Aniracetam 750mg Capsules

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  • Aniracetam 750mg Capsules
  • Aniracetam 750mg Capsules


Notice: This product is sold as a nootropic compound used for research purposes only. Any usage is based on your own research, please consider all warnings and recommendations before completing purchase. By purchasing this product, you agree to potential risks associated with this particular ingredients and our terms & conditions.

Ingredient List: Aniracetam Powder, Vegetarian Capsules (Vegetable Cellulose)

Aniracetam is a pyrrolidinone compound of the racetam family,[1] 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. 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.[1]

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.[1]

Aniracetam has been found to specifically decrease the rate of receptor desensitization in lab animal hippocampus (specifically quisqualate receptors)[2], suggesting a potential benefit to memory formation. It does not seem affect choline uptake into hippocampal cells in any way,[3] and actually encourages acetylcholine release.[4]

Study:Allosteric potentiation of quisqualate receptors by a nootropic drug aniracetam.[2]
Abstract - 1. Allosteric potentiation of the ionotropic quisqualate (iQA) receptor by a nootropic drug aniracetam (1-p-anisoyl-2-pyrrolidinone) was investigated using Xenopus oocytes injected with rat brain mRNA and rat hippocampal slices. 2. Aniracetam potentiates the iQA responses induced in Xenopus oocytes by rat brain mRNA in a reversible manner. This effect was observed above the concentrations of 0.1 mM. Kainate. N-methyl-D-aspartate and gamma-aminobutyric acid responses induced in the same oocytes were not affected. 3. The specific potentiation of iQA responses was accompanied by an increase in the conductance change of iQA and alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) responses, but the affinity of receptors for agonist and the ion-selectivity of the channels (reversal potentials) were not changed. 4. Aniracetam reversibly potentiated the iQA responses recorded intracellularly from the pyramidal cells in the CA1 region of rat hippocampal slices. The excitatory postsynaptic potentials (EPSPs) in Schaffer collateral-commissural-CA1 synapses were also potentiated by aniracetam. 5. Population EPSPs recorded in the mossy fibre-CA3 synapses as well as Schaffer-commissural synapses were also potentiated by aniracetam. The amplitudes of the potentiation were not changed by the formation of long-term potentiation.[2]

Study:The effects of various cognition-enhancing drugs on in vitro rat hippocampal synaptosomal sodium dependent high affinity choline uptake.[3]
Abstract -The purpose of the present study was to compare the effect of seven drugs, that have been reported to enhance cognitive functions, on rat hippocampal cholinergic neuronal activity. The latter was assessed by measuring the effects of the drugs on in vitro sodium-dependent high affinity choline uptake (HACU) into rat hippocampal synaptosomes 30 minutes after their in vivo administration. 3,4-Diaminopyridine (0.1 mg/kg IP), like pramiracetam (44 and 88 mg/kg IP), increased HACU with higher or lower doses being ineffective. Centrophenoxine (100 mg/kg IP) decreased HACU. Piracetam (100 and 500 mg/kg IP), aniracetam (10-200 mg/kg PO), lysine vasopressin (0.005-0.05 mg/kg IM) and 4-aminopyridine (0.01-3.0 mg/kg IP) were ineffective. The results indicate that 3,4-diaminopyridine and centrophenoxine, like pramiracetam may be increasing cognitive function in part by affecting hippocampal cholinergic neuronal activity. In addition, the findings indicate the usefulness of using in vitro HACU as a biochemical measurement to assess the potential effect of cognitive-enhancing drugs on cholinergic neuronal activity in vivo.[3]

Study:The effect of aniracetam on cerebral glucose metabolism in rats after lesioning of the basal forebrain measured by PET.[4]
Abstract -To evaluate the effect of aniracetam, a potent modulator of the glutamatergic and cholinergic systems, on the altered cerebral glucose metabolism after lesioning of the basal forebrain, we measured the cerebral metabolic rate of glucose (CMRGlc) with positron emission tomography and the choline acetyltransferase (ChAT) activity in the frontal cortex of the lesioned rats after treating them with aniracetam. Continuous administration of aniracetam for 7 days after the surgery prevented CMRGlc reduction in the frontal cortex ipsilateral to the lesion while the lesioned rats without aniracetam showed significant CMRGlc reduction in the frontal cortex. The level of CMRGlc in the lesion-side basal forebrain was lower in all rats regardless of the aniracetam treatment. Biochemical studies showed that aniracetam did not alter the reduction in the frontal ChAT activity. These results showed that aniracetam prevents glucose metabolic reduction in the cholinergically denervated frontal cortex with little effect on the cortical cholinergic system. The present study suggested that a neurotransmitter system other than the cholinergic system, e.g. the glutamatergic system, plays a central role in the cortical metabolic recovery after lesioning of the basal forebrain.[4]


