Nootropics
Evidence: animal_plus_anecdotal
Non-classical racetam that modulates all three groups of metabotropic glutamate receptors (mGluR Groups I, II, and III) and upregulates GABA-B receptors — a unique mechanism that distinguishes it from other racetams. Also enhances high-affinity choline uptake (HACU) and stimulates acetylcholine release. Does not significantly affect adrenergic, serotonergic, or dopaminergic receptors. The GABA-B upregulation is particularly notable as it may counteract GABA-B receptor downregulation caused by phenibut or baclofen tolerance.
Standard: 20-100 mg 1-3 times daily (sublingual or oral)
Maintenance: 20-50 mg twice daily
Administration: oralsublingual
Timing: Morning and afternoon. Sublingual administration may provide faster onset and higher bioavailability. With or without food.
Duration: Cycles of 4-8 weeks on, 2-4 weeks off. Limited long-term safety data.
One of the most pharmacologically interesting racetams due to its unique mGluR modulation and GABA-B upregulation properties. The Elia et al. 2018 trial in Nature Communications showed significant symptom improvement in ADHD adolescents with mGluR gene variants — but this represents roughly 10% of ADHD cases, and fasoracetam is likely ineffective in the other 90%. The GABA-B upregulation property has made it popular in the nootropic community for recovering from phenibut tolerance/dependence, though this use is entirely anecdotal. The original Phase 3 trial for vascular dementia failed to meet endpoints, which is why Nippon Shinyaku abandoned it. Evidence base is thin — one small ADHD trial and animal data. Mechanism is promising but clinical validation is insufficient.
Research chemical — no pharmaceutical-grade product exists. Originally developed by Nippon Shinyaku as NS-105 for vascular dementia (shelved after Phase 3 failure in Japan). Licensed to Aevi Technologies (now NFC-1) for ADHD trials. Available from nootropic vendors — demand CoA with HPLC purity >98%. Low doses make purity especially critical.
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