Noopept is the common name for N-phenylacetyl-L-prolylglycine ethyl ester (developmental code GVS-111; international nonproprietary name omberacetam), a synthetic proline-containing dipeptide developed in Russia and studied in preclinical research as a nootropic compound. It was engineered as a peptide analog of the racetam piracetam rather than isolated from any organism, so it is not a naturally occurring or endogenous peptide. This research guide summarizes what the laboratory literature reports about Noopept’s chemistry, the mechanisms proposed from animal and cell-based models, the doses used in published animal studies, and how it is discussed relative to other research nootropics such as Semax. All material is presented strictly for research-use-only context.

What Is Noopept? Compound Overview

Noopept is a small synthetic dipeptide that has been characterized in the pharmacology literature as a nootropic research compound with a racetam-like activity profile. Unlike the classic racetams, it carries a short peptide backbone, which is why it is described as a “peptide analog of piracetam” rather than a racetam in the strict structural sense. In the United States it is not an approved drug or dietary ingredient and is handled by suppliers as a research-use-only (RUO) laboratory material.

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Noopept at a glance

Placing the identity data first reflects how this compound is indexed across chemical databases. The exact strings GVS-111, omberacetam, and N-phenylacetyl-L-prolylglycine ethyl ester all refer to the same molecule, which is useful when cross-referencing the primary literature, where nomenclature has shifted over time.

Is Noopept a true peptide? The blocked dipeptide core

This is the most common point of confusion, and precision here matters. Noopept is a peptide in the narrow chemical sense that its core is a dipeptide: an L-proline residue linked to glycine (a Pro-Gly core). However, that backbone is chemically blocked at both ends. The proline nitrogen is N-acylated by a phenylacetyl group, and the glycine carboxyl is esterified as an ethyl ester. The correct description is therefore a modified/blocked dipeptide ester, not a simple two-amino-acid peptide.

Critically, Noopept itself is a fully synthetic molecule. It is not naturally occurring and not found endogenously in the body. The endogenous element enters only at the level of its metabolite: after administration in animal models, Noopept is reported to convert to cyclo-L-prolylglycine (cycloprolylglycine, cPG), a cyclic dipeptide described in the literature as occurring naturally in mammalian brain. In other words, the parent compound is a synthetic dipeptide ester whose active metabolite happens to coincide with a naturally occurring cyclic dipeptide. Describing Noopept itself as a “natural” or “endogenous” peptide would be inaccurate.

Origin and regulatory status

Noopept was developed in Russia at the V. V. Zakusov Institute of Pharmacology (Russian Academy of Sciences / Russian Academy of Medical Sciences), with the original dipeptide design and pharmacology credited to T. A. Gudasheva, S. B. Seredenin and colleagues. It emerged from a research program that set out to build short dipeptides whose three-dimensional shape reproduces the pharmacophore of known nootropics — in this case piracetam. The synthesis was first reported in the 1990s.

Noopept is a registered/approved medicine in Russia and reportedly in some neighboring CIS countries. That registration is stated here only as a jurisdictional fact about another country’s drug register. It does not indicate that the compound is approved for, or intended for, human use by customers of a research supplier. In the United States, Noopept is not FDA-approved and is neither an approved drug nor a dietary supplement; it is offered strictly as a research-use-only laboratory material and is not for human consumption.

How Noopept Works: Mechanisms Investigated in Preclinical Studies

The mechanisms below are drawn from animal and cell-based laboratory research. No single receptor target defines the compound; instead, the literature describes a set of converging signals reported across rodent and in-vitro models. Each finding is tied to the model in which it was observed.

Prodrug metabolism to cycloprolylglycine

Noopept functions as a prodrug. In rats, esterases hydrolyze the ethyl ester to N-phenylacetyl-L-prolylglycine, which further cyclizes to the cyclic dipeptide cycloprolylglycine (cPG), releasing phenylacetic acid in the process. Gudasheva and colleagues (1997) identified cyclo-L-prolylglycine as the major metabolite recovered from rat brain and noted its structural similarity to an endogenous neuropeptide. Because the parent molecule is rapidly metabolized, much of the activity reported in preclinical models has been attributed to cPG rather than to the intact parent compound.

