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Aniracetam is a compound in the group of racetams due to its common pyrrolidone structure. It is one of the more common Racetamic structures. It is fat-soluble and thus needs to be ingested with fatty acids. Additionally, Aniracetam is Cholinergic
Aniracetam acts as a positive modulator of some excitatory receptors known as AMPA receptors and decreases the rate of receptor desensitization. This typically manifests as a controlled and prolonged neurological stimulation effect. Since AMPA receptors differ in structure across the brain, different AMPA modulators affect the brain in different ways.
Anecdotally, Aniracetam has been know to aid in 'collective and holistic thinking', or putting the pieces of the puzzle together. It also increases blood flow and activity in the area of the brain known for this action, the association cortex.
Aniracetam, as an AMPA modulator, is currently being studied for usage in depression and other CNS disorders such as Alzheimer's disease.
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1-p-anisoyl-2-pyrrilidinone, Ro 13-5057, CAS 72432-10-1, 1(4-methoxybenzoyl)-2-pyrrolidinone
As is the nature of dissecting a brain, the majority of the studies on Aniracetam have been done in laboratory animals such as mice and monkeys. Extrapolation is used in many cases when applied to humans, which is an unavoidable consequence since cellular studies would require taking brain tissue out of a living human.Examine.com Medical Disclaimer
Doses between 10 mg/kg bodyweight and 100 mg/kg bodyweight have been used in rats with efficacy in laboratory settings. Limited human evidence finds that oral doses in the 1,000-1,500 mg range (over the course of a day) tend to be effective.
Doses as low as 400 mg have been reported to have some efficacy, and it is common to take the above 1,000-1,500 mg aniracetam in two divided doses of 500-750 mg twice daily with meals.
Aniracetam powder has a highly bitter taste, so capsules may be a better purchase for those who wish to avoid that.
Aniracetam is a pyrrolidinone compound of the racetam family, and has an additional anisoyl ring with a methoxy group at the lone para position. (replacing the amine group of piracetam) with an O-methoxy group on the furthest binding point. Its structure is dissimilar to that of Oxiracetam (which is quite similar to piracetam) and Pramiracetam (fairly unique structure) yet closely related to that of Nefiracetam.
Aniracetam is a piracetam molecule in which the amine is replaced by a methylated phenyl group, this modification was made to enhance fat solubility and underlies differences between piracetam and aniracetam
Aniracetam appears to be greatly taken up from the gut even in a fasted state, but is subject to extensive first pass hepatic metabolism. Due to this, it has an overall bioavailabiliy of around 8.6-11.4%. Bioavailability is presumed higher when taken with fatty acids, but unexplored.
Is fat-soluble and logically enhanced when taken with fatty acids, does not appear to need fatty acids to be absorbed
Plasma levels of aniracetam have been noted to peak at 2.3mcg/L (300mg) and 14.1mcg/L (1200mg) with an elimination half life of 35 minutes following ingestion of aniracetam. It appears to have extensive first pass metabolism in the liver with the main metabolites being N-anisoyl-GABA, 2-pyrrolidinone, and anisic acid. 95.8% of the dose is recovered, mostly in the urine, 28 hours post ingestion.
In a study of healthy male volunteers, Aniracetam showed a Cmax (max concentration) of 8.75+/-7.82 and 8.65+/-8.7ng/mL over two testing periods which correspond to a Tmax (time at max) of 0.4+/-0.1 hour each time; in response to 400mg oral Aniracetam. The plasma elimination half-lives were 47+/-0.16 and 49+/-0.24 hours and plasma AUC 4.53+/-6.62 and 4.76+/-6.65ng/h/mL in this study as well. These relatively low peaks of Aniracetam may be due to extensive metabolism after oral administration.
It appears that superloading Aniracetam (50-100mg/kg bodyweight) does not augment the Cmax or Tmax significantly, and tends to only prolong the AUC to 1.7-2.1 hours.
Appears to be rapidly absorbed in under 30 minutes, and rapidly metabolized; higher doses do not change the time it takes to work, but may prolong the AUC (Area-Under-Curve) of Aniracetam, either by delaying excretion or metabolism
The main human metabolite of Aniracetam is a compound known as N-Anisoyl-GABA (aka. 4,p-Anisaminobutyric acid or ABA), which accounts for 70% of orally ingested Aniracetam by weight after hepatic (liver) biotransformation. Alternate pathways lead to production of P-Anisic Acid (which can be conjugated by wither glucuronic acid or glycine) and 2-pyrrolidinone (which then goes on to the Kreb's Cycle to produce energy via the succinate intermediate).
One study that confirmed protective effects against amnesia in a choice reaction test with aniracetam (10-100mg/kg) subsequently tested all metabolites, with both P-anisic acid and 2-pyrrolidinone failing to exert anti-amnesiac effects while N-anisoyl-GABA at 30mg/kg was similarly effective.
