Noopept (Peptide Note)
Also known as: N-phenylacetyl-L-prolylglycine ethyl ester · GVS-111
A small proline-containing dipeptide derivative — technically a peptidomimetic — developed in Russia as an orally active cognitive enhancer with structural lineage to piracetam.
Noopept is an oral peptidomimetic (N-phenylacetyl-L-prolylglycine ethyl ester) approved in Russia for cognitive indications; active metabolite is cycloprolylglycine.
Evidence tier: B — clinical evidence (trials or approved use in some jurisdictions)
- Category
- Cognitive Enhancement
- Half-life
- Oral bioavailability; parent compound rapidly metabolised to active cycloprolylglycine
- Formula
- C₁₇H₂₂N₂O₄
- Weight
- 318.37 g/mol
Section 1
Overview
Noopept is, strictly speaking, a small peptidomimetic rather than a classical research peptide — a proline-containing dipeptide ester developed in Russia as an orally active analogue of the racetam-class nootropics. It is included on this site because its mechanism of action and discovery history are firmly within the peptide research tradition, and because peer-reviewed literature continues to position it alongside Semax and Selank as part of the Russian cognitive-peptide family.
After oral administration Noopept is rapidly metabolised to cycloprolylglycine, an endogenous cyclic dipeptide that is itself a putative cognitive enhancer. The parent compound and metabolite together produce the pharmacological effects characterised in research.
Reported potency is approximately three orders of magnitude greater than piracetam on equivalent endpoints in animal models, with a broader profile that includes anxiolytic and neuroprotective effects alongside the core pro-cognitive activity.
Section 2
Discovery & History
- Developed in Russia in the 1990s by Skoldinov, Ostrovskaya, and colleagues at the V. V. Zakusov Institute of Pharmacology, as part of a programme to find more potent and orally active successors to piracetam through structural analogue design.
- The molecule was engineered around a proline-glycine core, exploiting the observation that cyclic proline-glycine dipeptides could be endogenously formed from the parent ester and carry pharmacological activity in their own right.
- Granted clinical approval in the Russian Federation in 2011 for cognitive indications — mild cognitive impairment, cerebrovascular disease-associated cognitive decline, and cognitive component of asthenic syndromes.
- Internationally available only as a research chemical; the compound has not entered Western regulatory pipelines despite substantial peer-reviewed interest.
- Subject to a continuing peer-reviewed literature on mechanism, pharmacokinetics, and behavioural pharmacology, with the metabolite cycloprolylglycine now recognised as a distinct pharmacologically-active entity in its own right.
Section 3
Mechanism of Action
- 1Rapid metabolism to cycloprolylglycine (CPG) — an endogenous cyclic dipeptide with intrinsic neuropeptide-like activity — providing a two-component pharmacological profile in which both parent and metabolite contribute.
- 2Modulation of AMPA and NMDA glutamate receptor function in hippocampal neurons, with reported potentiation of AMPA-mediated currents and modulation of NMDA-mediated calcium influx at physiologically-relevant concentrations.
- 3Increased BDNF and NGF expression in the hippocampus after sustained oral dosing — paralleling the Semax/Selank mechanism and providing the mechanistic root for the pro-cognitive effects observed in the Russian clinical work.
- 4Antioxidant effects, including upregulation of endogenous antioxidant enzyme activity (superoxide dismutase, catalase) and measurable reductions in lipid peroxidation markers under stress conditions.
- 5Anxiolytic effects in animal stress models — measurable improvements in open-field, elevated plus-maze, and forced-swim behaviour attributed to modulation of corticosterone responses and glutamatergic tone rather than direct GABA-A binding.
- 6Neuroprotection in ischaemic and excitotoxic injury models — reduced neuronal death, preserved synaptic integrity, and improved functional recovery in cell-culture and in-vivo preparations following controlled injury.
- 7Modulation of cerebral blood flow and cerebrovascular tone — reported vasoactive effects in some experimental models plausibly contributing to the cerebrovascular-indication clinical use in Russia.
- 8Anti-amyloid effects in transgenic Alzheimer's disease models — reduced amyloid-beta accumulation and preserved cognitive performance in some published animal work.
Section 4
Researched Benefits
Findings reported in the published preclinical and clinical literature. Effects in research contexts do not constitute claims of therapeutic benefit in humans.
- 1Improved memory consolidation in animal learning paradigms — replicated across radial-arm maze, passive avoidance, and Morris water-maze tasks in rat and mouse models.
- 2Cognitive improvement in Russian clinical trials in mild cognitive impairment populations, with measurable MMSE and MoCA improvements over placebo and durability at 3-month follow-up.
- 3Anxiolytic effects in animal stress models — a secondary but consistently-reported pharmacological effect that positions Noopept alongside Selank in the anxiolytic-adjacent category.
- 4Neuroprotection against ischaemic and oxidative injury in research models — reduced neuronal death and functional recovery in cerebrovascular models.
- 5Oral bioavailability — distinctive among the broader nootropic peptide family and the practical differentiator that makes Noopept the most-accessible research-context cognitive peptide.
- 6Reported tolerability in long-term clinical use in Russia — the licensed clinical experience covers courses up to 3 months, an unusually long safety database for a small research-tradition molecule.
- 7Anti-amyloid effects in transgenic AD model systems — a plausible mechanism-based angle for cognitive-decline research applications.
- 8Reported effects on subjective clarity and mental fatigue in operator-population research — early behavioural pharmacology work on healthy adults.
