Fasoracetam Nootropics Racetams Reviews

Fasoracetam: How This Nootropic May Help You Focus Better

Originally known as NS-105, Fasoracetam is one of the newest nootropics on the market. Besides being the latest racetam to be discovered, it has some unique properties unlike any other racetam on the market. Let’s find out what makes this substance a truly unique nootropic, and why you should (or should not) try it.

One of the primary effects of Fasoracetam is the modulation of metabotropic glutamate receptors II and III (mGluR).[1] mGlu receptors have been shown to be involved in synaptic plasticity and neuroprotection. In addition, LY354740, am mGlu2/3 agonist, has been shown to be effective in generalized anxiety disorder.[2]

Fasoracetam is also the only racetam that significantly enhances cAMP formation[3] and that has been shown to be potentially effective in individuals with glutamatergic gene variants that are suffering from ADHD[4]. A Phase III clinical trial is near completion, but the drug is not currently listed as an ADHD treatment by the FDA.

Fasoracetam has also shown to have antidepressant effects[5] and to counteract learned helplessness, an avoidance behavior typically associated with depression. Fasoracetam, however, does not act on serotonin and other monoamines, and researchers think the antidepressant effect may stem from its ability to upregulate GABA-B receptors.[6]

Generally speaking, Fasoracetam has shown to be more effective with chronic use, and, in the ADHD study, most benefits were felt at week five onward.[7]
Fasoracetam ADHD

Mechanism of Action

In rat studies, fasoracetam restores the function of key receptors, glutamate mGluR II and III[8].  It also upregulates GABA-B receptors through receptor antagonism[9], a fact which may be related to its ability to reverse phenibut tolerance (which is one of the few supplements reported to relieve anhedonic depression). The GABA-B receptor is very important and has been found to play a role in cognition[10], anxiety and mood.

Alcohol, a very disinhibiting and fog-inducing compound (with pleasurable effects similar to phenibut) is thought to achieve its activity by activating GABA-B and A receptors (as well as dopamine).  However, because it downregulates these receptors, prolonged use may cause anxiety and cognitive disruptions.  Phenibut binds in a similar fashion to GABA-B.

FasoracetamBecause of its relatively narrow range of receptor targets, fasoracetam does not feel like a classic stimulant nor does it alter one’s feeling of wakefulness.  It lacks clinical dopamine activity but remarkably still managed to address ADHD symptoms, according to the study.  It is not clear how fasoracetam has such a specific utility in treating ADHD, more research on other neurotransmitters may be turned up in coming years, but judging on present evidence, it seems that Fasoracetam could reduce ADHD symptoms by modulating glutamatergic receptors.

That being said, the FDA does not list Fasoracetam as an ADHD medication and it should not be used as such. Only a professional can prescribe medications for ADHD and you should not self medicate.

Although it is a newer supplement without much of a user-base, it does appear to be well-tolerated even in large doses or extended periods. Among college students, it may soon become a mainstay, alongside other trusted nootropics such as Bacopa, Modafinil, and Noopept.


In addition to the findings surrounding glutamate and ADHD, rat studies have also revealed fasoracetam to have profound cholinergic activity.  Many common nootropics work by controlling acetylcholine, including several drugs used in the treatment of Alzheimer’s.

It increases the uptake of choline at sites in key brain regions involved in intelligence and mood, the hippocampus and cerebral cortex.  This, in turn, results in increased production and release of acetylcholine.[11]
This, similarly to what has been commonly reported with piracetam, may explain a need for choline supplementation in the case of symptoms such as low mood, headache or brain-fog.

Although I personally have only ever tried piracetam and aniracetam (and found, despite a slight cognitive boost, that they both caused a slightly lowered mood, with piracetam being more stimulating and anxiety-prone while aniracetam was calm and relaxing), I haven’t read any complaints of fasoracetam and depression (on the contrary it appears to be a robust antidepressant nootropic, similar to tianeptine). This is remarkable because excessive acetylcholine production is typically associated with low mood and depression. Even with something as mild as bacopa, reports of moodiness are easy to pin down.

Since all three of the mentioned racetams seem to operate through a shared mechanism of acetylcholine, it’s not clear how fasoracetam achieves a similar cognitive boost without side effects on mood.  Perhaps it has been less trialed and as more users sample it, more negative reports will pour in.  This seems unlikely, however, given multiple reports of antidepressant effects, and at higher doses, near euphoria.

