Noopept, international nonproprietary name omberacetam and development code GVS-111, is a small synthetic molecule built from two amino acids. It was designed at the V. V. Zakusov Institute of Pharmacology in Moscow as a peptide-based analog of piracetam. In the body it acts largely as a prodrug: one of its breakdown products, cycloprolylglycine, is a cyclic dipeptide that also occurs naturally in the brain.

In Russia, Noopept is a registered medicine sold as 10 mg tablets for memory and attention problems after brain injury or with cerebrovascular disease. In the US it is not an approved drug. FDA has sent warning letters to companies selling it online, stating that Noopept is not a dietary supplement. The human evidence is thin: a handful of small, open-label Russian studies, and we found no published placebo-controlled trial.

This page summarizes what the Russian product information, the published studies and the FDA record report. It is for education only and is not medical advice.

Property	Detail
Class	Nootropic (ATC N06BX); dipeptide analog of piracetam
Names	Noopept; omberacetam (INN); GVS-111
Russian product	Noopept 10 mg tablets (holder OTCPharm); the current Russian product information lists it as available without a prescription
Route	Oral
Labeled dose (Russia)	10 mg twice daily, up to 10 mg three times daily; courses of 1.5–3 months
Half-life	0.38 h in plasma (Russian product information); time to peak about 15 minutes
Active metabolite	Cycloprolylglycine, a cyclic dipeptide also found naturally in the brain
US status	Not FDA-approved; FDA warning letters say it does not qualify as a dietary supplement
WADA	Not named on the WADA 2026 Prohibited List (phenylpiracetam is)

What it is

Noopept is a dipeptide-based molecule: a core made of the amino acids proline and glycine, capped with a phenylacetyl group on the proline end and an ethyl ester on the glycine end. Its formula is C₁₇H₂₂N₂O₄ and its molecular weight is 318.4 g/mol (PubChem). It is usually grouped with the “racetams,” but its chemical structure is quite different from piracetam’s (Araj et al., J Pharm Biomed Anal 2025). Its designers describe it as a dipeptide built to mimic the shape of piracetam (Gudasheva et al., Curr Pharm Des 2018).

The design idea, according to the developers, was to turn a non-peptide drug into a short peptide that the body could handle like a natural regulator. Dipeptides are short enough to survive oral dosing and cross biological barriers, unlike longer peptides. Out of a series of proline-containing compounds, the phenylacetyl ethyl ester was chosen as the most active and practical to make. The name combines “nootropic” and “peptide” (Gudasheva et al., 2018).

The same group later identified cycloprolylglycine as a natural substance in rat brain, at about 2.8 nmol per gram of tissue, with memory effects of its own in rats (Gudasheva et al., FEBS Lett 1996). In rats, Noopept itself could not be detected in the brain 1 hour after an injection, while cycloprolylglycine rose about 2.5-fold. The authors concluded that Noopept acts as a prodrug of this cyclic dipeptide (Gudasheva et al., Eur J Drug Metab Pharmacokinet 1997). They later argued that Noopept also has activity of its own, because in their animal tests it affected more phases of memory than cycloprolylglycine alone (Gudasheva et al., 2018).

Mechanism claims

Almost all mechanism work comes from the developers’ institute and from animal or cell studies. The proposed mechanisms include:

Neurotrophins (in rats). Repeated dosing for 28 days increased mRNA for nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) in the hippocampus (Ostrovskaya et al., Bull Exp Biol Med 2008).
HIF-1 activation (in cell culture). At 10 μM in human kidney cells, Noopept increased the activity of HIF-1, a transcription factor that switches on genes involved in the response to low oxygen, and did not affect eight other factors tested. Piracetam did not have this effect. The authors propose this as Noopept’s primary mechanism (Vakhitova et al., Acta Naturae 2016).
Antioxidant protection (in cell culture). In cultured human cortical neurons exposed to hydrogen peroxide, Noopept improved neuron survival in a dose-dependent way, more than piracetam or vitamin E did (Pelsman et al., Int J Dev Neurosci 2003).
Broader claims. The developers’ 2002 review attributes its effects to antioxidant and anti-inflammatory actions, protection against excess calcium and glutamate, and improved blood flow properties (Ostrovskaya et al., Eksp Klin Farmakol 2002).