Section 5
Theoretical Dosing & Protocols
| Route | Dosage | Frequency | Duration |
|---|---|---|---|
| Oral (clinical use in Russia) | Typical clinical doses 10–30 mg per day | Twice or three times daily | Cycles of 1.5–3 months in published clinical practice |
Note: Not licensed in the UK; this information is provided for educational reference only.
Section 6
Administration Routes
- Oral administration — the molecule's defining feature, made possible by the peptidomimetic chemistry (specifically the N-phenylacetyl protection at the N-terminus and the ethyl ester at the C-terminus) that resists gastrointestinal proteolysis and enables first-pass survival.
- Sublingual administration is anecdotally reported in some non-clinical use contexts, though the peer-reviewed pharmacokinetic characterisation is limited.
- Parenteral (subcutaneous, intramuscular, intravenous) routes are used in some animal research contexts where dose-response control or precise pharmacokinetic characterisation is prioritised over administration convenience.
- Intranasal delivery has been examined but offers no clear advantage over the oral route for a molecule with genuine oral bioavailability.
Section 7
Safety Profile
Commonly reported
- · Mild transient headache — the most commonly-reported adverse effect at initial exposure; typically resolves within the first several days of a course.
- · Sleep disturbance if dosed late in the day — the mild alerting effect argues for morning-and-early-afternoon administration in cycled protocols.
- · Occasional irritability at higher doses — a dose-dependent effect that typically resolves with dose reduction.
- · Mild gastrointestinal upset in a minority of subjects, usually resolving with continued dosing.
- · Transient decreases in blood pressure reported in some subjects; typically clinically insignificant.
Rare / theoretical
- · Hypersensitivity reactions to the excipients or the peptidomimetic components — theoretical concern based on chemistry; documented rate is low.
- · Long-term Western safety data is limited to the Russian clinical experience; chronic-use safety beyond 3 months has not been formally characterised outside licensed clinical practice.
- · Theoretical pharmacodynamic interaction with monoamine-modulating drugs (MAOIs, SSRIs) — extrapolated from mechanistic considerations rather than documented cases.
- · Rare reports of transient elevations in blood pressure at higher doses in cerebrovascular-indication subjects.
Contraindications
- · Not licensed for human use in the UK — supply for human consumption is prohibited under the Human Medicines Regulations 2012.
- · Severe hepatic or renal impairment (per Russian labelling in approved clinical use) — the ester hydrolysis and downstream metabolite clearance are compromised in these settings.
- · Pregnancy and lactation — no controlled human data; excluded from published Russian trial protocols in these populations.
- · Acute hypertensive crisis or uncontrolled severe hypertension — theoretical contraindication based on the reported blood-pressure effects.
Section 8
UK & EU Regulatory Context
United Kingdom
Not licensed as a medicine in the UK. Research chemical only.
European Union
Not approved by the EMA. Used clinically in the Russian Federation.
Section 9
Clinical Studies Summary
Noopept in mild cognitive impairment — randomised trial
Russian randomised controlled trial in a mild-cognitive-impairment population (n>50) reporting cognitive improvement over 8 weeks of Noopept 20 mg/day oral versus placebo, with measurable MMSE and MoCA gains that persisted at the 12-week follow-up assessment. The trial informed the 2011 Russian clinical approval decision.
Noopept and hippocampal BDNF expression
Preclinical molecular-pharmacology study demonstrating that sustained oral dosing of Noopept over 21 days produced significant increases in hippocampal BDNF protein and mRNA expression in rodent models, providing the molecular-mechanism scaffold for the observed cognitive-endpoint improvements in the human clinical work.
Cycloprolylglycine as the active metabolite of Noopept
Pharmacokinetics-mechanism study demonstrating that the rapidly-formed metabolite cycloprolylglycine (CPG) carries a substantial portion of the parent compound's pharmacological activity — direct CPG administration reproduced the cognitive-endpoint effects, confirming a two-component pharmacology in which both parent and metabolite contribute.
Noopept in Alzheimer's disease model systems
Behavioural and molecular study in APP/PS1 transgenic Alzheimer's disease mice, reporting preservation of Morris water-maze performance, reduced amyloid-beta 42 accumulation, and increased BDNF expression in the Noopept-treated cohort versus vehicle controls — extending the mechanistic evidence base beyond ischaemic/oxidative neuroprotection into amyloid-relevant pathology.
Noopept anxiolytic effect characterisation
Behavioural pharmacology study characterising the anxiolytic profile of oral Noopept in the standard rodent anxiety paradigms (elevated plus-maze, open-field, novelty-suppressed feeding), demonstrating a measurable anxiolytic effect distinct from the pro-cognitive endpoint and providing the empirical scaffold for the anxiolytic-adjacent positioning of the compound.
Section 10
Frequently Asked Questions
Section 10a
Practical Research Guidance
Cycle guidance
Reconstitution & storage
UK sourcing notes
Section 11
Sourcing for Laboratory Research
Sourcing Noopept (Peptide Note) for laboratory research
Researchers in the United Kingdom and elsewhere typically obtain Noopept (Peptide Note) from specialist research-chemical suppliers. Purity, third-party testing, and supplier transparency are the principal differentiators worth evaluating before placing an order. The two suppliers below are commonly referenced in UK research contexts.
Reminder: research peptides are sold strictly for in vitro and preclinical laboratory purposes. Importation or supply for human consumption is not permitted under UK medicines legislation.