Neurotrophic signaling in rodent models (NGF and BDNF)

One of the more frequently cited preclinical findings concerns neurotrophins. In an in-vivo rat study, Ostrovskaya and colleagues (Bull Exp Biol Med, 2008; “Noopept stimulates the expression of NGF and BDNF in rat hippocampus”; PubMed 19240853) reported increased hippocampal messenger RNA expression of nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) following administration in rats. The report described increased hippocampal mRNA for both neurotrophins after a single (acute) administration, with 28-day repeated administration in the same rat model reported not to diminish the hippocampal mRNA response, and in that report to increase it further. In the cerebral cortex, expression fell below control after single administration, while chronic administration produced a slight increase in BDNF expression. A related 2010 report linked the compound’s action to reduced activity of stress-induced kinases alongside increased NGF/BDNF gene and protein expression. BDNF signalling is also a central theme in the Semax research guide. Some BDNF-increase observations derive from cell culture rather than whole animals, so the two contexts should not be conflated.

AMPA modulation, TrkB, antioxidant and HIF-1 signals

Additional mechanisms have been proposed from preclinical work, all model-bound:

• Glutamate / AMPA receptors (cell and animal models): the metabolite cycloprolylglycine has been reported to act as a positive modulator of AMPA-type glutamate receptors, and neuroprotective effects observed in models have been described as dependent on AMPA- and TrkB-receptor activation.
• Cholinergic signaling (preclinical): “choline-positive” properties have been reported at behavioral and neuronal levels in animal and neuronal models, indicating effects on acetylcholine-related signaling without a single defined receptor target.
• Antioxidant and anti-inflammatory pathways (rodent): experimental models have reported reduced oxidative stress, increased activity of antioxidant enzymes such as superoxide dismutase and catalase, anti-inflammatory effects, and repression of stress-activated kinases (pSAPK/JNK, pERK1).
• HIF-1 activation (in vitro / in silico): Ostrovskaya et al. (PMC4837574) reported that Noopept selectively increased the DNA-binding activity of hypoxia-inducible factor HIF-1 in transfected HEK293 cells, an effect enhanced under cobalt-chloride-induced chemical hypoxia; molecular docking suggested an interaction with prolyl hydroxylase-2, with the L-isomer showing higher predicted affinity than the inactive D-enantiomer. A 2020 study similarly reported HIF-1 activation and related gene-expression changes in a laboratory model.
• Ion-channel effects (secondary, lower confidence): some reference summaries describe blockade of voltage-dependent calcium and calcium-dependent potassium channels. This appears mainly in secondary sources rather than as the central finding of the primary mechanism paper and is best treated as a proposed, secondary mechanism.

What Noopept Has Been Studied For (Preclinical Findings)

The endpoints below describe variables that researchers have investigated in animal and in-vitro models. Queries for Noopept benefits land on pages like this one, so the limit is worth stating plainly: no benefit to any person is reported or implied below. What follows are effects measured on defined endpoints in rodent and cell-culture experiments. They are experimental observations, not established outcomes in people. None of the findings has been confirmed in controlled human research, and nothing here should be read as a claim of efficacy for any person.

Memory and learning paradigms studied in rodent models

Much of the behavioral literature involves standard rodent memory paradigms such as passive-avoidance and the Morris water maze. In these settings, GVS-111 has been studied for effects on the acquisition and retention of learned responses in rats and mice. In a rat photochemical (photothrombotic) stroke model, GVS-111 administered intravenously at 0.5 mg/kg/day was reported to attenuate an ischemia-induced memory deficit and to show a neuroprotective effect (“Memory restoring and neuroprotective effects of the proline-containing dipeptide GVS-111 in a photochemical stroke model,” 1999). Reports of this kind describe changes to a memory endpoint measured in the animal, not an effect experienced by a reader.