None of these mechanisms has been confirmed in people.

Pharmacokinetics

Human pharmacokinetic data are limited to the Russian product information and a short report from the developers’ institute.

Parameter	Value	Source
Absorption	Enters the bloodstream unchanged from the gut	Russian product information
Time to peak	About 15 minutes on average	Russian product information
Plasma half-life	0.38 h (≈23 minutes)	Russian product information
Metabolites	Phenylacetic acid, phenylacetylproline and cycloprolylglycine	Russian product information
Brain penetration	Reported to reach higher levels in brain than in blood	Russian product information; shown in rats

The product information is reproduced in the Vidal drug reference (Russia). It also states that the drug does not accumulate and that stopping it causes no withdrawal syndrome; these statements come from the manufacturer’s labeling rather than from published trials.

Species differ a lot. In rats, Noopept is cleared very quickly and heavily metabolized. In rabbits it circulates unchanged for longer, and in humans elimination is slower still, with considerable variation between people. No metabolites were found in human plasma in that work, which the authors attributed to the small dose (Boiko et al., Eksp Klin Farmakol 2004). In rats, oral Noopept was absorbed and crossed the blood-brain barrier unchanged (Boiko et al., Bull Exp Biol Med 2000), and cycloprolylglycine had different kinetics from the parent drug (Boyko et al., Biomed Khim 2018).

The very short half-life of the parent drug is one reason researchers suspect that the longer-lasting effects, if any, depend on the metabolite.

Regulatory status

Russia

Noopept is registered in Russia as a 10 mg tablet. Its developers state that it passed clinical trials for mild cognitive impairment of cerebrovascular or post-traumatic origin and has been on the market since 2006 (Gudasheva et al., 2018). The current Russian product information lists the following uses: problems with memory, attention and other cognitive functions, and emotional instability, in people with (Vidal):

after-effects of traumatic brain injury, including post-concussion syndrome;
cerebrovascular insufficiency (encephalopathies of various causes);
asthenic (fatigue-related) disorders;
other states with reduced mental productivity.

The labeled dose is 10 mg twice daily after meals, raised to 10 mg three times daily if needed, not taken after 6 pm, for 1.5–3 months. The same source lists the product as dispensed without a prescription. A 2025 European market survey described Noopept as a prescription medicine in Russia (Vanhee et al., J Xenobiot 2025), so sources differ on this point.

United States

Noopept has no FDA approval. In a February 2019 warning letter to an online seller, FDA listed Noopept among products that are “not dietary supplements or conventional foods,” and called the products unapproved “new drugs” based on the seller’s disease claims (FDA warning letter, Peak Nootropics, 2019). A 2022 letter to another seller named its “Noopept Powder” as an unapproved new drug (FDA warning letter, Crystal Clear Supplements, 2022).

Europe and Australia

A market surveillance study by 12 official medicines control laboratories found that Noopept was the most often detected racetam-type drug in samples collected from January 2020 to September 2024, most of them from the illegal market. It noted that Noopept is not authorized in the EU or Australia, and it was often found as bulk raw powder (Vanhee et al., 2025).

What the research shows

Human studies

The best-known human study compared Noopept with piracetam in patients with mild cognitive disorders after vascular disease or brain trauma (Neznamov & Teleshova, Neurosci Behav Physiol 2009). It is an English translation of a 2008 Russian paper from the developers’ institute, and no abstract is indexed in PubMed. As summarized by the Alzheimer’s Drug Discovery Foundation (ADDF Cognitive Vitality report, 2020):

Feature	Detail
Design	Open-label comparison, no placebo group
Arms	Noopept 10 mg twice daily vs piracetam 400 mg three times daily
Duration	56 days
Noopept arm	31 patients
Reported result	Both drugs improved several mood and cognition measures; in the Noopept group, MMSE rose from 26 to 29
Reported side effects (Noopept)	Raised blood pressure 7 of 31; sleep disturbance 5 of 31; irritability 3 of 31