Fasoracetam and coluracetam are interesting racetams with multiple mechanisms of action compared to piracetam. Although they both share a cholinergic effect, the former modulates mGlu receptors (as well as GABA-B receptors) while the latter interacts with a process named high-affinity choline uptake.  This may explain their calm, clear effects when compared with the more bland effects of piracetam.


Of the eight known metabotropic glutamate receptors, only one and five are believed to increase NMDA receptor activity and neural excitation (these two are postsynaptic).  The other six receptors all function to lower NMDA (and are presynaptic), lessen excitation and thus reduce potential neurotoxicity.

By slightly lowering glutamate activity and at the same time boosting GABA-B levels, fasoracetam offers a collected state of mind compared to piracetam’s more scattered one.  Normal tasks would flow much easier, and performance would be improved without adverse effect.
While OCD and more recently schizophrenia have been described as hyperglutamatergic, ADHD has always been thought of as a condition of low glutamate.[12]

However, fasoracetam may very well regulate the metabotropic receptors in both directions and benefit everyone equally (restoring both high and low activity of the receptors to normal).

It is not clear how to explain the remarkable improvements reported in samples of both schizophrenia and ADHD. An explanation may be the selectiveness for the presynaptic mGluRs (mGluR1 and mGluR5) coupled with the fact that these receptors both elevate cAMP and lower NMDA activity. Levels of these receptors in the body are both altered in schizophrenia (so fasoracetam would produce two favorable alterations for the schizophrenic patient).

Despite all this fine talk about schizophrenia and glutamate, most of the reports surrounding fasoracetam are concerned with ADHD symptoms, specifically motivation and focus.  It is not widely known for its use as psychiatric medicine, and it may be considered by ADHD patients who have not responded well to conventional treatments. Again, it is not approved by the FDA as an ADHD treatment, and we are not suggesting people suffering from that disease to use it without a medical prescription.


As stated above fasoracetam appears to have GABA-B antagonistic properties[13], and it may upregulate these receptors and thus diminish the tolerance to GABA-B agonists like Phenibut, Baclofen, and Alcohol, and may even act as an “antidote” to a Phenibut overdose.

Before many of the newer designer supplements hit the market and much was known about fasoracetam, Noopept was one of the more recommended supplements for alcoholics to recover cognitive capacities. But in light of this newer evidence, fasoracetam may address the issue more directly. Because of its activity here, fasoracetam may eventually find use in treating age-related memory decline, dementia, and even depression. For now, the research and hype seem to surround the potential treatment of ADHD symptoms.

Dosage and half-life

Buy Fasoracetam CapsulesNo dependence potential was noted in the rhesus monkey over the course of four weeks.[14]  However. users cannot be completely absolved of concern, due to interspecies differences and the possibility of an only mildly addictive substance requiring an exceptionally long habituation period.

If its use is not completely discouraged in elderly patients, significant caution and close monitoring are recommended.  Its metabolism and clearance depend heavily on the kidneys and at least one studied has reported significant accumulation in the elderly (whose renal function is typically compromised).[15]

It is typically taken at 10mg twice daily, but it is probably best to start with 5 mg and taper up. Even though the dosage is very low, bitterness is still a problem and the use of capsules or parachuting is recommended.

Although some work their way up to 30 mg in one dose, this may not be the most effective strategy (due to a short half-life of the compound) and this pattern of use is more likely to be helped along by a large meal.  A potent nootropic with a half-life of around 90 minutes, taking it even once a day may be enough for active levels to build up in your system, but tolerance will be close behind.

You can buy Fasoracetam capsules and powder at Nootropics Depot. Fasoracetam is not approved by the FDA as an ADHD treatment.

Reviewer 8.8

References   [ + ]


The 14 Best Nootropics for Anxiety

As we collect evidence provided to us by our ever-expanding group, we’ve come up with a few good remedies. Anxiolytic drugs are known to “relieve anxiety”.[1] Many of us suffer from anxiety ranging from slight to severe impairment. It is wise to note that some drugs, such as Bacopa, have enhanced efficacy after chronic administration.[2] Others, such as Tenoten, are applied sublingually and can be used to treat acute anxiety.[3] Any of the information here is not to be used or substituted for medical advice.


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Bacopa monnieri nootropics for anxiety
Bacopa monnieri

Bacopa monnieri (also known as Brahmi) is one of the most important herbs in Ayurvedic medicine. It has been used for centuries as a mental tonic originating in India.