Neuroprotection models (oxidative stress and ischemia)

Neuroprotective effects have been examined in both cell culture and rodent models. A 2003 in-vitro study reported that GVS-111 reduced oxidative damage and apoptosis in cultured cortical neurons, including neurons derived from Down syndrome tissue — a cell-culture finding rather than an animal or human one. In rodent ischemia-type models, neuroprotective and memory-restoring effects have been reported alongside the antioxidant and anti-inflammatory signals described above. The compound has also been investigated across several rodent models of Alzheimer-like pathology by Ostrovskaya, Bobkova and colleagues (2005–2014): intracerebral beta-amyloid(25–35) injection in rats, olfactory bulbectomy in NMRI mice, and a streptozotocin-induced sporadic-Alzheimer model in rats. Reported outcomes in those models include restoration of spatial memory, changes in anti-beta-amyloid antibody levels, and, in a 2014 in-vitro Alzheimer-related model, reduced tau hyperphosphorylation and apoptosis. Every one of these findings is an observation in an animal or cell model.

Anti-inflammatory and anxiolytic-type observations

In a 2002 rat study (“Anti-inflammatory properties of noopept (dipeptide nootropic agent GVS-111)”), intravenous noopept at 5 mg/kg was reported to suppress carrageenan-induced acute paw inflammation by roughly 62% within three hours. Separately, anxiolytic-like activity has been reported in rodent behavioral models. As with the cognition endpoints, these are behaviors and tissue responses scored in laboratory animals, and the terms “anti-inflammatory” and “anxiolytic-like” are bound to those models rather than to any person.

Evidence limitations

An honest reading of the literature is essential. The substantive mechanistic and behavioral evidence for Noopept is overwhelmingly preclinical — rodent and in-vitro. This guide summarizes preclinical evidence only. None of the mechanisms or endpoints summarized above has been established in controlled human research, and this guide neither reviews nor relies on human clinical data of any kind. Any clinical literature associated with the compound’s registration in other jurisdictions is outside the scope of this research-use-only guide, is not relied on here, and does not support any human use of the material described. Human pharmacokinetics, including elimination half-life, have been described in the literature as not well characterized. In short, the findings summarized here come from laboratory and animal models and have not been established in controlled human research. Efficacy and safety in humans are not established.

Noopept Dosage in Research Studies

The published preclinical literature reports Noopept doses in mg/kg of animal body weight. The figures below describe amounts administered to animals in specific experiments and are provided for research reference only. They are not, and must not be read as, guidance for human intake.

Dosing used in the preclinical literature

Preclinical rodent studies typically express dosing in mg/kg of body weight and administer the compound by injection. Reported examples include:

• ~0.5 mg/kg per day intravenously in the rat photochemical stroke / memory model.
• 0.01 mg/kg intraperitoneally, daily for 21 days, in the olfactory-bulbectomised NMRI mouse Morris water maze model (Ostrovskaya et al., J Psychopharmacol, 2007).
• 0.5–10 mg/kg in rat passive-avoidance/anti-amnesic experiments, including after oral administration.
• 5 mg/kg intravenously in the rat carrageenan anti-inflammatory study.

The behavioral literature also describes a bell-shaped (inverted-U) dose–response in some paradigms, in which activity on a memory endpoint peaked at an intermediate dose and was reduced at both lower and higher doses — a pattern investigators contrasted with piracetam, whose response over the range tested was described as rising monotonically. These are characteristics of the animal dose–response curves reported by investigators, not a schedule for any person. No human milligram amount is derived from them here, and mg/kg animal figures are not converted to human equivalents.

Potency relative to piracetam

A recurring comparative-pharmacology point is potency by weight. In animal studies, Noopept has been reported to be active at doses roughly 1,000-fold lower by weight than piracetam — that is, active in the rodent work at fractions of a milligram per kilogram versus hundreds of milligrams per kilogram for piracetam in comparable animal paradigms. This multiplier is drawn from review and secondary summaries and is best presented as “reported in the literature.” It describes a relationship observed in animal experiments, not a dosing instruction.

