Noopept (GVS-111, N-Phenylacetyl-L-Prolylglycine Ethyl Ester): A Dipeptide Cognition-Research Compound

Research summary. Noopept (development code GVS-111; chemical name N-phenylacetyl-L-prolylglycine ethyl ester) is a small dipeptide-derived research compound originally developed in Russia as a structural analogue and pharmacological successor to the racetam-class nootropic piracetam. It is a dipeptide ester of phenylacetic acid linked to L-proline-glycine, and is studied across cognition, neuroprotection, oxidative-stress, and amyloid-related neurotoxicity research models. Noopept holds approved status in Russia for cognition-related indications but is not approved by the FDA or EMA. The supporting biological literature is concentrated in a Russian research programme with limited Western replication of human-trial endpoints.

Molecular profile

• Chemical name: N-phenylacetyl-L-prolylglycine ethyl ester
• Class: Dipeptide ester (Pro-Gly backbone with N-phenylacetyl cap and C-terminal ethyl ester)
• Molecular formula: C₁₇H₂₂N₂O₄
• Molecular weight: ~318.4 g/mol
• PubChem CID: 180496
• CAS Number: 157115-85-0
• Synonyms: GVS-111, Noopept, Omberacetam (in some sources, though this name is occasionally disputed)

Mechanism of action

Noopept is interpreted as a multi-target cognition-research compound. Reported mechanisms include:

• Cycloprolylglycine release. Noopept is metabolised in vivo to release cycloprolylglycine (cPG), an endogenous cyclic dipeptide present in mammalian brain with its own reported nootropic and neuroprotective activity. Noopept is sometimes interpreted as a prodrug-like delivery vehicle for cPG.
• BDNF and NGF modulation. Increases in brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) expression have been reported in rodent CNS following noopept administration.
• Antioxidant and anti-apoptotic activity. Cell-culture and rodent studies have reported reductions in reactive-oxygen-species generation, preservation of mitochondrial membrane potential, and reductions in apoptotic markers under stress conditions.
• Calcium-handling and excitotoxicity buffering. Reports include modulation of intracellular calcium homeostasis under glutamate-toxicity stress.
• Tau-pathology modulation in cell-culture models. Reductions in tau hyperphosphorylation have been reported in Aβ-stressed neuronal cultures.
• AMPA/NMDA receptor modulation. Some studies have reported indirect modulation of glutamatergic signalling.

Preclinical research highlights

Amyloid-β neurotoxicity models. Cell-culture work using Aβ25–35-induced toxicity in neuronal preparations has reported that noopept reduces apoptosis, preserves mitochondrial function, reduces tau hyperphosphorylation, and supports neurite integrity. This is one of the most cited lines of evidence positioning noopept as a multi-target neuroprotective research compound.

Cognitive endpoints in rodents. Rodent studies have reported improvements in spatial-learning and passive-avoidance paradigms, with effects reported across both healthy and cognitively compromised animal models.

Cerebral ischaemia models. Rodent ischaemia-reperfusion studies have reported reduced infarct size and improved functional recovery with noopept administration.

Oxidative-stress models. Rodent and cell-culture work has reported reductions in lipid-peroxidation markers and improvements in endogenous antioxidant-enzyme activity.

Anxiolytic activity. Rodent paradigms have reported anxiolytic-like effects, with mechanism proposed to involve cycloprolylglycine release and BDNF-mediated neurotrophic support rather than direct GABAergic activity.

Limitations of the evidence base

Several caveats apply:

• The supporting biological literature is concentrated in a Russian research programme, with limited independent Western replication.
• Clinical-trial data exists primarily within the Russian regulatory framework; major Western trial registries contain comparatively little late-stage noopept-specific data.
• The proposed prodrug-like relationship to cycloprolylglycine is not universally accepted as the dominant mechanism, and a unified mechanistic account remains an active research question.
• The "racetam-related" framing in marketing literature is partly historical — noopept's chemical structure is distinct from the canonical racetam scaffold (it is a phenylacetyl-Pro-Gly ester rather than a 2-pyrrolidone derivative).

Current research status

Noopept is an investigational research compound outside the Russian regulatory framework. It is not approved by the FDA or EMA. Research interest is concentrated in cognition, BDNF/NGF biology, amyloid-related cellular injury models, and post-ischaemic neuroprotection.

For research-supplier contexts, noopept is supplied as a research-grade investigational compound and is not intended for self-administration.

Key takeaways for researchers

• Noopept (GVS-111, N-phenylacetyl-L-prolylglycine ethyl ester) is a dipeptide-ester research compound originally developed in Russia.
• Reported mechanisms include in vivo release of cycloprolylglycine, BDNF and NGF modulation, antioxidant activity, calcium-handling buffering, and tau-pathology modulation in cell-culture models.
• Preclinical research has reported effects across cognition, amyloid-related neurotoxicity, cerebral ischaemia, and anxiolytic-like endpoints.
• Supporting literature is concentrated in a Russian research programme with limited Western replication of clinical endpoints.
• Noopept is not FDA- or EMA-approved.

References

1. 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.
2. Ostrovskaya RU, Vakhitova YV, Kuzmina USh, et al. Neuroprotective effect of novel cognitive enhancer noopept on AD-related cellular model involves the attenuation of apoptosis and tau hyperphosphorylation. J Biomed Sci. 2014;21:74.

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This article is provided for educational and research purposes only. Noopept is a research compound. It is not an FDA- or EMA-approved drug and is not intended for human consumption, diagnosis, treatment, cure, or prevention of any disease or condition. All work involving this compound should be conducted by qualified personnel within an appropriate research setting and in compliance with applicable institutional and regulatory requirements.