Noopept

An orally active dipeptide-derived small molecule — INN omberacetam — registered as a prescription nootropic in Russia and sold on the Western research market with no randomized or placebo-controlled human trial, no registered clinical study, and no FDA approval.

Also referenced as: Omberacetam, GVS-111, SGS-111, N-phenylacetyl-L-prolylglycine ethyl ester, ethyl phenylacetyl-Pro-Gly

Also appears in: Neuroprotection

What is Noopept?

Noopept is a brand name for omberacetam (development code GVS-111), the ethyl ester of N-phenylacetyl-L-prolylglycine — C17H22N2O4, molecular weight about 318.4, CAS 157115-85-0, PubChem CID 180496. It was designed at the V. V. Zakusov Institute of Pharmacology in Moscow as an orally active dipeptide analog of piracetam, part of a long-running program there that worked backward from known non-peptide drugs to short peptide prototypes and then forward again to orally dosed dipeptide mimetics (Gudasheva, Vestnik Rossiiskoi Akademii Meditsinskikh Nauk, 2011;(7):8–16).

It is not a peptide in the sense the research market uses the word. The molecule is built on a proline-glycine dipeptide core, but both ends are chemically capped — a phenylacetyl group on the amino terminus, an ethyl ester on the carboxyl terminus — which leaves a 318-dalton, orally bioavailable small molecule rather than a peptide that has to be reconstituted and injected. It appears alongside peptides in this market because of that dipeptide scaffold and because the Russian nootropic compounds it is sold with, such as Semax and Selank, genuinely are peptides.

How it works

• Prodrug conversion to cyclo-L-prolylglycine. One hour after 5 mg/kg intraperitoneal dosing in rats, the parent compound was undetectable in brain, while of three candidate metabolites only cyclo-prolylglycine had risen — 2.5-fold — and its formation from the parent was reproduced in vitro with plasma and brain enzymes. The authors read this as evidence that the drug is a prodrug for a cyclic dipeptide identical to an endogenous compound with nootropic activity (Gudasheva et al., European Journal of Drug Metabolism and Pharmacokinetics, 1997;22(3):245–252). Later rat work from the same institute found the metabolite’s pharmacokinetics differ substantially from the parent’s (Boyko et al., Biomeditsinskaya Khimiya, 2018;64(5):455–458).
• Selective HIF-1 activation. In HEK293 cells transfected with luciferase reporters for nine transcription factors — CREB, NFAT, NF-κB, p53, STAT1, GAS, VDR, HSF1, and HIF-1 — 10 µM Noopept raised the DNA-binding activity of HIF-1 and of nothing else, while 1 mM piracetam moved none of them; molecular docking suggested the L-isomer and its N-phenylacetylprolyl metabolite bind prolyl hydroxylase 2. The authors proposed this HIF-positive effect as the compound’s primary mechanism (Vakhitova et al., Acta Naturae, 2016;8(1):82–89). It is reporter-assay evidence in a kidney-derived cell line, not a measurement in neurons.
• Neurotrophin expression, region by region. A single dose raised NGF and BDNF mRNA in rat hippocampus, and 28-day dosing potentiated rather than tolerized the effect. The same experiment found expression of both factors in the cerebral cortex below control after a single dose — a directional split that is usually left out when this study is cited (Ostrovskaya et al., Bulletin of Experimental Biology and Medicine, 2008;146(3):334–337).
• α7 nicotinic receptor–dependent interneuron activation. In rat hippocampal slices, 5 µM Noopept increased the firing frequency of GABAergic interneurons in the stratum radiatum of CA1. That effect was almost completely abolished by the α7 nAChR antagonists α-bungarotoxin and methyllycaconitine, which also eliminated the accompanying rise in spontaneous IPSCs in CA1 pyramidal cells (Kondratenko et al., Neuroscience Letters, 2022;790:136898).

Research status

The preclinical record is large; the human record is thin and uncontrolled. A PubMed search for “noopept” returns roughly 106 records and one for “omberacetam” roughly 91, as of August 2026 — the great majority from the originating Zakusov Institute and collaborating Russian groups, covering amyloid and streptozotocin models of Alzheimer’s disease, glutamate toxicity in HT-22 neurons, anti-inflammatory and cytokine effects, and antiamnestic behavior in rodents. Non-Russian groups have taken it up more recently: an intranasal forskolin-plus-Noopept formulation reversed motor deficits and dopamine-neuron loss in PINK1 knockout rats (Dagda et al., International Journal of Molecular Sciences, 2022;24(1):690 — the authors disclose founding the company commercializing that formulation), and a Turkish group reported attenuation of diabetes-related neuropathic pain through TRPV1 inhibition in rats (Düzova et al., Molecular Neurobiology, 2021;58(10):5031–5051).

The human evidence. There is a human literature, but it is a handful of small, open-label, single-country reports rather than a controlled program. The study nearly every claim about Noopept in people traces back to is Neznamov and Teleshova, a comparison of Noopept against piracetam in patients with mild cognitive disorders in organic brain diseases of vascular and traumatic origin (Neuroscience and Behavioral Physiology, 2009;39(3):311–321; the Russian original is Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova, 2008;108(3):33–42). Both authors were at the Clinical Psychopharmacology Laboratory of the institute that developed the compound, and neither the English nor the Russian record carries an abstract on PubMed — so sample size, randomization, blinding, and dose cannot be verified from the indexed literature, and secondhand descriptions of this trial circulating online do not agree with one another. Around it sit a few reports of similar scale: EEG changes on Noopept in patients with post-traumatic and vascular cognitive disturbance, from the same center (Bochkarev et al., Zhurnal Nevrologii i Psikhiatrii imeni S.S. Korsakova, 2008;108(11):47–54); an open prospective study in 60 stroke patients reporting improved MMSE and association scores after two months at 20 mg daily (Amelin et al., ibid., 2011;111(10 Pt 1):44–46); two-page papers on neurasthenia (Chutko et al., ibid., 2008;108(12):51–52) and on discirculatory encephalopathy (Barantsevich et al., ibid., 2009;109(5):62–64); and a healthy-volunteer climate-adaptation study (Shabanov et al., Eksperimental’naya i Klinicheskaya Farmakologiya, 2007;70(6):41–47).