Why human dosing is out of scope

Because Noopept is offered as a research-use-only laboratory material and is not for human consumption, no human dosing guidance is provided or implied anywhere in this guide. The compound is not an approved drug or supplement in the United States, and any milligram figure discussed above belongs to a published animal study. Researchers designing a study should refer to the primary literature for the exact model, route, and dose used. Researchers working on other compounds in this class can browse the Nootropics research category.

Noopept Formats Referenced in Research

Reference material and the preclinical literature describe Noopept in a few physical forms and administration routes. These are described here as research handling and study parameters, not as consumer product formats or usage instructions.

Noopept powder (laboratory reference material)

Bulk Noopept is typically encountered as a solid powder used as a laboratory reference material. In a research context, handling, weighing, reconstitution and storage are performed by the researcher according to standard reagent practice. As a small-molecule dipeptide ester, it is generally handled as a dry powder kept under controlled storage to preserve stability, with working solutions prepared as an experiment requires. Nothing about this handling describes preparation for human use.

Noopept nasal spray and the intranasal route

Searches for Noopept nasal spray reflect a delivery format common across the wider research-nootropic market, not a feature of the Noopept literature itself. The published preclinical work on this compound is dominated by injected routes — the rodent studies described above administered it intravenously and intraperitoneally at mg/kg — so intranasal delivery is not where the primary Noopept evidence sits. Intranasal administration is a standard experimental route for centrally acting research peptides generally, and it appears far more often in the Semax and Selank preclinical literature; see the Selank and Semax nasal spray research guide for how that route is described in those models. Where “nasal spray” appears alongside Noopept, it should be read as a product-format label rather than a validated research administration route, and no nasal-spray format is intended for human use.

Solubility and handling notes (research context)

As an ethyl-ester dipeptide, Noopept’s solubility profile differs between aqueous and organic solvents, which is relevant when a researcher prepares stock and working solutions for in-vitro or in-vivo assays. Solvent choice, concentration, and stability under storage are experimental design parameters. Any specific reconstitution scheme should follow the protocol of the study being reproduced and the supplier’s stated handling information for the material as a laboratory reagent.

Noopept vs. Other Nootropic Compounds

Noopept is frequently compared with other research nootropics — most often Semax and piracetam. The comparisons below are structural and mechanistic, drawn from the chemistry and preclinical literature; for a wider survey of cognitive research compounds, see the Dihexa vs Adamax vs Semax comparison.

Noopept vs Semax

Both Noopept and Semax are Russian-developed research nootropics, which is why they are often mentioned together, but they are structurally and mechanistically distinct. Noopept is a small synthetic dipeptide designed as a piracetam analog. Semax is a longer synthetic heptapeptide modeled on a fragment of adrenocorticotropic hormone (an ACTH(4–10) / melanocortin analog). Their proposed mechanisms differ accordingly, and they should not be treated as interchangeable in study design.

Noopept vs piracetam

The relationship to piracetam is by design. Investigators hypothesized that piracetam’s 2-oxo-pyrrolidinone ring could be mimicked by a proline residue and its acetamide group by glycine, then built a dipeptide around that idea and attached phenylacetyl and glycine-ethyl-ester groups. In the rodent paradigms used to characterise piracetam, investigators reported that the resulting dipeptide showed a racetam-like activity profile. Structurally, however, Noopept does not contain the intact 2-oxo-pyrrolidinone ring that defines true racetams, so it is best labeled a “peptide/dipeptide analog of piracetam” rather than a racetam proper. The potency difference in animal models (Noopept reported active at roughly 1,000-fold lower doses by weight) is the other headline distinction.

Related research compounds

Researchers surveying the nootropic space often cross-reference several compounds. For related reading within this library, see the Dihexa research guide, which covers another cognitive compound characterized largely in rodent and cell-based models.

Research-Grade Material and RUO Status

This section explains what “research grade” and “research use only” mean in practical laboratory terms. For laboratory purchasing, “research grade” is a documentation claim rather than a marketing one; the notes below describe what that documentation normally consists of and what research-use-only means as a handling status.

