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Nefiracetam n-(2,6-dimethylphenyl)-2-oxo-1-pyrrolidineacetamide 77191-36-7
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Nefiracetam is a nootropic cognitive enhancer of the racetam family with similarities to Aniracetam. It seems to enhance both GABAergic and cholinergic signalling, and long term usage appears to be both neuroprotective and Nootropic. Nefiracetam’s cytoprotective actions are mediated by enhancement of GABAergic, cholinergic, and monoaminergic neuronal systems.
Nefiracetam was derived initially from the parent molecule Piracetam but it shares more structural similarity to Aniracetam. Both nefiracetam and aniracetam are fat soluble racetam compounds used for the purpose of memory enhancement or the treatment of cognitive decline.
ITEM |
STANDARD |
RESULTS |
Appearance |
White to off white crystalline powder |
Comply |
Melting point |
166-170°C |
167.3-168.1°C |
Identification |
Positive reaction |
Positive reaction |
Related substances |
≤1.0% |
0.16% |
Loss on drying |
≤0.5% |
0.06% |
Residue on ignition |
≤0.1% |
0.02% |
Chloride |
≤0.014% |
<0.014 |
Heavy Metals |
≤20ppm |
<20ppm |
Clarity of solution |
Conform to standard |
Complies |
Microbial Limit |
≤20ppm |
<20ppm |
Assay |
≥99.0% |
99.52% |
Nefiracetam appears to be able to increase memory formation when taken daily over a prolonged period of time (7 days or longer), which has been repeatedly shown in animal studies with some human evidence suggesting the same. Prolonged supplementation is also associated with a higher rate of neurogenesis (the process by which neurons are generated from neural stem and progenitor cells) which is not seen acutely.
The mechanisms of nefiracetam seem to be linked back to two pathways. One of these pathways is prolonging the opening of calcium channels (tied into PKA and a Gi/o protein) which enhances signalling of a receptor independent of the synapse, and the other pathway seems to be tied into PKC and CAMKII which then augments signalling through cholinergic receptors (which then releases most excitatory neurotransmitters from the presynaptic level in a manner similar to Nicotine).
The former pathway (calcium channels) appears to be critical for long-term potentiation, whereas the latter pathway (PKC/CAMKII) appears to be vital for neuronal signal enhancement.
Some other minor pathways include being a partial agonist at the Glycine binding site of the NDMA receptor (may enhance signalling when there are subpar levels of glycine, but attenuates excessive signalling) and increasing affinity of the muscarinic acetylcholine receptors for its ligand, acetylcholine.
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