|Summary sheet: Piracetam|
|Substitutive name||Avigilen, Memo-Puren, Nootron, Nootrop, Nootropil, Nootropyl, Normabrain, Norzetam, Geratam|
|Routes of Administration|
Piracetam (2-oxo-1-pyrrolidine acetamide) is a nootropic substance of the racetam class. It is a derivative of GABA.
Piracetam was first synthesized in 1964 by Corneliu E. Giurgea and other scientists at the Belgian pharmaceutical company UCB.
In the United Kingdom, piracetam is prescribed mainly for myoclonus (spasmodic jerky contraction of groups of muscles), but is used off-label for other conditions. In the United States, it is not approved by the Food and Drug Administration for any medical use and it is not permitted to be sold as a dietary supplement. However, it is still readily available and sold through online vendors. As a "smart drug", it is reported to enhance cognitive functions including memory, intelligence, and attention.
The active dose of piracetam is 100 times than that of noopept, making it both the earliest and least potent racetam. The standard piracetam dose for adults is between 1,200-4,800mg a day. The largest effective dose is 1,600mg taken three times a day for a total of 4,800mg.
Piracetam, or 2-oxo-1-pyrrolidine-acetamide, is a synthetic compound of the racetam family. Racetams share a pyrrolidine nucleus, a five member nitrogenous ring with a ketone bonded oxygen at R2. This 2-pyrrolidone ring is bound to the terminal carbon of an acetamide group, an ethyl amide chain with a ketone bond (C=O) at the alpha carbon.
Piracetam shares structural similarity to the neurotransmitter GABA, its pyrrolidine core is the cyclic counterpart of GABA and could theoretically be converted into an acetamide chain through a hydrolysis reaction into GABA.
Piracetam's mechanism of action, as with racetams in general, is not fully understood. The drug influences neuronal and vascular functions and influences cognitive function without acting as a sedative or stimulant. Piracetam is a positive allosteric modulator of the AMPA receptor. It is hypothesized to act on ion channels or ion carriers, thus leading to increased neuron excitability. GABA brain metabolism and GABA receptors are not affected by piracetam.
Among other things, it has also been found to increase blood flow and oxygen consumption in parts of the brain, but this may be a side effect of increased brain activity rather than a primary effect or mechanism of action for the drug. Piracetam also improves the function of the neurotransmitter acetylcholine via muscarinic cholinergic (ACh) receptors, which are implicated in memory processes.
Although it is not fully understood how, it's these multiple complex mechanisms of action which result in piracetams nootropic effects.
Disclaimer: The effects listed below cite the Subjective Effect Index (SEI), an open research literature based on anecdotal user reports and the personal analyses of PsychonautWiki contributors. As a result, they should be viewed with a healthy degree of skepticism.
It is also worth noting that these effects will not necessarily occur in a predictable or reliable manner, although higher doses are more liable to induce the full spectrum of effects. Likewise, adverse effects become increasingly likely with higher doses and may include addiction, severe injury, or death ☠.
In comparison to the effects of other nootropics such as noopept, this compound can be described as focusing primarily on physical stimulation over that of cognitive stimulation.
- Stimulation - The stimulation which piracetam presents can be considered as primarily subtle, comparable to that of caffeine.
- Headaches - Some users suggest that this effect may be alleviated with a choline source such as choline bitartrate, alpha-GPC or citicoline.
- Muscle spasms
There are currently no anecdotal reports which describe the effects of this compound within our experience index. Additional experience reports can be found here:
Toxicity and harm potential
Adverse effects, although rare and of short duration are limited to anxiety, insomnia, drowsiness, headaches and agitation. It may be safe for up to 18 months in humans at doses of 3.2g daily with one year-long study in ambulatory patients with Alzheimer's using 8g daily reporting no side effects. However, a possibility for adverse drug-drug interactions persists for piracetam due to it interacting with blood in an anti-clotting manner. Therefore, caution should be taken when pairing piracetam with pharmaceutical blood thinning agents such as Warfarin or potent nutraceutical options and individuals prone to brain hemorrhaging are discouraged from using piracetam.
Patients with renal insufficiency should also not use piracetam.
No fatal overdoses associated with piracetam use have been reported as of 2016. In animal models (rodents, dogs, and marmoset), an LD50 failed to be established at the dosage of 8-10g/kg.
Regardless, it is strongly recommended that one use harm reduction practices when using this substance.
The median lethal dosage (LD50) of piracetam has not been officially published as it has low abuse potential, but the typical dosage is two grams once to three times a day.
Dependence and abuse potential
The chronic use of piracetam can be considered as not addictive with a low potential for abuse. It does not seem to be capable of causing psychological dependence among certain users.