Aniracetam also increases the release of dopamine and serotonin via cholinergic mechanisms in the prefrontal cortex[5], with implications in improving judgement. This may also in part explain it's involvement as an anti-depressant.[6] Via either the same or alternate mechanisms (positive AMPA modulation) Aniracetam has also been shown to reduce impulsiveness in the rat.

Study:Aniracetam enhances cortical dopamine and serotonin release via cholinergic and glutamatergic mechanisms in SHRSP.[5]
Abstract - Aniracetam, a cognition enhancer, has been recently found to preferentially increase extracellular levels of dopamine (DA) and serotonin (5-HT) in the prefrontal cortex (PFC), basolateral amygdala and dorsal hippocampus of the mesocorticolimbic system in stroke-prone spontaneously hypertensive rats. In the present study, we aimed to identify actually active substances among aniracetam and its major metabolites and to clarify the mode of action in DA and 5-HT release in the PFC. Local perfusion of mecamylamine, a nicotinic acetylcholine (nACh) and N-methyl-D-aspartate (NMDA) receptor antagonist, into the ventral tegmental area (VTA) and dorsal raphe nucleus (DRN) completely blocked DA and 5-HT release, respectively, in the PFC elicited by orally administered aniracetam. The effects of aniracetam were mimicked by local perfusion of N-anisoyl-gamma-aminobutyric acid [corrected] (N-anisoyl-GABA), one of the major metabolites of aniracetam, into the VTA and DRN. The cortical DA release induced by N-anisoyl-GABA applied to the VTA was also completely abolished by co-perfusion of mecamylamine. Additionally, when p-anisic acid, another metabolite of aniracetam, and N-anisoyl-GABA were locally perfused into the PFC, they induced DA and 5-HT release in the same region, respectively. These results indicate that aniracetam enhances DA and 5-HT release by mainly mediating the action of N-anisoyl-GABA that targets not only somatodendritic nACh and NMDA receptors but also presynaptic nACh receptors.[5]

Study:Antidepressant activity of memory-enhancing drugs in the reduction of submissive behavior model.[6]
Abstract - The present study tests the activity of nootropic drugs in a behavioral test linked to depression. This test measures the reduction of submissive behavior in a competition test as the relative success of two food-restricted rats to gain access to a feeder. Nootropic drugs tested include piracetam (2-oxo-1-pyrrolidineacetamide), aniracetam (1-(4-methoxybenzoyl)-2-pyrrolidinone), the Ampakine, Ampalex, 1-(quinoxalin-6-ylcarbonyl)piperidine, and analogs were compared to the antidepressants, fluoxetine ((+/-)-N-methyl-gamma-(4-[trifluoromethyl]phenoxy)-benzenepropanamine) and desimpramine (5H-dibenz[b,f]azepine-5-propanamine, 10,11-dihydro-N-methyl-, monohydrochloride), while the anxiolytic diazepam (7-chloro-1-methyl-5-phenyl-3H-1,4-benzodiazepin-2(1H)-one) served as a control. Drugs were given intraperitoneally for 3 weeks. The antidepressant and nootropic drugs reduced submissive behavior over time. The effect was dose dependent as measured for fluoxetine and Ampakines. The reduction of submissive behavior by Ampakines gradually faded after cessation of treatment and had a more rapid onset of activity (during the 1st week of treatment) than fluoxetine (after 2 weeks). The results suggest that Ampakines may have antidepressant activity. The potential of depression treatment with memory-enhancing drugs is hypothesized and the link between cognition and depression is discussed.[6]

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These statements have not been evaluated by the Food & Drug Administration. This product is not approved by the FDA. This product is not intended to diagnose, treat, cure or prevent any diseases.

Keep out of the reach of children. Do not take this or any other compound if under the age of 18, pregnant or nursing a baby, or if you have any known or suspected medical conditions and/or taking prescription drug(s) or OTC medication(s). Always consult with a qualified health physician before taking any new compound.

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