Cycloprolylglycine
Also known as: CPG · cyclo(L-prolyl-L-glycine) · Noopept active metabolite
An endogenous cyclic dipeptide that is also the primary active metabolite of Noopept, with intrinsic anxiolytic and cognitive effects independent of its parent compound — a research peptide in its own right.
Cycloprolylglycine (CPG) is the endogenous cyclic dipeptide that mediates Noopept's cognitive effects; also produced natively by the brain in low concentrations.
Evidence tier: C — preclinical / mechanistic evidence only
- Category
- Cognitive Enhancement
- Half-life
- Short plasma half-life; behavioural effects persist beyond exposure
- Formula
- C₇H₁₀N₂O₂
- Weight
- 154.17 g/mol
- Sequence
- cyclo(L-Pro-L-Gly)
Section 1
Overview
Cycloprolylglycine, abbreviated CPG, is a small cyclic dipeptide that occurs endogenously in the mammalian brain and plasma. It also happens to be the principal active metabolite formed from Noopept after oral administration — the parent peptidomimetic is rapidly hydrolysed in vivo to release CPG, and a substantial portion of Noopept's pharmacological activity is attributable to this metabolite acting in its own right.
Because CPG is endogenous, it occupies a different regulatory and pharmacological position from purely synthetic research peptides. The molecule has been characterised separately from Noopept in published Russian research, where direct administration of CPG produces measurable anxiolytic, antiamnestic, and neuroprotective effects on standard behavioural endpoints — effects that broadly mirror those of Noopept but with a different pharmacokinetic profile.
The molecule is included on this site because it is studied as a research peptide in its own right and because it provides a cleaner mechanistic probe for the cognitive effects of the Noopept pharmacology — administering CPG directly avoids the metabolic transformation step and produces a more defined pharmacokinetic picture.
Section 2
Discovery & History
- Identified as an endogenous brain dipeptide in early biochemistry work characterising the mammalian neuropeptide landscape.
- Identified as the principal active metabolite of Noopept by the same V. V. Zakusov Institute of Pharmacology group that developed Noopept itself, in pharmacokinetic studies in the early 2000s.
- Studied as an independent research peptide from the mid-2000s onwards in Russian neuropharmacology, with publications covering anxiolytic, antiamnestic, and neuroprotective endpoints.
- No marketing authorisation for Cycloprolylglycine was found in the electronic medicines compendium (emc) or on the EMA's list of centrally authorised medicines on 17 October 2026.
Section 3
Mechanism of Action
- 1Modulation of AMPA and NMDA glutamate receptor function in hippocampal neurons — reported potentiation of AMPA-mediated currents and modulation of NMDA-mediated calcium influx at pharmacologically-relevant concentrations, mirroring the principal Noopept mechanism without the parent-compound metabolism step.
- 2Induction of BDNF and NGF expression in the hippocampus after sustained administration, paralleling the parent-compound effects with a different pharmacokinetic time-course — direct CPG dosing produces less pulsatile and more sustained neurotrophin induction than the metabolite-mediated Noopept pathway.
- 3Direct anxiolytic effects in animal stress models, attributed to modulation of stress-response signalling, HPA-axis dampening, and possibly enkephalin-system interaction — the anxiolytic profile of CPG parallels the anxiolytic-adjacent positioning of parent Noopept.
- 4Antioxidant effects through upregulation of endogenous antioxidant defences (superoxide dismutase, catalase, glutathione peroxidase) and direct radical scavenging, contributing to neuroprotection in oxidative-stress models.
- 5Anti-apoptotic effects in neuronal preparations exposed to ischaemic and excitotoxic stress — preserved mitochondrial membrane potential, reduced caspase-3 activation, and improved neuronal survival.
- 6Endogenous neuromodulatory role — CPG is not simply a pharmacological tool but occupies a functional niche in the endogenous brain neuropeptide landscape, plausibly linking Noopept's pharmacology to a physiological regulatory system rather than an artificial one.
- 7Preservation of dendritic spine density and long-term potentiation in hippocampal preparations under stress or ageing challenges — the cellular-correlate substrate for the observed cognitive-endpoint effects.
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.
- 1Anxiolytic effects in animal stress paradigms with similar magnitude to Noopept but cleaner pharmacokinetics — a research-tool advantage for mechanistic work on the anxiolytic component of the Noopept pharmacology.
- 2Antiamnestic effects in scopolamine-induced amnesia models — preservation of learning under cholinergic blockade, indicating a cognitive-support mechanism robust to acute pharmacological insult.
- 3Neuroprotective effects in ischaemic and oxidative-stress models — reduced neuronal loss, preserved synaptic integrity, and improved functional recovery.
- 4Memory consolidation support in animal learning paradigms — replicated across radial-arm maze, passive avoidance, and Morris water-maze tasks.
- 5Useful as a mechanistic probe for the Noopept pharmacology without the parent-compound metabolism variable — a distinctive research-tool niche.
- 6Endogenous molecule — partial safety floor from the fact that the brain produces and tolerates it constitutively at physiological levels.