The MMSE (Mini-Mental State Examination) is a 30-point screening test for cognitive impairment. The study’s design limits how much it can show:

No placebo. Without a placebo arm, practice effects on repeated testing and natural recovery cannot be separated from a drug effect.
Open-label. Patients and raters knew the treatment, which can bias subjective ratings of mood and cognition.
Small and short. About 30 patients per drug, followed for 8 weeks.
Developer-run. The study came from the institute that created the drug, and it has not been replicated by independent groups.
Active comparator only. Matching piracetam, a drug whose own memory benefit is uncertain, cannot show that either drug beats no treatment.

A second Russian report described an open study of 60 patients after stroke. It reported better MMSE and word-association test scores than controls after 2 months of Noopept 20 mg daily (Amelin et al., Zh Nevrol Psikhiatr 2011). It shares the same limits: open design, small sample, and no independent replication.

There are no controlled trials showing that Noopept improves memory or focus in healthy people.

Animal and cell studies

Most of the published literature is in animals or cell culture, and almost all of it comes from one research group. These results do not show that the drug works in people.

Memory tests in rats. Oral Noopept at 0.5–10 mg/kg kept its anti-amnesia effect in a passive avoidance task (Ostrovskaya et al., Bull Exp Biol Med 2001).
Alzheimer-like model in mice. In mice with the olfactory bulbs removed (a model with some Alzheimer-like changes), 0.01 mg/kg for 21 days restored spatial memory in a water maze (Ostrovskaya et al., J Psychopharmacol 2007).
Potency claims. The developers report effective doses in animals about 1,000 times lower than piracetam’s (Ostrovskaya et al., 2002). This compares milligram doses in rodent tests and says nothing about the size of any benefit in humans.

The ADDF review adds that almost all studies used non-standard animal models and outcome measures and came from a single laboratory (ADDF, 2020).

Side effects and risks

What the label and studies report

The Russian product information lists allergic reactions and, in patients with high blood pressure (mainly severe hypertension), a rise in blood pressure (Vidal). In the open-label comparison, raised blood pressure was the most frequent reported side effect, followed by sleep problems and irritability (ADDF summary of Neznamov 2009).

Long-term human safety data are lacking. In rabbits given 10 or 100 mg/kg orally for 6 months, the developers reported no irreversible organ changes (Kovalenko et al., Eksp Klin Farmakol 2002); this is an animal finding.

Who should not use it (Russian label)

The Russian product information lists these contraindications (Vidal):

severe liver or kidney impairment;
pregnancy and breastfeeding;
age under 18;
lactose intolerance (the tablets contain lactose);
hypersensitivity to the ingredients.

Interactions

The label states that no interactions were found with alcohol, sleeping pills, blood pressure drugs or stimulants. Independent interaction studies have not been published, and the ADDF review describes drug interactions as unknown.

Quality and contamination

Products sold online as supplements are not made to pharmaceutical standards. When researchers bought US “cognitive enhancement” supplements labeled as containing omberacetam or other unapproved racetams (Cohen et al., Neurol Clin Pract 2021):

one serving could contain up to 40.6 mg of omberacetam, about four times the typical 10 mg pharmacological dose;
several products contained drugs not declared on the label, and the products overall also contained phenibut, vinpocetine and picamilon;
75% (9 of 12) of declared drug quantities were inaccurate.

Piracetam is the drug Noopept was designed to imitate; it is licensed in the UK only for cortical myoclonus. Phenylpiracetam is another Russian nootropic, with a different structure and a stimulant profile, and it is named on the WADA list. Semax and Selank are other neuroactive peptides developed in Russia. Both are longer, seven-amino-acid peptides, and their human evidence likewise comes mostly from small Russian studies.