Tolerance to many of the effects of piracetam develops with prolonged and repeated use. This results in users having to administer increasingly large doses to achieve the same effects. After that, it takes about 3 - 7 days for the tolerance to be reduced to half and 1 - 2 weeks to be back at baseline (in the absence of further consumption). Piracetam may presents cross-tolerance with all racetam nootropics, meaning that after the consumption of piracetam certain nootropicss such as aniracetam and pramiracetam may have a reduced effect.
Piracetam showed nonselective MAO activity in a rat study. Piracetam and MAOIs are a potentially dangerous combination. It is likely that MAOIs could increase the effects of piracetam unpredictably. Taking this chemical while on prescription MAOIs is strongly discouraged.
This legality section is a stub.
As such, it may contain incomplete or wrong information. You can help by expanding it.
Piracetam, being a member of the racetam family, currently is legally available to buy and sell in most countries, but may still vary by region.
- Germany: Piracetam is a prescription medicine, according to Anlage 1 AMVV.
- Switzerland: Piracetam is listed as a "Abgabekategorie B" pharmaceutical, which requires a prescription.
- United Kingdom: Piracetam and other racetams are prescription only drugs; however, there is no penalty for possession or importing them.
- New Zealand: Piracetam is considered a prescription drug, and as such will be seized by the Ministry of Health. It is not able to be imported without a signed note from a doctor.
- Piracetam (Wikipedia)
- Piracetam (Erowid Vault)
- Piracetam (TiHKAL / Isomer Design)
- Piracetam (Examine)
- ↑ Henderson, D. R. (2012), Nootropil (piracetam)
- ↑ Erowid Piracetam Vault : FAQ : Frequently Asked Questions v0.7
- ↑ Malykh, A. G., Sadaie, M. R. (12 February 2010). "Piracetam and piracetam-like drugs: from basic science to novel clinical applications to CNS disorders". Drugs. 70 (3): 287–312. doi:10.2165/11319230-000000000-00000. ISSN 1179-1950.
- ↑ Winblad, B. (2005). "Piracetam: a review of pharmacological properties and clinical uses". CNS drug reviews. 11 (2): 169–182. doi:10.1111/j.1527-3458.2005.tb00268.x. ISSN 1080-563X.
- ↑ Ahmed, A. H., Oswald, R. E. (11 March 2010). "Piracetam defines a new binding site for allosteric modulators of alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) receptors". Journal of Medicinal Chemistry. 53 (5): 2197–2203. doi:10.1021/jm901905j. ISSN 1520-4804.
- ↑ Gouliaev, A. H., Senning, A. (May 1994). "Piracetam and other structurally related nootropics". Brain Research. Brain Research Reviews. 19 (2): 180–222. doi:10.1016/0165-0173(94)90011-6.
- ↑ Giurgea, C. E. (1982). "The nootropic concept and its prospective implications". Drug Development Research. 2 (5): 441–446. doi:10.1002/ddr.430020505. ISSN 0272-4391.
- ↑ Jordaan, B., Oliver, D. W., Dormehl, I. C., Hugo, N. (September 1996). "Cerebral blood flow effects of piracetam, pentifylline, and nicotinic acid in the baboon model compared with the known effect of acetazolamide". Arzneimittel-Forschung. 46 (9): 844–847. ISSN 0004-4172.
- ↑ Winnicka, K., Tomasiak, M., Bielawska, A. (October 2005). "Piracetam--an old drug with novel properties?". Acta Poloniae Pharmaceutica. 62 (5): 405–409. ISSN 0001-6837.
- ↑ Fedi, M., Reutens, D., Dubeau, F., Andermann, E., D’Agostino, D., Andermann, F. (May 2001). "Long-term efficacy and safety of piracetam in the treatment of progressive myoclonus epilepsy". Archives of Neurology. 58 (5): 781–786. doi:10.1001/archneur.58.5.781. ISSN 0003-9942.
- ↑ Stancheva, S. L., Alova, L. G. (June 1988). "[Effect of centrophenoxine, piracetam and aniracetam on the monoamine oxidase activity in different brain structures of rats]". Farmakologiia I Toksikologiia. 51 (3): 16–18. ISSN 0014-8318.
- ↑ Trabucchi, M., Govoni, S., Battaini, F. (April 1986). "Changes in the interaction between CNS cholinergic and dopaminergic neurons induced by L-alpha-glycerylphosphorylcholine, a cholinomimetic drug". Il Farmaco; Edizione Scientifica. 41 (4): 325–334. ISSN 0430-0920.
- ↑ Anlage 1 AMVV - Einzelnorm