Bacopa has been shown in studies to relieve anxiety, improve cognition, and enhance memory formation.[4] [5] In a rat study, Bacopa increased the levels of serotonin and enhanced the gene expression of serotonin transporters[6]. Studies have shown a relationship between high levels of serotonin and positive mood.[7] [8]

Bacopa also appears to have an adaptogenic effect by reducing the biochemical effects of stress.[9]

To fully appreciate the positive effects of Bacopa, it needs to be taken consistently. Studies have shown more improvement as time passes. [10]


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Withania somnifera, commonly known as Ashwagandha, is a popular herb used in Ayurvedic medicine. In Sanskrit, Ashwagandha means “the smell of a horse”, because of its unmistakable smell. It is also believed to give vitality and the “strength of a stallion”.

Ashwagandha is believed to act as a neuroprotector, anxiolytic, anti-inflammatory, thyroid-booster, and libido enhancer.

Ashwagandha activates GABA-A receptors, the mechanism of action responsible for its anxiolytic and sleep-inducing effects.[11]

It has been shown to be as effective as fluoxetine for obsessive-compulsive disorder (OCD) in a mice study.[12]


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Matcha is a Japanese green tea with a very high Theanine content

L-Theanine is a natural amino acid contained in green tea. Most store-bought teas contain minimal amounts of L-Theanine, however, concentrations are greater in teas such as matcha, gyokuro, and kabusecha.

L-Theanine is structurally similar the neurotransmitters glutamate and GABA.[13] L-Theanine is also a neuroprotective agent[14] which increases the amounts of serotonin, dopamine, and GABA in various areas of the brain.[15] It’s commonly used with stimulants, — like caffeine or amphetamines —, to reduce side effects, but it is also effective by itself.


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Inositol is a sugar involved in cellular signaling and as a component of cell membranes. There are nine different inositol molecules. The most abundant of these being myo-inositol.

Inositol was once considered a B vitamin (formerly Vitamin B8). It was later found to be producible by the human body, disproving it as an essential nutrient. It is naturally found in small quantities in milk products, fruits, and vegetables.

Research shows high dose Inositol supplementation (18 g) was as effective as fluvoxamine (150 mg) in decreasing the number of panic attacks[16] and reducing the symptoms of obsessive-compulsive disorder (OCD). [17]


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Phenibut is a gamma-aminobutyric acid (GABA) derivative.

GABA is the major inhibitory neurotransmitter in the brain. The mechanism of action of conventional anxiolytics, hypnotics, and sedatives (such as benzodiazepines, barbiturates, and alcohol) increase GABA levels. This is what gives them anti-anxiety, sleep-inducing, tranquilizing, and anticonvulsive effects.

Phenibut was developed in the Soviet Union in the 1960s as a non-sedative alternative to benzodiazepines. Phenibut is part of the Russian cosmonaut medical kit as a treatment for stress.

Phenibut activates GABA-B receptors[18] and boosts dopamine levels.[19]


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Picamilon is another Russian nootropic made by combining niacin (vitamin B3) and GABA. This allows Picamilon to cross the blood–brain barrier[20] and have anxiolytic and vasodilating[21] effects.

It is used in Russia as a treatment for anxiety, depression[22], alcoholism[23], and brain damage.[24]


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Aniracetam (known as Ampamet in Europe) is a compound of Racetam family. It is a fat-soluble derivative of Piracetam.

Aniracetam modulates AMPA receptors. AMPA is one of the main three excitatory neurotransmitters (the other two being NMDA and kainate receptors). Compounds that act on AMPA receptors are called AMPAkines.

AMPAkines are substances which exhibit neuroprotective and cognition enhancing effects[25]. Some of these have been investigated as treatment for Alzheimer’s disease and other neurodegenerative conditions[26]. Aniracetam is also a potential anxiolytic[27] and antidepressant.[28] Anecdotal evidence states that Aniracetam is effective in some individuals, while others are non-responders.


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Coluracetam is a relatively new Japanese nootropic drug with little clinical backing. Unlike Piracetam, Coluracetam directly affects High Affinity Choline Uptake.[29] It was shelved after failing to demonstrate efficacy for Alzheimer’s.

Phase IIa clinical trials have demonstrated efficacy for comorbid MDD with GAD (Generalized Anxiety Disorder).

Anecdotal reports state Coluracetam is responsible for a sensation of “HD Vision” as well as lowered anxiety.


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Fasoracetam, a novel nootropic
Fasoracetam, a potent and novel nootropic which shows promise to relieve anxiety, as well as reduce ADHD symptoms.

Fasoracetam, also referred to as NS-105, is a novel cognitive enhancer. Fasoracetam is a high-affinity choline reuptake inhibitor, similar to Coluracetam.[30] Many refer to this particular mechanism of action as “HD vision”.

