Noopept

omberacetam (INN), GVS-111, N-phenylacetyl-L-prolylglycine ethyl ester, Ноопепт

Cognitive & neuro

Awaiting medical reviewEN ES DE FR PT ZH+ Follow for updates

Note on this profile. Noopept is an approved medicine in Russia and some neighbouring countries, where it is sold as 10 mg tablets for cognitive complaints after head injury or in vascular brain disease. It is not approved anywhere else. This page explains the published science; use outside those approvals is unapproved.

Summary

Class: Synthetic dipeptide-derived small molecule: the dipeptide L-prolyl-glycine with a phenylacetyl group on one end and an ethyl ester on the other. It is a "peptide mimetic" rather than a plain peptide, and it is taken by mouth
Mechanism: Broken down in the body to cycloprolylglycine, a dipeptide the brain makes itself; in rodents it raises NGF and BDNF in the hippocampus, protects neurons from oxidative and amyloid-related damage and modulates glutamate signalling
Routes studied: Oral tablets (human, approved use); intraperitoneal and oral (rodents). Community: oral, sublingual, occasionally intranasal
Dose range reported: Russian label: 10 mg twice daily, increased to 30 mg/day if needed, for 1.5–3 months. Rodent studies: 0.01–10 mg/kg. Community-reported: 10–30 mg/day oral or sublingual
Half-life: Short for the parent compound (about 15–20 minutes in rats); human plasma levels are low and the active metabolite is thought to carry much of the effect. Human pharmacokinetics are poorly published
Storage: Tablets and powder: room temperature, dry, away from light. Solutions degrade (the ethyl ester hydrolyses) — not usually stored in liquid form
Regulatory status: Approved medicine in Russia and some CIS countries; unapproved everywhere else. See region table

Doses are as reported in studies or by the community — never recommendations.

1What it is

Noopept was developed in the 1990s at the Zakusov Institute of Pharmacology in Moscow (Ostrovskaya, Gudasheva, Seredenin and colleagues) as a deliberate attempt to build a small, orally active molecule that mimicked the memory-related dipeptide structures the group had found in piracetam research. The result is a prolyl-glycine dipeptide with chemical caps on both ends, which is why it is often grouped with racetams and sometimes with peptides. It is neither exactly: chemically it is a dipeptide ester, pharmacologically it behaves like a prodrug for cycloprolylglycine, an endogenous (naturally occurring) cyclic dipeptide found in rat brain.

It was approved in Russia in the 2000s under the brand name Noopept and received the INN omberacetam. Outside Russia it has circulated since the 2010s as a "nootropic" powder or capsule, which is where most of the English-language community discussion comes from. Almost all primary research is from the originating institute, published in Russian journals and their English translations (chiefly Bulletin of Experimental Biology and Medicine).

2How it's thought to work

Several mechanisms are proposed, almost all from rodent and cell work:

Prodrug for cycloprolylglycine. Noopept is hydrolysed to cyclo(Pro-Gly), which the originating group describes as an endogenous nootropic and anxiolytic dipeptide. Much of the sustained effect is attributed to this metabolite.

Neurotrophins. Single and repeated doses increased NGF and BDNF mRNA in rat hippocampus (Ostrovskaya 2008), offered as the explanation for effects that outlast the drug's short .

Neuroprotection. Reduced oxidative stress, calcium overload and cell death in cultured neurons and in rodent models of amyloid toxicity and ischaemia; it reduced aggregation and toxicity of alpha-synuclein and amyloid-beta.

Glutamate and cholinergic modulation. Reported to sensitise AMPA/NMDA-type signalling and to have cholinergic-like effects in some paradigms; this is less well characterised.

Anxiolytic component. The metabolite shows anxiolytic activity in rodent tests, which the label leans on when describing "anxiolytic" properties.

Proposed: a synthetic dipeptide reported to raise BDNF and NGF in rodent brain, with cognitive effects attributed to that rather than to a receptor of its own. It is a prescription nootropic in Russia and unapproved elsewhere; controlled human data are limited.Schematic — not to scale

None of these has been directly confirmed in human mechanistic studies.

3What the research shows

Mild cognitive disorder after head injury or in vascular brain disease

The main human study is a comparative trial of noopept (20 mg/day) versus piracetam (1,200 mg/day) in 53 patients with mild cognitive impairment of traumatic or vascular origin over about two months (Neznamov & Teleshova 2009, Neurosci Behav Physiol). Noopept patients improved more on several cognitive and anxiety scales and had fewer side effects. It was not placebo-controlled and not blinded in the way Western regulators would expect. Other Russian clinical reports exist but are small and hard to access; treat the human base as thin. [4]

Memory and learning in rodents

Extensive rodent work shows improved passive-avoidance and spatial memory, restoration of memory after various insults (amyloid injection, hypoxia, cholinergic lesions, electroshock) and retained activity after oral dosing (Ostrovskaya 2002, 2007, 2014; many others). Effects are reported at doses far lower than piracetam, which is the basis for the "1,000 times more potent than piracetam" claim often repeated online — a potency comparison in rats, not a human efficacy claim. [2][3][7]

Graded C/D

Neuroprotection, Alzheimer's models

Rat models of Alzheimer's disease (amyloid-beta injection into the basal forebrain) showed restored spatial memory and reduced amyloid-related changes (Ostrovskaya 2007, J Psychopharmacol). Cell studies show protection against alpha-synuclein and amyloid aggregates (Jia 2011, J Mol Biol). No human disease-modification data. [2][6]

Graded C/B

Anxiety, mood

Rodent anxiolytic effects via the metabolite (Gudasheva 1996). The 2009 human trial reported reduced anxiety and irritability scores as secondary outcomes. No dedicated human anxiety trial. [5]

Healthy-adult cognitive enhancement

No controlled trials in healthy people. Community reports are mixed: some describe clearer thinking and better recall, others nothing or irritability.

