Fasoracetam – Review of Benefits, How it works, Side effects, Dosage

Last updated on October 13th, 2016 at 02:18 am

Fasoracetam is a nootropic of the racetam-class family. It has been shown to reduce ADHD symptoms and is currently undergoing a clinical trial for the treatment of ADHD.

Also Known AsNS-105, NFC-1, (+)-5-oxo-d-prolinepiperidinamide monohydrate
Main benefits
  • Decreases ADHD symptoms in adolescents
  • Improves memory and learning in rats
  • Prevents memory impairments by baclofen in rats
  • Acts as an antidepressant in rats
Synergistic with
  • Possibly antidepressants
  • Possibly stimulants for ADHD
Does not go well with
  • Forskolin – The cAMP increase is inhibited by fasoracetam in rats
How to takeOrally, in the morning with food.
Typical dose50 mg twice a day
Best takenChronically
Half-lifeAbout 1 hour in animals – see below
Mechanism of actionIncreases glutamate activity
Upregulates GABAB receptors
Increases acetylcholine release and synthesis
Where to BuyNootropics Depot – Bulk powder and capsules


Fasoracetam appears to improve the symptoms of ADHD in adolescents. It decreases depression in rats with similar efficacy of desipramine, prevents amnesia in rats with cholinergic dysfunction and reverses memory impairments caused by baclofen.

The few studies thus far show its mechanism of action includes increasing glutamate activity, upregulating GABAB receptors and increasing acetylcholine release and synthesis.


Summary of benefits

ADHDSignificant decrease in symptoms with stronger effects the longer it was taken50 - 500 mg twice a dayAdolescents with ADHD and a gene variant of the glutamate receptor
Memory and learningImproved memory

Reversed memory disruptions caused by baclofen
10 mg/kg (rats)Rats
DepressionStrong decrease comparable to desipramine1-100 mg/kg (rats)Rats

Attention deficit hyperactivity disorder (ADHD)

In a study involving 30 adolescents, 29 of which completed it, there was a significant decrease in ADHD symptoms and subsequently Vanderbilt scores, which measures ADHD symptoms. Mean scores at week 1 were 29.1 which decreased to 22.5 by week 5. Doses started at 50 mg twice a day at week 1 and increased weekly to a maximum of 500 mg twice a day at week 5. ADHD symptoms improved at week 2 of the study and continued improving until the end of the study of week 5.[1]

Graph showing fasoracetam improves ADHD Symptoms
Weekly improvements in ADHD symptoms following fasoracetam treatment (source)


In rats, fasoracetam demonstrates a potent antidepressant effect comparable to that of desipramine.[2]

Memory and learning

Fasoracetam exhibits antiamnesic properties in rats with cholinergic dysfunction and reverses the memory disruptions caused by baclofen.[3]


Schizophrenia is purported to be associated with hypoglutamatergic activity.[4] Fasoracetam was found to reduce ADHD symptoms in adolescents with low glutamate neurotransmission.[1] Extrapolating these results, it seems likely that it may also benefit patients with schizophrenia. However, no studies have been done to assess this hypothesis.

Mechanism of action



In the ADHD population, there is a significantly higher copy-number variant(duplication of a gene) affecting the metabotropic glutamate receptors genes resulting in hypoglutamatergic activity.[5] Fasoracetam is purported to increase glutamatergic activity and was found to significantly reduce the symptoms of ADHD in adolescents.[1]

Animals and lab studies

AcetylcholineIncreased levelsIncreased release and synthesisImproved memoryRats with choline dysfunction
DopamineNo changeNoneNoneRats
Noradrenaline and adrenalineNo changeNoneNoneRats
GABAPossible increase in activityUpregulation of GABAB receptors
  • Decreased in depression

  • Reversal of baclofen-induced memory impairments
GlutamateIncreased activityUnknownPossible decrease in ADHD symptomsRats


In the cerebral cortex and the hippocampus, fasoracetam increases high affinity choline uptake (HACU) which increases acetylcholine synthesis. Additionally, there is an increase in acetylcholine release in the cerebral cortex.[3]

Dopamine and noradrenaline

It appears fasoracetam does not alter dopamine, noradrenaline and adrenaline levels nor does it bind to the beta-adrenoreceptors.[2]


Fasoracetam binds to the GABAB receptor in rats effectively blocking the memory disruptions caused by baclofen. However, it’s unclear whether it activates the receptor (agonist), blocks it (antagonist), or acts in a more complex-manner, i.e. partial-agonist or inverse agonist.[3]

Regardless, it appears to upregulate the GABAB receptors in the cerebral cortex of rats which may contribute to its antidepressant effect.[2]


In the rat brain, fasoracetam inhibits forskolin-induced cAMP formation in the cerebral cortex by stimulating the metabotropic glutamate receptors.[6][7][8]


No change was seen in serotonin levels in rats. Likewise, it did not appear to bind to the 5-HT2 receptor.[2]