Fasoracetam can act as a sustainable anxiolytic since long-term administration upregulates GABA-B receptors.[31] Anecdotal reports have noted both acute and chronic anxiolytic effects.

Treatment of ADHD, by NS-105, is mediated through modulation of mGluR glutamate receptors.[32] In other words, those suffering from ADHD and/or anxiety may benefit from Fasoracetam’s purported effects.


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Tianeptine is a tricyclic antidepressant (TCA) developed in France circa 1960. Tianeptine embodies a unique mechanism of action, unlike other TCAs.

Tianeptine was originally believed to be a Serotonin Reuptake Enhancer. Recent research suggests its antidepressant effect is due to the activation of μ-opioid and δ-opioid receptors[33] as well as modulation of AMPA and NMDA receptors.[34]

Tianeptine efficacy is comparable to fluoxetine, amitriptyline, and imipramine (with significantly fewer side effects).[35]


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Tenoten is a simultaneous nootropic and anxiolytic with novel properties. Unlike GABA agonists, Tenoten treats anxiety “based on antibodies to the brain-specific protein S-100B”.[36]

“Testing at the Russian Institute of Molecular Biology and Biophysics indicate Tenoten was as clinically effective as amitryptiline (Elavil), sertraline (Zoloft), and phenazepam (a benzodiazepine) for the reduction of anxiety but without sedation. It further recommended Tenoten for patients with moderate cognitive impairment”.[37]

“[Tenoten] demonstrated considerable improvement of the control over brain frontal compartment effector functions”.[38]

In a small trial group of 50 children, Tenoten showed efficacy for the treatment of ADHD symptoms.[39]


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Selank, is an analog of the endogenous peptide tuftsin. Since tuftsin has innate immunomodulatory capabilities, Selank is also able to regulate T cell cytokines.[40] In this way, Selank can be seen as having immunomodulatory properties.

Unlike common anxiolytics, Selank does not cause sedation or cognitive impairment. It is non-habit forming and does not cause withdrawal symptoms.

Selank modulates monoamine transmitters[41] and catalyzes the metabolism of serotonin.[42] Selank causes rapid elevation of BDNF, solidifying its place as a cognitive enhancer.[43]

Although Selank’s mechanism of action is largely misunderstood, evidence suggests it lowers levels of tau(1/2) leu-enkephalin.[44]


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Afobazole (also known by its scientific name Fabomotizole) is a Russian anxiolytic drug which does not possess sedative properties unlike most anxiolytics. Afobazole, similar to Fasoracetam, upregulates GABA receptors.[45] Afobazole restores GABA to healthy levels following ischemia.[46] This is widely regarded to be Afobazoles main anxiolytic mechanism of action.

Fabomotizole also induces BDNF and NGF release, agonizes MT3 receptors, and reversibly inhibits MAO-A [47] [48] [49] [50] [51]. Since Afobazole directly effects BDNF and NGF, it is also classified as a nootropic. Caution should be taken when combining Afobazole with other MAO inhibiting substances. Afobazole may also have an antidepressant effect.


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Kava is a GABAergic drug which affects the GABA-A receptor in several ways. Kava exhibits reverse tolerance. It is a less-harmful alternative to common GABA-A benzodiazepine receptor agonists. The alkaloids chiefly responsible for Kava’s mechanism of action are called kavalactones.[52] It is becoming apparent that although Kava is confirmed to modulate GABA-A receptors, it may do so in a different method than direct agonism.[53] It appears Kava potentiates GABA-A through poorly understood means.[54] GABA-A receptor density increased following administration of Kava, suggesting both upregulating and sensitizing properties.[55]

A common concern for Kava usage lies in its purported hepatotoxicity. Hepatotoxicity of Kava is a direct result of the extract or plant matter obtained, suggesting quality is paramount to avoiding liver damage. “Risk factors included overdose, prolonged treatment, and comedication with synthetic drugs and dietary supplements”.[56] Indigenous tribes have been using Kava for centuries, with minimal consequences. One can assume toxicity is directly affected by the quality of the plant used.