Aniracetam is heavily metabolized into N-anisoyl-GABA and P-Anisic Acid, which should be considered for bioactivity in the body
AMPA is one of the three subsets of glutamate (excitatory) receptors, of which the other two are kainate and NMDA (N-methyl-D-Aspartate). These AMPA receptors mediate fast excitatory amino acid transmission, and are heterogenously expressed in the brain as heteromers with eight possible subunits (GluR1 through R4, each in a flip or flop variant).
Aniracetam is a modulator of the AMPA receptor that works by binding to a non-active site of AMPA receptors and allosterically modifying the binding site, of which the final result is a reduced rate of desensitization in the presence of positive stimuli (such as glutamate, which is intrinsically produced). This occurs in the concentration range of 1-5mM.
AMPA receptors appear to be positively modulated by aniracetam, similar to other basic racetam compounds
May have a positive influence on kainate receptors, does not appear to interact with NMDA receptors much if at all
Activation of AMPA receptors is able to release noradrenaline from neurons, and 100µM (but not 10µM) of aniracetam is able to potentiate AMPA's effects on noradrenaline release in these hippocampal cells.
Kyurenic acid is able to attenuate the ability of NDMA to release noradrenaline from cells, and this inhibition is attenuated in the presence of aniracetam (EC50 in the range of 10-100nM and near full inhibition at 1µM) without inherently affecting basal outflow or NMDA induced release of noradrenaline at this dose; blocking the AMPA receptor failed to block this effect, and while kyurenic acid also suppresses AMPA receptor activation aniracetam (1-100µM) does not antagonize this effect (cyclothiazide, however, was effective).
Aniracetam appears to be able to potentiate signalling via nicotinic α4β2 receptors at 0.1nM via interactions with GS proteins, independent of protein kinases.
Aniracetam has been shown at 50mg/kg oral ingestion (rats) to decrease the turnover rates for dopamine in the striatum and reducing dopamine levels in the hypothalamus and striatum; serotonin levels decreased in the hypothalamus but increased in the cortex and striatum, where it reduced turnover (hypothalamus) and increase turnover (cortex, striatum, brain stem).
Aniracetam seems to be able to alleviate damage done to memory and learning impairment caused by various agents and traumas such as cholinergic antagonists, cerebral ischaemia and electroconvulsive shock. Aniracetam can also protect against scopolamine-induced damage, and does so (at 1.5g) to a greater extent than Piracetam (at 2.4g).
Aniracetam has been shown to reduce measures of anxiety in rats, and has anecdotally reported to do the same in humans. It is suspected to do so via a mix of serotonergic, dopaminergic, and cholinergic interactions. Improvements as measured by social interactions were seen in doses ranging from 10mg/kg body weight to 100mg/kg bodyweight.
It has demonstrated efficacy in reducing depression in aged rats at 100mg/kg bodyweight, but was ineffective at exerting anti-depressive effects in younger mice. These effects were mimicked with Aniracetam metabolites, and were abolished with haloperidol and mecamylamine, and thus the mechanism was theorized to be enhancing dopaminergic signalling via the nicotinic acetylcholinergic receptors.
There may also be interactions with depression and downstream effects of Aniracetam's main mechanism of action, AMPA receptor modulation.
Aniracetam has been found to specifically decrease the rate of receptor desensitization in lab animal hippocampus (specifically quisqualate receptors), suggesting a potential benefit to memory formation. It does not seem affect choline uptake into hippocampal cells in any way, and actually encourages acetylcholine release.
Aniracetam also increases the release of dopamine and serotonin via Cholinergic mechanisms in the prefrontal cortex, with implications in improving judgement. This may also in part explain it's involvement as an anti-depressant. Via either the same or alternate mechanisms (positive AMPA modulation) Aniracetam has also been shown to reduce impulsiveness in the rat.
Through the general mechanism of AMPA modulation (and thus applicable to Piracetam and Oxiracetam), Ampakines can upregulate Brain-derived Neurotrophic factor (BDNF) for periods longer than the Ampakine's AUC due to a long BDNF half-life. These effects may be free of downregulation given some time away from the ampakine's existence in serum exists. BDNF is implicated in increasing adult neural plasticity.
It is also being studied in other cognitive deficits such as Alzheimer's disease or other cognitive ailments as either a mechanism to biologically reverse neurological changes or to alleviate symptoms of said disorders.
Aniracetam has also been implicated in rats to alleviate some cognitive deficits in the hippocampus onset by Fetal Alcohol Syndrome (FAS) in a dosage of 50mg/kg bodyweight.
(Common misspellings for Aniracetam include aniractam, anracetam, aniracetm)
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