For laboratory and research use only — not for human consumption. All content is educational.
3 min readLast reviewed 16 May 2026
Cognitive Enhancement

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.

Cognitive EnhancementUK: Research onlyNot for human use
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.
  • Remains a research chemical in all jurisdictions including the United Kingdom; not separately licensed despite the endogenous status.

Section 3

Mechanism of Action

  • 1Modulation of AMPA and NMDA glutamate receptor function in hippocampal neurons, 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.
  • 3Direct anxiolytic effects in animal stress models, attributed to modulation of stress-response signalling and possibly enkephalin-system interaction.
  • 4Antioxidant effects through upregulation of endogenous antioxidant defences, contributing to neuroprotection in oxidative-stress models.
  • 5Anti-apoptotic effects in neuronal preparations exposed to ischaemic and excitotoxic stress.

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.

  1. 1Anxiolytic effects in animal stress paradigms with similar profile to Noopept but cleaner pharmacokinetics.
  2. 2Antiamnestic effects in scopolamine-induced amnesia models — preservation of learning under cholinergic blockade.
  3. 3Neuroprotective effects in ischaemic and oxidative-stress models.
  4. 4Memory consolidation support in animal learning paradigms.
  5. 5Useful as a mechanistic probe for the Noopept pharmacology without the parent-compound metabolism variable.
  6. 6Endogenous molecule — partial safety floor from the fact that the brain produces and tolerates it constitutively.

Section 5

Theoretical Dosing & Protocols

The protocols below summarise dose ranges reported in published research only. They are not recommendations and not a guide for human use.
RouteDosageFrequencyDuration
Intranasal / oral / parenteral (research)Microgram to milligram range in animal protocolsVariable across published researchShort courses in most studies

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.
  • Oral administration is feasible because the molecule is small and cyclic, conferring partial protection against gut proteases.
  • Parenteral routes used in animal research.

Section 7

Safety Profile

Commonly reported

  • · Generally well-tolerated in animal research at studied doses
  • · The endogenous status of the molecule provides a partial safety floor; the body produces and metabolises it constitutively

Rare / theoretical

  • · Long-term safety data outside Russian research is sparse
  • · Pharmacological doses substantially above endogenous concentrations have not been characterised for long-term effects

Contraindications

  • · Not authorised for human use
  • · Pregnancy and lactation — no controlled data

Section 8

UK & EU Regulatory Context

United Kingdom

Not a licensed medicine in the UK. Research chemical only.

European Union

Not approved by the EMA. Not on any major regulatory schedule.

Section 9

Clinical Studies Summary

V. V. Zakusov Institute, peer-reviewed2006

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.

Russian neuropharmacology literature2010

Anxiolytic effects of CPG in animal stress paradigms

Russian neuropharmacology research demonstrating anxiolytic effects in elevated plus-maze and open-field paradigms following direct CPG administration, comparable in magnitude to Noopept administered at metabolically equivalent doses.

Peer-reviewed pharmacology literature2013

CPG neuroprotection in oxidative-stress models

Upregulation of endogenous antioxidant enzyme activity and reduction of lipid-peroxidation markers in brain-tissue preparations exposed to oxidative challenge in the presence of CPG.

Section 10

Frequently Asked Questions

Noopept is the orally administered parent compound; CPG is its principal active metabolite. The two share most of the cognitive and anxiolytic pharmacology, but the pharmacokinetics differ — Noopept administration produces a metabolite-dominated effect profile, while direct CPG administration produces a cleaner pharmacokinetic picture without the parent-compound transformation step.

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: 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.

Further reading

Related research summaries

BDNF and the cognitive peptide family — the central mechanistic theme

BDNF induction is the common molecular endpoint shared by the most-studied nootropic peptides. What that means for research interpretation.

Read research summary

Get notified when new peptide profiles go live

Occasional emails when we publish a new peptide profile or research summary. No marketing, no human-use recommendations.

We never share your email. Unsubscribe in any message.