In humans, a 100 mg tablet takes about 1.3 hours in young adults and about 2.1 hours in the elderly to reach maximum blood concentration.[9]

The half-life of fasoracetam varies depending on the species; 0.67 hours for rats, 2.1 hours for dogs, and 1.3 hours for monkeys. Its bioavailability was quite high due to a combination of a lack of first-pass metabolism and great absorption by the small intestine; 97% in rats, 90% in dogs, and 79% in monkeys. Oral bioavailability was comparable to that of intravenous. About 90% of fasoracetam is excreted unchanged in the urine of rats and monkeys with 60% for dogs.[10]

Chronic administration in rats does not affect liver drug-metabolizing enzymes.[11]


Fasoracetam may synergize well with antidepressants and ADHD medications. It appears to have a unique mechanism of action that greatly differs from that of traditional pharmaceutical medications. Because of this, it should not interact with them, but rather enhance their effects.

Side effects

In a small study involving adolescents with ADHD[1], the most common side effects were mild in nature and included:

  • Headache – 63.3% of subjects
  • Fatigue – 36.7%
  • Upper abdominal pain – 26.7%
  • Diarrhea – 23.3%
  • Irritability – 20%

However, it was not a double-blind study and as such there was no placebo-group to compare the side effects with. The researchers also noted that the side effects were not related to fasoracetam.


In a study involving 30 adolescents, fasoracetam was found to be safe and well-tolerated.[1]


  1. Jones, Grace. “Exploratory dose-escalation study of NFC-1 in ADHD adolescents with glutamatergic gene network variants.” 62nd Annual Meeting. AACAP, 2015.
  2. Shimidzu, Takako et al. “Effect of a Novel Cognition Enhancer NS-105 on Learned Helplessness in Rats: Possible Involvement of GABAB Receptor up-Regulation after Repeated Treatment.” European Journal of Pharmacology, vol. 338, no. 3, 1997, pp. 225–232. doi:10.1016/s0014-2999(97)81925-5.
  3. Ogasawara, Takashi et al. “Involvement of Cholinergic and GABAergic Systems in the Reversal of Memory Disruption by NS-105, a Cognition Enhancer.” Pharmacology Biochemistry and Behavior, vol. 64, no. 1, 1999, pp. 41–52. doi:10.1016/s0091-3057(99)00108-2.
  4. Itokawa, M., and T. Yoshikawa. “[Hypoglutamatergic hypothesis of schizophrenia: evidence from genetic studies].” Seishin shinkeigaku zasshi= Psychiatria et neurologia Japonica 105.11 (2002): 1349-1362.
  5. Elia, Josephine et al. “Genome-Wide Copy Number Variation Study Associates Metabotropic Glutamate Receptor Gene Networks with Attention Deficit Hyperactivity Disorder.” Nature Genetics, vol. 44, no. 1, Apr. 2011, pp. 78–84. doi:10.1038/ng.1013.
  6. Oka, Michiko et al. “Involvement of Metabotropic Glutamate Receptors in Gi- and Gs-Dependent Modulation of Adenylate Cyclase Activity Induced by a Novel Cognition Enhancer NS-105 in Rat Brain.” Brain Research, vol. 754, no. 1-2, 1997, pp. 121–130. doi:10.1016/s0006-8993(97)00064-4.
  7. Oka, Michiko et al. “A Novel Cognition Enhancer NS-105 Modulates Adenylate Cyclase Activity through Metabotropic Glutamate Receptors in Primary Neuronal Culture.” Naunyn-Schmiedeberg’s Archives of Pharmacology Naunyn-Schmiedeberg’s Arch Pharmacol, vol. 356, no. 2, 1997, pp. 189–196. doi:10.1007/pl00005040.
  8. Hirouchi, Masaaki et al. “Role of Metabotropic Glutamate Receptor Subclasses in Modulation of Adenylyl Cyclase Activity by a Nootropic NS-105.” European Journal of Pharmacology, vol. 387, no. 1, 2000, pp. 9–17. doi:10.1016/s0014-2999(99)00785-2.
  9. Kumagai, Y., et al. “Comparison of pharmacokinetics of NS-105, a novel agent for cerebrovascular disease, in elderly and young subjects.”International journal of clinical pharmacology research 19.1 (1998): 1-8.
  10. Mukai, Hideya, et al. “Pharmacokinetics of NS-105, a Novel Cognition Enhancer.” Arzneimittelforschung 49.11 (1999): 881-890.
  11. Mukai H, Sugimoto T, Ago M, Morino A, Takaichi M, Ogawa Y, Seki H, Matsuura C, Esumi Y. Pharmacokinetics of NS-105, a novel cognition enhancer. 2nd communication: distribution and transfer into fetus and milk after single administration, and effects of repeated administration on pharmacokinetics and hepatic drug-metabolizing enzyme activities in rats. Arzneimittelforschung. 1999 Dec;49(12):977-85. PubMed PMID: 10635441.

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