racetam nootropics.

When administered to aged mice, 500mg/kg of Piracetam for 14 days was found to elevate N-methyl-D-aspartate (NMDA) glutamate receptor density. Deficits of NMDA receptors may be one cause for age-associated cognitive impairments. It is theorized that Piracetam may help to reduce these impairments. In vitro studies have demonstrated that Piracetam can enhance the release of glutamate from neuronal synapses.

Membrane Fluidity

Neuronal membrane fluidity gradually declines with aging and may lead to diminished functions associated with age-related cognitive decline. Piracetam appears to increase neuronal membrane fluidity as measured by decreased anisotropy of a membrane probe. This effect appears to be limited to aged animals. In vitro analysis showed that chronic treatment of 300 mg/kg Piracetam once daily significantly enhanced membrane fluidity in aged rats and humans, but not in young rats. The same treatment was correlated with improvements in avoidance learning only in the aged rats.

Hippocampal neuron membranes from patients with Alzheimer’s Disease show significantly lower membrane fluidity compared to elderly patients not diagnosed with Alzheiemer’s Disease. Piracetam was found, in vitro, to reverse the differences in hippocampal membrane fluidity. Following administration, neurons from the Alzheimer’s group showed the same level of fluidity as those from the control group.

Cholinergic Receptors

Administering 500 mg/kg a day orally for two weeks was found to increase muscarinic cholinergic receptor density in the frontal cortex in aged female mice by 30-40%. However, there was no effect on m-cholinoceptor density for young mice. This limited efficacy could explain why memory-enhancing effects of Piracetam are more pronounced in elderly adults. Administration of Piracetam has been demonstrated to decrease acetylcholine concentrations in the hippocampus.

Supplementing choline alongside treatment with Piracetam has been observed to increase the cognitive enhancement effects of the nootropic. In one memory study, mice were given two sessions within a photo-cell activity cage and measured of activity were used to determine retention of information. One group of mice received 2000 mg/kg piracetam IP and 50 mg/kg piracetam plus 50 mg/kg choline IP administered post-session. Additional groups received either choline alone (between 10 to 200 mg/kg IP) or piracetam alone (between 10 to 1000 mg/kg IP) as well as other combinations of piracetam and choline. The first group performed the best at the memory test. This suggests a synergistic mechanism of action, though studies have not yet been conducted in humans.

Piracetam Safety and Side Effects


Piracetam shows extremely low toxicity in non-human acute exposure studies. Lethal doses were observed at 18.2 g/kg and higher in mice, but were not observed in rats at 21 g/kg or in dogs at 10 g/kg. The dosage 18.2 g/kg is greater than 100 times the standard therapeutic dose in humans.  By comparison, the median lethal dose (LD50) in mice for table salt is 3 g/kg and the lethal dose for caffeine is 192 mg/kg. Therefore, Piracetam shows lower toxicity than both table salt and caffeine in animal models.


Adverse Effects

Piracetam exhibits few mild side effects and no serious side effects when used on its own by healthy adults. It is well-tolerated and has been found safe when administered in humans at dosages of 3.2g per day for up to 18 months. In one trial, patients with early probably Alzheimer’s Disease reported no side effects during one year of 8g dosages per day.

Some patients reported drowsiness during the first two week of use. When administered with synthetic thyroid hormones (T3 and T4), some patients reported sleep disorders, confusion and irritability. Common adverse reactions (affecting between 1 – 10 users out of 100) can include nervousness, weight gain and hyperkinesia. Uncommon side effects (affecting less than 1 out of 100 users) can include depression, somnolence, asthenia and depression. Additional rare side effects can include agitation, anxiety, confusion, hypersensitivity, hallucinations, ataxia, balance impairment, headache, aggravation of epilepsy symptoms, insomnia, abdominal pain, diarrhea, nausea and vomiting.


Due to Piracetam’s effect on platelet aggregation, it should not be used by patients with blood-clotting disorders. Its use is contraindicated in patients with disorders of hemostasis, cerebral hemorrhage, Huntington’s Chorea or individuals undergoing major surgery. Caution is recommended before combining this drug with pharmaceutical blood thinners or using in patients at risk of internal bleeding including gastrointestinal ulcer. It is also contraindicated for patients with severe renal impairment as measured by a renal creatinine clearance of lower than 20 mL/min.

Piracetam should not be used by pregnant or breastfeeding mothers. This compound is excreted in human breast milk. There has not been sufficient research to determine safety of this compound if ingested by developing fetuses or breastfeeding children, therefore caution is advised by medical experts.

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