4Reported side effects and interactions

Literature-reported

The Russian label lists irritability, sleep disturbance and rises in blood pressure in people with pre-existing hypertension; it advises against use in pregnancy, breastfeeding, severe liver or kidney impairment and under 18. The 2009 trial reported fewer adverse events than piracetam. Long-term safety data in the Western sense are absent.

Community-reported

headache (the most common), irritability or a "flat" mood, brain fog at higher doses, insomnia when taken late, occasional dizziness. Some report rapid tolerance.

Theoretical. glutamate-sensitising effects raise the usual, unproven question about long-term excitatory load; no human signal.

Interactions. none formally studied. The label cautions about combining with other centrally acting drugs; community stacks with choline sources (to offset headache) are anecdotal.

Markers researchers commonly monitor

No compound-specific lab markers are established. Based on the label and physiology:

Marker	Why it's watched
Blood pressure	the Russian label warns of rises in hypertensive patients; a home cuff before and during a course is the one marker that directly follows from the label.
Liver enzymes (ALT/AST) and creatinine/eGFR	the compound is hepatically metabolised and renally cleared; the label restricts use in severe liver or kidney impairment.
Sleep quality	insomnia is community-reported; a simple sleep log catches it.
A short, repeatable cognitive test	if cognition is the goal, a baseline on the same test (e.g. a validated digit-span or word-recall task) is the only honest way to tell effect from expectation.
CBC and CMP	general baseline for a compound with little published long-term human safety data.

Free for everyone. Safety information is never behind a paywall.

5Reconstitution and handling

Noopept is an oral compound, supplied as tablets, capsules or bulk powder; it is not for injection. Powder doses are small (tens of milligrams), so a milligram scale, not a scoop, is the honest way to measure it. It is poorly soluble in water and its ester bond breaks down in solution, so community practice is to take powder dry or sublingually rather than store it in liquid. The calculator is not relevant for this compound.

Open in calculator, pre-loaded →

6Commonly studied alongside

Semax (#36) and Selank (#37) in Russian neuro-pharmacology; piracetam and other racetams as comparators; Cerebrolysin; choline sources (community practice). Dihexa and P21 appear in the same community conversations without any combined study.

Informational cross-links. Not stack recommendations.

7Regulatory status by region

Region	Status (checked —)
United States	Not FDA-approved. Sold as a "nootropic"; FDA does not recognise it as a lawful dietary ingredient and has objected to its sale as a supplement †. Not on the Category 2 compounding list to our knowledge †
European Union	Not authorised as a medicine; not a permitted food supplement ingredient
United Kingdom	Not licensed. Supply likely falls under the Psychoactive Substances Act 2016 †
Australia	Not approved; treated as a prescription-only substance for import purposes †
South Africa	Not registered with SAHPRA
Russia / CIS	Approved medicine (10 mg tablets); available without prescription in Russia †
Sport (WADA)	Not on the Prohibited List as of review date †

8Open questions

Human pharmacokinetics: how much cycloprolylglycine reaches the brain after an oral dose, and for how long?
Any placebo-controlled, blinded trial — in patients or healthy adults — outside the originating institute.
Whether the neurotrophin effects seen in rats occur in humans at label doses.
Tolerance with repeated use, which the community reports and the literature does not address.

9References

1Ostrovskaya RU et al. (2008). Noopept stimulates the expression of NGF and BDNF in rat hippocampus. Bull Exp Biol Med. PubMed · DOI
2Ostrovskaya RU et al. (2007). The nootropic and neuroprotective proline-containing dipeptide noopept restores spatial memory and increases immunoreactivity to amyloid in an Alzheimer's disease model. J Psychopharmacol. PubMed · DOI
3Ostrovskaya RU et al. (2002). Proline-containing dipeptide GVS-111 retains nootropic activity after oral administration. Bull Exp Biol Med. PubMed · DOI
4Neznamov GG, Teleshova ES (2009). 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. PubMed · DOI
5Gudasheva TA et al. (1996). Anxiolytic activity of endogenous nootropic dipeptide cycloprolylglycine in elevated plus-maze test. Bull Exp Biol Med. PubMed
6Jia X et al. (2011). Neuroprotective and nootropic drug noopept rescues alpha-synuclein amyloid cytotoxicity. J Mol Biol. PubMed · DOI
7Ostrovskaya RU et al. (2014). Noopept efficiency in experimental Alzheimer disease (cognitive deficiency caused by beta-amyloid 25–35 injection into Meynert basal nuclei of rats). Bull Exp Biol Med. PubMed

References are being resolved to PubMed/DOI identifiers; links search PubMed for the citation until then.

† Being confirmed by our reviewers against current sources.

10Community

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Self-reported side effects Phase 2

Not enough data yet. 0 of the 50 members needed have logged this compound for 4+ weeks. We don't show anything below 50, so no one can be identified.

11Page history

26 Oct 2026Profile published — awaiting medical review

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