Fasoracetam

Overview

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.

Mechanism of Action

Fasoracetam is characterized in the human trial literature and rodent pharmacology as a metabotropic glutamate receptor (mGluR) activator/modulator rather than a classical ionotropic glutamate agent. Rodent studies (Shirayama et al., 1999) demonstrated that it increases acetylcholine release in the cerebral cortex, enhances high-affinity choline uptake in cortex and hippocampus without changing choline acetyltransferase activity, and reverses memory disruption induced by the GABA-B agonist baclofen—suggesting a dual mechanism of facilitating cholinergic neurotransmission and suppressing GABA-B-receptor-mediated responses. No receptor-binding affinity (Ki/EC50) data for specific mGluR subtypes have been located in primary sources.

Research Summary

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).

Vendors selling Fasoracetam

Scored vendors carrying Fasoracetam, ranked by trust grade. Grades are computed from indexed Certificates of Analysis. Full $/mg pricing is on the comparison page.

Reported Side Effects

• Headache (63.3% in NCT02286817 trial)
• Fatigue (36.7% in NCT02286817 trial)
• Three serious adverse events in trial (assessed as unrelated to study drug)
• No established human safety profile beyond small trial populations
• Gray-market material carries unverified purity/identity risks

Compare Fasoracetam with Others

Research References

• Fasoracetam compound record, CID 198695.
• Fasoracetam in adolescents with ADHD and glutamatergic gene network variants disrupting mGluR neurotransmitter signaling. 2018. PMID 29339723.
• Involvement of cholinergic and GABAergic systems in the reversal of memory disruption by NS-105, a cognition enhancer. 1999. PMID 10494996.
• ClinicalTrials.gov record NCT02286817 (Phase 1 PK / dose-escalation study of NFC-1 in adolescents with ADHD).

Frequently asked questions

Has Fasoracetam been independently lab-tested?

Disclosed Labs has collected 1 Certificate of Analysis (COA) for Fasoracetam from 1 independent testing lab. 1 vendor has submitted material for testing. Products average 99.7% tested purity across the corpus. Full testing data is available at https://www.disclosedlabs.com/peptides/fasoracetam/testing.

Where can researchers source Fasoracetam?

1 vendor with Disclosed Labs trust grades currently list Fasoracetam, including Kimera Chems. Compare live prices and lab-verified COAs at https://www.disclosedlabs.com/prices/fasoracetam.

How does Fasoracetam work?

Fasoracetam is characterized in the human trial literature and rodent pharmacology as a metabotropic glutamate receptor (mGluR) activator/modulator rather than a classical ionotropic glutamate agent. Rodent studies (Shirayama et al., 1999) demonstrated that it increases acetylcholine release in the cerebral cortex, enhances high-affinity choline uptake in cortex and hippocampus without changing choline acetyltransferase activity, and reverses memory disruption induced by the GABA-B agonist baclofen—suggesting a dual mechanism of facilitating cholinergic neurotransmission and suppressing GABA-B-receptor-mediated responses. No receptor-binding affinity (Ki/EC50) data for specific mGluR subtypes have been located in primary sources.

What does the research say about Fasoracetam?

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).