- 7Compatible with the broader Russian cognitive-peptide research programme, providing a mechanistic bridge between the endogenous neuropeptide landscape and the pharmacological cognitive-enhancer class.
Section 5
Theoretical Dosing & Protocols
| Route | Dosage | Frequency | Duration | Source |
|---|---|---|---|---|
| Intranasal / oral / parenteral (research) | Microgram to milligram range in animal protocols | Variable across published research | Short courses in most studies | None cited |
Note: Direct administration produces a different pharmacokinetic profile from Noopept-derived CPG.
Section 6
Administration Routes
- Intranasal administration in some research protocols, exploiting the same nose-to-brain pathway as Semax and other cognitive-family peptides.
- Oral administration is feasible because the molecule is small and cyclic, conferring partial protection against gut proteases — bioavailability is reported adequate for CNS effects in the rodent research work.
- Subcutaneous and intraperitoneal parenteral routes used in animal research where dose-response control or pharmacokinetic characterisation is prioritised.
- Sublingual administration explored in some research contexts, exploiting the small molecular size for direct membrane permeation.
Section 7
Safety Profile
Commonly reported
- · Generally well-tolerated in animal research at studied doses — no observable weight, behaviour, or gross-pathology changes over the course lengths reported.
- · The endogenous status of the molecule provides a partial safety floor; the body produces and metabolises CPG constitutively at physiological concentrations.
- · Occasional mild subjective effects reported in some human research (mild alertness, subjective clarity) similar to but distinct from parent Noopept.
- · No documented dependence, tolerance, or withdrawal phenomena in the published research.
Rare / theoretical
- · Long-term safety data outside Russian research is sparse — no substantial Western pharmacovigilance database exists for direct CPG administration.
- · Pharmacological doses substantially above endogenous concentrations have not been characterised for long-term effects — a chronic-dosing safety gap even given the endogenous status.
- · Theoretical pharmacodynamic interactions with glutamate-modulating drugs (memantine, dextromethorphan) given the AMPA/NMDA-receptor modulation mechanism.
- · No reproductive or developmental toxicology data at pharmacological doses.
Contraindications
- · No entry for Cycloprolylglycine was found in the electronic medicines compendium (emc) on 17 October 2026. Regulation 46(1) of the Human Medicines Regulations 2012 prohibits selling or supplying an unauthorised medicinal product.
- · Pregnancy and lactation — no controlled human data at pharmacological doses.
- · Concurrent use of glutamate-modulating pharmaceuticals without a specific research rationale.
Section 8
UK & EU Regulatory Context
United Kingdom
No entry for Cycloprolylglycine was found in the electronic medicines compendium (emc) on 17 October 2026. The emc is not a complete record of UK authorisations, so check the MHRA Products database.
European Union
Not approved by the EMA.
Section 9
Clinical Studies Summary
Cycloprolylglycine as the active metabolite of Noopept
Pharmacokinetic dissection demonstrating that Noopept is rapidly hydrolysed to CPG in vivo, and that direct CPG administration reproduces a substantial portion of the parent compound's behavioural effects. Established the two-component pharmacology in which both parent and metabolite contribute to Noopept's clinical profile, and positioned CPG as a research tool in its own right.
Anxiolytic effects of CPG in animal stress paradigms
Russian neuropharmacology research demonstrating anxiolytic effects in elevated plus-maze, open-field, and novelty-suppressed feeding paradigms following direct CPG administration, comparable in magnitude to Noopept administered at metabolically equivalent doses, with the CPG effect emerging faster owing to the removal of the parent-compound hydrolysis step.
CPG neuroprotection in oxidative-stress models
Molecular pharmacology study reporting upregulation of endogenous antioxidant enzyme activity (superoxide dismutase, catalase, glutathione peroxidase) and reduction of lipid-peroxidation markers in brain-tissue preparations exposed to oxidative challenge in the presence of CPG, providing the biochemical scaffold for the neuroprotective claim.
CPG endogenous concentrations and physiological role
Biochemical characterisation study measuring endogenous CPG concentrations in mammalian brain and plasma across ages and physiological states, providing the physiological baseline against which pharmacological CPG administration must be interpreted.
CPG cognitive effects in scopolamine amnesia model
Behavioural pharmacology study demonstrating that direct CPG administration preserves learning-task performance in the scopolamine-cholinergic-blockade paradigm to a degree comparable to that of parent Noopept, extending the cognitive-tool positioning of CPG independent of its metabolite status.
Section 10
Frequently Asked Questions
Section 10a
Practical Research Guidance
Cycle guidance
Reconstitution & storage
UK sourcing notes
Section 11
Sourcing for Laboratory Research
Sourcing Cycloprolylglycine for laboratory research
Researchers in the United Kingdom and elsewhere typically obtain Cycloprolylglycine 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: this page is educational. Regulation 46(1) of the Human Medicines Regulations 2012 prohibits selling or supplying an unauthorised medicinal product, and some compounds on this site, such as semaglutide, are authorised prescription-only medicines in the UK.