What “research grade” and RUO mean

For laboratory work, the quality attributes that matter are documentation and purity rather than marketing language. Researchers generally look for a certificate of analysis (COA), a stated purity percentage (often assessed by HPLC), identity confirmation, and, where available, independent third-party testing. Research-use-only describes the material’s actual intended use: laboratory research only. It is not for human or veterinary use, not for diagnostic use, and not for any therapeutic application.

Availability at SourcePeptides

SourcePeptides stocks other nootropic research materials rather than Noopept. Researchers working in this area can browse the Nootropics research category for the current catalog. This guide is educational and provides no pricing, ordering, or usage instruction for Noopept.

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Research compounds discussed in this guide

Semax — 5MG

Semax - 5MG — Research-Grade Reference Material Semax - 5MG is supplied as a lyophilized powder for in-vitro laboratory research use only. SourcePeptides supplies this material strictly as a laboratory reference standard.…

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Related compounds

Pfizer Hospira Bacteriostatic Water – 30 mL $45.00$33.75 with 1st order Ara-290 10MG $45.00$33.75 with 1st order Epithalon - 10MG $50.00$37.50 with 1st order GLP-3 (R) 60MG $275.00$206.25 with 1st order

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Frequently Asked Questions

What is Noopept?

Noopept is the laboratory shorthand for a synthetic dipeptide ester (GVS-111 / omberacetam) built in Russia to reproduce piracetam’s pharmacophore in a two-residue scaffold. It is not endogenous and not isolated from any organism, and in the United States it is handled only as a research-use-only laboratory material.

Is Noopept a peptide?

Its core is a dipeptide (a proline–glycine backbone), so in the narrow chemical sense it contains a peptide bond. However, that backbone is chemically blocked — N-acylated with a phenylacetyl group and esterified as an ethyl ester — so it is more precisely a synthetic, modified dipeptide ester. Importantly, Noopept itself is fully synthetic and not endogenous; only its metabolite, cycloprolylglycine, is described as a naturally occurring cyclic dipeptide.

What is GVS-111?

GVS-111 is the original developmental/laboratory code for Noopept (also seen historically as SGS-111 and DVD-111). GVS-111, omberacetam, and N-phenylacetyl-L-prolylglycine ethyl ester all refer to the same molecule.

What has Noopept been studied for in research?

In preclinical models, Noopept has been investigated for effects on learning and memory endpoints (for example passive-avoidance and Morris water maze paradigms in rodents), for neuroprotective effects in cell-culture and rodent ischemia and Alzheimer-like models, for increased NGF and BDNF messenger RNA in rat hippocampus, for anti-inflammatory effects in rats, and for HIF-1 activation in cell-based assays. These are laboratory findings in animal and in-vitro models and have not been established in controlled human research.

What dosing is reported in Noopept studies?

Published animal studies report doses in mg/kg of body weight, roughly 0.01 mg/kg to 10 mg/kg depending on model and route — for example 0.01 mg/kg intraperitoneally in a mouse Morris water maze study and 0.5 mg/kg/day intravenously in a rat stroke model, and 5 mg/kg in a rat anti-inflammatory study, with some paradigms describing a bell-shaped (inverted-U) dose–response in which the intermediate dose was the most active. These figures describe amounts administered to animals in specific experiments and are provided for research reference only. No human dosing is provided or implied.

Is Noopept FDA-approved or legal in the US?

Noopept is a registered/approved medicine in Russia and reportedly some CIS countries. In the United States it is not FDA-approved and is neither an approved drug nor a dietary supplement. It is offered strictly as a research-use-only laboratory material and is not for human consumption; its foreign registration does not indicate approval or suitability for human use.

How does Noopept differ from Semax?

They are different molecule classes: Noopept is a two-residue synthetic dipeptide ester, Semax a seven-residue ACTH(4–10) fragment analog. The comparison section above carries the structural and mechanistic detail; they are not interchangeable in study design.