No placebo control, and no registered trial. A PubMed search combining noopept or omberacetam with “placebo” or “double-blind” returns exactly one record, and it is a cross-maze behavioral study in BALB/c and C57BL/6 mice (Vasil’eva et al., Eksperimental’naya i Klinicheskaya Farmakologiya, 2012;75(7):3–7). No record under either name carries the randomized-controlled-trial or Phase 1–3 publication types at all. ClinicalTrials.gov returns zero registered studies as of August 2026 — not for noopept, not for omberacetam, and not for either development code. There is no failed Western trial to report because no development program under any of the compound’s codes ever reached a registry-listed study. Human pharmacokinetics do exist, but thinly and from the originating institute: an interspecies comparison found elimination slowing from rats to rabbits to humans, with considerable individual variability and no metabolites detectable in human plasma (Boyko et al., Eksperimental’naya i Klinicheskaya Farmakologiya, 2004;67(1):40–43). The Russian registration rests on a domestic evidence package that has not been independently replicated.

What surveillance has found instead. Analytical work has repeatedly found the compound in products it should not be in. Testing of ten over-the-counter supplements marketed for memory and cognition detected omberacetam and aniracetam plus three further unapproved drugs — phenibut, vinpocetine, and picamilon — with a recommended serving of one product delivering 40.6 mg of omberacetam against a typical pharmacologic dose of 10 mg; several detected drugs were undeclared, several declared drugs were absent, and 9 of 12 stated quantities were inaccurate (Cohen et al., Neurology: Clinical Practice, 2021;11(3):e303–e307). A market-surveillance study run by twelve official medicines control laboratories across Europe and Australia documented 159 samples between January 2020 and September 2024 and singled out noopept, phenylpiracetam, and phenibut — drugs available only on prescription in Russia and unauthorized in the participating countries — as having been intercepted in large bulk quantities of raw material (Vanhee et al., Journal of Xenobiotics, 2025;15(3):88).

Common dosage forms

Because it is orally active, Noopept is sold in formats that are unusual for this market: bulk powder, capsules and tablets, sublingual tablets and solutions, and occasionally intranasal solutions. Lyophilized powder in sealed vials for reconstitution — the default presentation for research peptides — is uncommon here, which follows from the compound being orally available in the first place; the animal literature has dosed it orally, intraperitoneally and intranasally, and one non-Russian group has formulated it into a dissolving microneedle patch (Srivastava & Thakkar, European Journal of Pharmaceutical Sciences, 2021;164:105909). The compound also turns up as one component of multi-ingredient nootropic capsule blends, where its content per capsule is often not stated separately, and the NIH Dietary Supplement Label Database carries US supplement labels listing Noopept as an ingredient even though FDA’s position is that it is not a lawful dietary-supplement ingredient. This section describes formats only and is not dosing guidance.

Key considerations

• Not a peptide, with a practical consequence for verification. A capped Pro-Gly core at 318 daltons is a peptidomimetic small molecule, not a peptide, and confirming identity and purity follows small-molecule analytics — chromatography and mass spectrometry against a defined 318-dalton target — rather than the sequence-and-mass conventions of a peptide certificate of analysis. A certificate written for peptide work does not automatically say anything useful about this compound.
• Unapproved in the United States; FDA has said so in writing. In a warning letter dated February 5, 2019 to a nootropics seller, FDA identified Noopept among products it deemed unapproved new drugs and misbranded drugs, and stated that they “are not dietary supplements or conventional foods.” Registration in Russia — where the multi-country control-laboratory study describes it as prescription-only — is not an FDA pathway and carries no US legal standing.
• The human evidence is small, open-label, and single-country. A handful of Russian studies, the most-cited of them an active-comparator trial from the institute that developed the compound with no abstract indexed. No randomized or placebo-controlled trial exists under either name, there is no ClinicalTrials.gov registration, and no long-term safety data has been published; the human pharmacokinetics that do exist come from a single interspecies study by the developing institute. Preclinical breadth is not a substitute for any of that, and the compound has been in clinical use in one country for years without producing an independently replicated controlled trial.
• The active species may not be the molecule being sold. The rat data support conversion to cyclo-L-prolylglycine, an endogenous cyclic dipeptide, with the parent undetectable in brain an hour after dosing. If most of the pharmacology belongs to that metabolite, purity of the parent compound says little about exposure to the active species — and cyclo-L-prolylglycine is itself sold separately, which makes the two easy to conflate.
• Naming is unreliable at both the chemical and the label level. “Noopept” is a brand name, omberacetam is the INN, and GVS-111 and SGS-111 are development codes for the same molecule — four names for one compound, which is why product listings and citation trails for it are so easy to double-count; the racetam-style suffix groups it with piracetam even though its ring is the plain pyrrolidine of proline rather than the 2-pyrrolidinone that defines that class, a mismatch noted in the most detailed physicochemical characterization published to date, whose authors observe that very little is known about the compound’s structural properties despite the volume of pharmacodynamic work (Araj et al., Journal of Pharmaceutical and Biomedical Analysis, 2025;252:116474). On the label side, the supplement-testing and control-laboratory findings above mean a product named for this compound is not a reliable guide to what it contains or how much.