Most, but not all, of clinical studies, have demonstrated Kava’s efficacy as an anxiolytic. Standardized extract demonstrated the highest efficacy versus placebo. 1 week of chronic administration may be necessary to feel its effects. Evidence suggests Kava may aid in the treatment of insomnia and sleeplessness.[57]

References   [ + ]

1. Definition of anxiolytic by Merriam-Webster
2, 10. Enhanced dendritic arborization of hippocampal CA3 neurons by Bacopa monniera extract treatment in adult rats.
3. The use of tenoten and tenoten (pediatric formulation) as a drug for premedication in adults and children during outpatients dentist visit.
4. Randomized controlled trial of standardized Bacopa monniera extract in age-associated memory impairment.
5. Bacopa monniera, a reputed nootropic plant: an overview.
6. Bacopa monniera leaf extract up-regulates tryptophan hydroxylase (TPH2) and serotonin transporter (SERT) expression: implications in memory formation.
7. Associations between whole-blood serotonin and subjective mood in healthy male volunteers.
8. Serotonergic function in the central nervous system is associated with daily ratings of positive mood.
9. Adaptogenic effect of Bacopa monniera (Brahmi).
11. Pharmacological effects of Withania somnifera root extract on GABAA receptor complex.
12. Influence of Withania somnifera on obsessive compulsive disorder in mice.
13, 14. Neuroprotective effects of theanine and its preventive effects on cognitive dysfunction
15. The neuropharmacology of L-theanine(N-ethyl-L-glutamine): a possible neuroprotective and cognitive enhancing agent.
16. Double-blind, controlled, crossover trial of inositol versus fluvoxamine for the treatment of panic disorder.
17. Inositol treatment of obsessive-compulsive disorder.
18. On neurotransmitter mechanisms of reinforcement and internal inhibition.
19. Phenibut (beta-phenyl-GABA): a tranquilizer and nootropic drug.
20. Pikamilon pharmacokinetics in animals.
21. The new cerebrovascular preparation pikamilon.
22. The results of clinical study of the drug Picamilon (analysis of data of neurologic and psychiatric clinics) – AP Huaichenko, RP Kruglikova-Lvova
23. Picamilon Application in Therapy of Patients with Alcoholism, – Novikov VE, Kovaleva LA
24. Picamilon Application in the Complex of Regenerative Therapy of Patients after Insultus
25. AMPA receptor potentiators for the treatment of CNS disorders.
26. Benzofurazan compounds which enhance AMPA receptor activity
27. Anxiolytic effects of aniracetam in three different mouse models of anxiety and the underlying mechanism.
28. Antidepressant-like effects of aniracetam in aged rats and its mode of action.
29. MKC-231, a choline uptake enhancer, ameliorates working memory deficits and decreased hippocampal acetylcholine induced by ethylcholine aziridinium ion in mice
30. Involvement of cholinergic and GABAergic systems in the reversal of memory disruption by NS-105, a cognition enhancer.
31. Effect of a novel cognition enhancer NS-105 on learned helplessness in rats: possible involvement of GABA(B) receptor up-regulation after repeated treatment.
32. A novel cognition enhancer NS-105 modulates adenylate cyclase activity through metabotropic glutamate receptors in primary neuronal culture.
33. The atypical antidepressant and neurorestorative agent tianeptine is a μ-opioid receptor agonist.
34. The neurobiological properties of Tianeptine (Stablon): from monoamine hypothesis to glutamatergic modulation
35. Tianeptine: a review of its use in depressive disorders.
36, 37, 38. Tenoten in the therapy of patients with moderate cognitive impairment.
39. Clinical efficacy of tenoten for children in treatment of attention deficit and hyperactivity disorder
40. Immunomodulatory effects of selank in patients with anxiety-asthenic disorders
41. Effects of heptapeptide selank on the content of monoamines and their metabolites in the brain of BALB/C and C57Bl/6 mice: a comparative study
42. Comparison of the effects of selank and tuftsin on the metabolism of serotonin in the brain of rats pretreated with PCPA
43. Intranasal administration of the peptide Selank regulates BDNF expression in the rat hippocampus in vivo.
44. Efficacy and possible mechanisms of action of a new peptide anxiolytic selank in the therapy of generalized anxiety disorders and neurasthenia
45, 46. Effects of afobazole on the content of neurotransmitter amino acids in the striatum in global transient ischemia.
47. Clinical study of the selective anxiolytic agent afobazol
48. Gabaergic mechanism of cerebrovascular and neuroprotective effects of afobazole and picamilon
49. Effects of afobazole on the BDNF content in brain structures of inbred mice with different phenotypes of emotional stress reaction
50. Selective anxiolytic afobazole increases the content of BDNF and NGF in cultured hippocampal HT-22 line neurons
51. Interaction of afobazole with sigma1-receptors
52, 57. Kava kava | University of Maryland Medical Center
53, 54, 55. Kavapyrone enriched extract from Piper methysticum as modulator of the GABA binding site in different regions of rat brain.
56. Kava hepatotoxicity–a clinical review.