Fasoracetam
Cognition, Mood
Elimination half-life reported at 4-6.5 h in humans; 5.25 h is the midpoint.
In short
- A racetam with a genuinely distinctive mechanism — it acts on metabotropic glutamate receptors, not primarily on cholinergic pathways.
- One of the better-studied racetams: it reached phase 2 trials in adolescent ADHD with specific glutamatergic gene variants.
- Elimination half-life of roughly 4-6.5 hours in humans.
- Originally developed by Nippon Shinyaku for vascular dementia; that programme was discontinued.
- Not approved anywhere despite reaching clinical trials.
Structure
How it works
Fasoracetam upregulates metabotropic glutamate receptors, particularly group II and III mGluRs, and this is the basis for the ADHD programme — the trials specifically enrolled adolescents carrying disruptive variants in mGluR network genes, making it one of the few genuinely pharmacogenomic approaches in this space.
It also has reported effects on the cholinergic system, upregulating acetylcholine release and high-affinity choline uptake, and on GABA-B receptors, where chronic administration reportedly upregulates receptor density — the opposite of the desensitisation most GABAergic agents produce.
What the research shows
A phase 2 trial in adolescents with ADHD and mGluR network gene variants reported improvement on ADHD rating scales. The programme did not proceed to approval.
The original vascular dementia programme in Japan was discontinued after failing to demonstrate sufficient benefit.
Animal work supports antidepressant-like and anti-amnesic effects.
Reports of anxiolytic and cognitive effects in healthy people are anecdotal.
Dosing in the literature
Figures below are quoted from published studies, with the species or population they were measured in. They are records of what was studied, not recommendations.
| Studied in | Amount | Route | Source |
|---|---|---|---|
| Human — phase 2 ADHD trial in adolescents | 50–400 mg twice daily, titrated | oral | PubMed Central |
| Human — pharmacokinetics | Elimination half-life approximately 4–6.5 h | oral | PubMed |
Commonly reported ranges
These are amounts people report using. They are not from any study, have not been evaluated for safety, and are reproduced here only because they circulate widely and are better seen alongside the evidence than instead of it.
| Reported by | Amount | Route |
|---|---|---|
| Commonly reported | 10–50 mg, one to three times daily | oral or sublingual |
Note the direction: the trial doses were substantially HIGHER than typical community use, which is the opposite of the usual pattern in this library. The trials also enrolled a genetically selected population, which is not the same as the general population.
Handling and storage
Oral, as capsules or powder. Sublingual use is commonly described though comparative bioavailability data is not available.
The 4–6.5 hour half-life supports divided dosing if sustained effect is the goal.
Side effects
The phase 2 trial reported a generally acceptable safety profile in adolescents, which is real human safety data — uncommon in this section.
Community reports mention headache, fatigue, and gastrointestinal upset.
Long-term safety data does not exist. The GABA-B upregulation reported with chronic use has not been characterised for consequences on discontinuation.
Combinations
Commonly paired with a choline source (alpha-GPC, citicoline) on the reasoning that racetams increase cholinergic demand and that headache reflects choline depletion. This is a widely repeated community model rather than an established mechanism, and controlled evidence for the pairing is absent.
Research status
Developed by Nippon Shinyaku in the 1990s for vascular dementia, then licensed and taken into ADHD trials by Aevi Genomic Medicine with a pharmacogenomic enrolment strategy.
The published human literature is small but genuine, including registered trials.
Legal status
Not approved in any jurisdiction. Reached clinical trials but not approval. Sold as a research chemical or, misleadingly, as a dietary supplement in some markets — it does not meet the US definition of a dietary supplement.
WADA status
Not specifically named on the Prohibited List. Falls under WADA class S0, which prohibits any pharmacological substance not currently approved by any governmental regulatory health authority for human therapeutic use. Treat it as prohibited in sport.
Conclusion
Fasoracetam is the most clinically advanced racetam here and the one with the most interesting mechanism — the mGluR pharmacogenomic angle is genuinely novel rather than a variation on the cholinergic theme.
It is worth noting the trials enrolled adolescents selected for specific gene variants at doses higher than most people take. That is a narrower finding than "fasoracetam works".
Sources
- [1]Fasoracetam in adolescents with ADHD and mGluR gene variantsPubMed Central
- [2]Fasoracetam pharmacology — mGluR, cholinergic and GABA-B effectsPubMed
- [3]PubChem CID 198695PubChem
- [4]WADA Prohibited List (current)WADA
Track your own Fasoracetam protocol
Peppers logs your doses, models your levels from this half-life, tracks your vials and tells you when you will run out. Free on iPhone.
Reference and educational information only. Not medical advice. Nothing here diagnoses, treats, or prescribes, and nothing here is a recommendation to use any compound. The compounds described are research chemicals and are not approved for human consumption. Legal and anti-doping status change — the review date above is when these claims were last checked. Talk to a qualified clinician about anything you intend to take.