Key takeaways

A prodrug of a brain dipeptide. Noopept is a capped two-amino-acid molecule that is cleared from plasma within minutes (half-life 0.38 h) and is partly converted to cycloprolylglycine, which is thought to carry much of its activity.
Registered in Russia, not in the US. It is sold in Russia as 10 mg tablets for cognitive problems after brain injury or vascular disease. FDA has stated in warning letters that it is not a dietary supplement.
Very limited human evidence. The key trial was small, open-label, 56 days long and had no placebo; it compared Noopept only with piracetam.
Mechanism data are preclinical. Claims about BDNF, NGF, HIF-1 and antioxidant effects come from rats and cell culture, mostly from the developers’ own institute.
Supplement products are unreliable. Tested US products contained up to four times the pharmacological dose and undeclared drugs.

Sources

National Center for Biotechnology Information. Noopept (omberacetam), PubChem CID 180496. PubChem.
Noopept (omberacetam) 10 mg tablets, Russian product information (instructions for use), as reproduced in the Vidal drug reference. Vidal.
Gudasheva TA, Ostrovskaya RU, Seredenin SB. Novel Technologies for Dipeptide Drugs Design and their Implantation. Curr Pharm Des. 2018;24(26):3020–3027. PubMed.
Ostrovskaia RU, Gudasheva TA, Voronina TA, Seredenin SB. The original novel nootropic and neuroprotective agent noopept [in Russian]. Eksp Klin Farmakol. 2002;65(5):66–72. PubMed.
Gudasheva TA, Boyko SS, Akparov VKh, et al. Identification of a novel endogenous memory facilitating cyclic dipeptide cyclo-prolylglycine in rat brain. FEBS Lett. 1996;391(1-2):149–152. PubMed.
Gudasheva TA, Boyko SS, Ostrovskaya RU, et al. The major metabolite of dipeptide piracetam analogue GVS-111 in rat brain and its similarity to endogenous neuropeptide cyclo-L-prolylglycine. Eur J Drug Metab Pharmacokinet. 1997;22(3):245–252. PubMed.
Boiko SS, Ostrovskaya RU, Zherdev VP, et al. Pharmacokinetics of new nootropic acylprolyldipeptide and its penetration across the blood-brain barrier after oral administration. Bull Exp Biol Med. 2000;129(4):359–361. PubMed.
Boĭko SS, Korotkov SA, Zherdev VP, et al. Interspecies differences of noopept pharmacokinetics [in Russian]. Eksp Klin Farmakol. 2004;67(1):40–43. PubMed.
Boyko SS, Zherdev VP, Shevchenko RV. Pharmacokinetics of noopept and its active metabolite cycloprolyl glycine in rats [in Russian]. Biomed Khim. 2018;64(5):455–458. PubMed.
Ostrovskaya RU, Gudasheva TA, Zaplina AP, et al. Noopept stimulates the expression of NGF and BDNF in rat hippocampus. Bull Exp Biol Med. 2008;146(3):334–337. PubMed.
Vakhitova YV, Sadovnikov SV, Borisevich SS, et al. Molecular Mechanism Underlying the Action of Substituted Pro-Gly Dipeptide Noopept. Acta Naturae. 2016;8(1):82–89. PubMed.
Pelsman A, Hoyo-Vadillo C, Gudasheva TA, et al. GVS-111 prevents oxidative damage and apoptosis in normal and Down’s syndrome human cortical neurons. Int J Dev Neurosci. 2003;21(3):117–124. PubMed.
Neznamov GG, Teleshova ES. Comparative studies of Noopept and piracetam in the treatment of patients with mild cognitive disorders in organic brain diseases of vascular and traumatic origin. Neurosci Behav Physiol. 2009;39(3):311–321. PubMed.
Alzheimer’s Drug Discovery Foundation. Noopept. Cognitive Vitality Reports, last updated March 20, 2020. ADDF.
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Ostrovskaya RU, Gruden MA, Bobkova NA, et al. The nootropic and neuroprotective proline-containing dipeptide noopept restores spatial memory and increases immunoreactivity to amyloid in an Alzheimer’s disease model. J Psychopharmacol. 2007;21(6):611–619. PubMed.
Kovalenko LP, Smol’nikova NM, Alekseeva SV, et al. Preclinical study of noopept toxicity [in Russian]. Eksp Klin Farmakol. 2002;65(1):62–64. PubMed.
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Noopept