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| Trade names | Breinox, Dinagen, Lucetam, Nootropil, Nootropyl, Oikamid, Piracetam, others |
| AHFS/Drugs.com | International Drug Names |
| Routes of administration | By mouth,parenteral,inhalation |
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| Pharmacokinetic data | |
| Bioavailability | ~100% |
| Onset of action | Swiftly following administration. Food delays time to peak concentration by 1.5 h approximately to 2–3 h since dosing.[2] |
| Eliminationhalf-life | 4–5 hours |
| Excretion | Urinary |
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| CompTox Dashboard(EPA) | |
| ECHA InfoCard | 100.028.466 |
| Chemical and physical data | |
| Formula | C6H10N2O2 |
| Molar mass | 142.158 g·mol−1 |
| 3D model (JSmol) | |
| Melting point | 152 °C (306 °F) |
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Piracetam is adrug that has efficacy incognitive disorders,vertigo, corticalmyoclonus,dyslexia, andsickle cell anemia; sources differ on its usefulness fordementia.[3][4][5] Piracetam is sold as a medication in many European countries. Piracetam in the United States is not approved for general use.[6]
Piracetam is in theracetams group, with chemical name2-oxo-1-pyrrolidine acetamide. It is a cyclic derivative of the neurotransmitterGABA[4] and shares the same 2-oxo-pyrrolidone base structure withpyroglutamic acid. Related drugs include the anticonvulsantslevetiracetam andbrivaracetam, and the putative nootropicsaniracetam andphenylpiracetam.
A 2001Cochrane review concluded that there was not enough evidence to support piracetam fordementia or cognitive problems.[5] A 2005 review found some evidence of benefit in older subjects with cognitive impairment.[4] In 2008, a working group of the BritishAcademy of Medical Sciences noted that many of the trials of piracetam for dementia were flawed.[7]
There is insufficient evidence of piracetam as a treatment forvascular dementia.[8]
Some sources suggest that piracetam's overall effect on loweringdepression andanxiety is higher than on improving memory.[9] However, depression is reported to be an occasional adverse effect of piracetam.[10]
Several clinical trials have looked at piracetam's efficacy as a treatment forADHD. Many of these have found that the drug fails to deliver the same therapeutic effects as current standard treatments for the disorder.[11][unreliable source?] However, more than one study has found piracetam to be highly synergistic with standard ADHD therapies, accelerating and potentiating their therapeutic effects. One 2008 clinical trial found that the combination of piracetam andatomoxetine was more effective than atomoxetine alone.[12]
While piracetam may be an effective adjuvant therapy for ADHD (when used with specific medications), there is no evidence that it is effective when used in isolation.
Piracetam may facilitate thedeformability of erythrocytes incapillary which is useful for cardiovascular disease.[4][3]
Peripheral vascular effects of piracetam have suggested its use potential forvertigo,dyslexia,Raynaud's phenomenon andsickle cell anemia.[4][3] There is no evidence to support piracetam's use in sickle cell crisis prevention[13] or forfetal distress during childbirth.[14] There is no evidence for benefit of piracetam withacute ischemic stroke,[15] though there is debate as to its utility during stroke rehabilitation.[16][17]
Piracetam has been found to diminisherythrocyteadhesion to vascular wallendothelium, making anyvasospasm in thecapillary less severe. This contributes to its efficacy in promotingmicrocirculation, including to the brain and kidneys.[4][3]
Symptoms includinganxiety,insomnia,irritability,headache,agitation,tremor, andhyperkinesia are occasionally reported.[10][18][19] Other reported side effects includesomnolence,weight gain,clinical depression,weakness, increasedlibido, andhypersexuality.[10]
According to a 2005 review, piracetam has been observed to have the following side effects: hyperkinesia,weight gain, anxiety, somnolence, depression, and weakness.[4]
Piracetam reducesplatelet aggregation as well asfibrinogen concentration, and thus is contraindicated to patients with cerebral hemorrhage.[4][3]
TheLD50 for oral consumption in humans has not been determined.[20] The LD50 is 5.6 g/kg for rats and 20 g/kg for mice, indicating extremely lowacute toxicity.[21] For comparison, in rats the LD50 ofvitamin C is 12 g/kg and the LD50 of table salt is 3 g/kg.
Piracetam'smechanism of action, as withracetams in general, is not fully understood. The drug influences neuronal and vascular functions and influences cognitive function without acting as asedative orstimulant.[4] Piracetam is apositive allosteric modulator of theAMPA receptor, although this action is very weak and its clinical effects may not necessarily be mediated by this action.[22] It is hypothesized to act on ion channels or ion carriers, thus leading to increased neuron excitability.[20]GABA brain metabolism andGABA receptors are not affected by piracetam[23]
Piracetam increases the action of theneurotransmitteracetylcholine viamuscariniccholinergic (ACh)receptors[citation needed], which are implicated inmemory processes.[24] Furthermore, piracetam may have an effect onNMDAglutamate receptors, which are involved withlearning andmemory processes. Piracetam is thought to increase cell membrane permeability.[24][25] Piracetam may exert its global effect on brain neurotransmission via modulation ofion channels (i.e., Na+, K+).[20] It has been found to increase oxygen consumption in the brain, apparently in connection toATP metabolism, and increases the activity ofadenylate kinase in rat brains.[26][27] Piracetam, while in the brain, appears to increase the synthesis ofcytochrome b5,[28] which is a part of theelectron transport mechanism inmitochondria. But in the brain, it also increases the permeability of some intermediates of theKrebs cycle through the mitochondrial outer membrane.[26]
Piracetam inhibitsN-type calcium channels. The concentration of piracetam achieved incentral nervous system after a typical dose of 1200 mg (about 100 μM)[29] is much higher than the concentration necessary to inhibitN-type calcium channels (IC50 of piracetam in rat neurons was 3 μM).[30]
Piracetam was first made some time between the 1950s and 1964 byCorneliu E. Giurgea.[31] There are reports of it being used for epilepsy in the 1950s.[32]
In 2009 piracetam was reportedly popular as a cognitive enhancement drug among students.[33]
Piracetam is an uncontrolled substance in the United States, meaning it is legal to possess without a license or prescription.[34] Use of piracetam in food, supplements, medical devices,insecticides, infant formula, cosmetics, animal feed, animal drugs, tobacco products, and drugs is unlawful and constitutes an act of misbranding.
In the United States, piracetam is not approved by theFood and Drug Administration.[1] Piracetam is not permitted in compounded drugs or dietary supplements in theUnited States.[35] Like most research chemicals, it has been available over-the-counter, self-regulated, and third-party lab tested by many U.S. companies for decades.[6] Nonetheless it is still, for the purposes of U.S. law, a "New Drug" as defined by 21 U.S. Code § 321(p)(1).
In the United Kingdom, piracetam is approved as a prescription drug[36] for adults withmyoclonus of cortical origin, irrespective of cause, and should be used in combination with other anti-myoclonic therapies.[37]
In Japan, piracetam is approved as a prescription drug.[38]
In the Czech Republic, piracetam is available without prescription.[39][40]
Piracetam has noDIN in Canada, and thus cannot be sold, but can be imported for personal use in Canada.[41]
In Hungary, piracetam was a prescription-only medication, but as of 2020, no prescription is required and piracetam is available as anover-the-counter drug under the name Memoril Mite, and is available in 600 mg pills.
Other medications have been considered or tried for the treatment of VCI or VaD. These include [...] piracetam. There is no convincing evidence about the efficacy of these medications in the treatment of VCI.
