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Head-to-head comparison of Fasoracetam and Nefiracetam — mechanism, side effects, legal status, and pricing.
Fasoracetam (NS-105, NFC-1) is a non-peptide racetam-class small molecule characterized as a metabotropic glutamate receptor (mGluR) activator that also modulates acetylcholine release and GABA-B signaling. A single Phase 1 trial in 30 adolescents with ADHD and mGluR-network gene variants showed clinical improvement on CGI scales, but broader development was discontinued and fasoracetam has never been approved in any jurisdiction. It is sold only as an unregulated research chemical/nootropic.
Nefiracetam is a non-peptide small molecule in the racetam (pyrrolidinone/2-oxopyrrolidine acetamide) class, investigated as a cognitive enhancer. It was never approved by the FDA, EMA, or Japan's PMDA; Daiichi Seiyaku withdrew its Japanese NDA (Translon) in February 2002 after a repeat Phase III trial in dementia failed to demonstrate efficacy. A US/Canada Phase II trial in poststroke depression (600 mg and 900 mg/day) showed no overall separation from placebo, though a subgroup analysis suggested benefit in the most severely depressed patients at 900 mg. No validated therapeutic dose or approved indication exists; it is sold by research-chemical and laboratory-reagent suppliers for research use only.
Fasoracetam
Nefiracetam
Category
Legal Status
Mechanism
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Fasoracetam
Nefiracetam
No pricing data yet.
Check Nefiracetam prices →COA corpus from Disclosed Labs — independently tested batches only.
Fasoracetam
1
COAs
99.7%
Avg purity
1
Labs
Nefiracetam
2
COAs
99.6%
Avg purity
2
Labs
Human data exist but the compound is not approved anywhere. The best-sourced human study is a completed Phase 1 open-label single-dose PK/single-blind placebo-controlled dose-escalation trial of NFC-1 (fasoracetam) in 30 adolescents (age 12–17) with ADHD carrying mGluR-network gene variants (NCT02286817; Elia et al. 2018, Nature Communications). CGI-I improved from 3.79 to 2.33 and CGI-S from 4.83 to 3.86 from baseline to week 5 (both P<0.001) in this small, largely uncontrolled sample. In rats (Wistar), fasoracetam reversed memory disruption across scopolamine-, NBM-lesion-, AF64A-, cerebral-ischemia-, baclofen-, and ECS-induced amnesia models, increased cortical acetylcholine release, and enhanced high-affinity choline uptake in cortex and hippocampus (Shirayama et al., 1999).
Human clinical data are limited and largely negative or mixed. Japanese Phase II/III trials in dementia/cognitive sequelae after cerebrovascular disorders showed improvement over placebo in some early trials, but a Ministry of Health-mandated repeat Phase III trial under revised guidelines failed to demonstrate efficacy, and Daiichi Seiyaku withdrew its Japanese NDA (Translon) in February 2002. A US/Canada multicenter randomized double-blind Phase II trial (28 sites, 1999–2001, n=159) tested nefiracetam 600 mg and 900 mg/day vs. placebo for poststroke depression; the drug did not separate from placebo overall (response >70%, remission >40% in both arms) but showed significant benefit in the most-severely-depressed subgroup at 900 mg (Robinson et al., J Neuropsychiatry Clin Neurosci 2008). A related post hoc analysis examined apathy outcomes in the same cohort. Preclinical findings include: rat cortical neurons showed potentiation of native α4β2-type nicotinic acetylcholine receptor currents via a G(s)-protein-dependent pathway; rat dorsal root ganglion neurons showed dual concentration-dependent effects on GABA_A receptor-channel currents mediated via cAMP-dependent protein kinase and Gi/Go proteins; rat neuronal preparations showed enhancement of high-voltage-activated N/L-type Ca²⁺ channel currents and modulation of NMDA receptor function via PKC-dependent phosphorylation; rat passive avoidance models showed reversal of apomorphine-induced amnesia and preservation of hippocampal NCAM-mediated memory consolidation during scopolamine disruption.
Fasoracetam and Nefiracetam are both in the Cognitive category and may have overlapping mechanisms. Researchers should review both profiles carefully, understand the mechanisms of action, and monitor the relevant biomarkers when combining compounds in the same class. As always, consult a licensed healthcare provider before making any decisions about combining research compounds.
This platform provides informational tools only, not medical advice. This comparison is for educational purposes only. Consult a licensed provider.
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