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COGNITIVEPEPTIDE PROFILE

Cortagen

Also known as Ala-Glu-Asp-Pro, AEDP tetrapeptide, Cortagen bioregulator

Cortagen is a synthetic tetrapeptide (Ala-Glu-Asp-Pro) developed by Professor Vladimir Khavinson as a brain cortex bioregulator. It belongs to the family of Khavinson short peptide bioregulators and is studied primarily for neuroprotection, peripheral nerve regeneration, and restoration of cortical function in aging. It acts on the central nervous system and has secondary effects on cardiac and immune tissue.

Last updated April 10, 2026

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Cortagen: quick citable summary

Cortagen is listed by PeptaHub as a cognitive peptide with a research only legal-status classification. The page summarizes mechanism, research context, common routes, safety notes, and references for writers and AI answer engines.

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PeptaHub. “Cortagen: Mechanism, Research Context, Safety.” peptahub.com, 2026. https://peptahub.com/peptides/cortagen. Licensed CC BY 4.0.

License: Creative Commons Attribution 4.0 International. Link back to https://peptahub.com/peptides/cortagen.

SAMEAS / EXTERNAL IDS
Cortagen CAS: 335591-03-2
QUICK ANSWER

What is Cortagen?

Cortagen is a synthetic tetrapeptide (Ala-Glu-Asp-Pro) developed by Khavinson as a brain cortex bioregulator. Its published data is rodent: altered cardiac gene expression in mice and reduced ischemic damage in rats. No human trial exists.

§ 01

Overview

Cortagen is a synthetic tetrapeptide (Ala-Glu-Asp-Pro) developed by Professor Vladimir Khavinson as a brain cortex bioregulator. It belongs to the family of Khavinson short peptide bioregulators and is studied primarily for neuroprotection, peripheral nerve regeneration, and restoration of cortical function in aging. It acts on the central nervous system and has secondary effects on cardiac and immune tissue.

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Mechanism of action

Cortagen is proposed to act as an epigenetic regulator in the Khavinson model: short peptides penetrate cell membranes and interact with DNA, modulating transcription. The transcriptomic result usually quoted for it comes from mouse heart, not brain. Anisimov and colleagues injected female CBA mice with Cortagen for 5 consecutive days and profiled 15,247 cardiac transcripts by cDNA microarray; 234 clones, matching 110 known genes, changed significantly, with maximum up- and down-regulation of +5.42 and -2.86 fold. The genes spanned various functional categories, and the study did not single out oxidative stress or apoptosis pathways. In rats with chronic brain ischemia, Cortagen and Cortexin accelerated behavioral recovery and limited lipid peroxidation. Heterochromatin decondensation is a proposed extension from the wider bioregulator literature rather than a Cortagen-specific result.

§ 03

Reported study ranges

PurposeRouteReported rangeFrequency
neuroprotection and nerve regeneration (research)subcutaneous15 mgonce daily

Reported ranges are for research context only. Consult a qualified healthcare professional before using any peptide.

Convert Cortagen research-range units

Need to convert mg to mcg, dose volume, or U-100 syringe units? The Cortagen dose calculator is preloaded with these ranges, or use the general dose unit converter.

§ 04

Research summary

Cortagen has a small but real literature, almost entirely Russian-language and preclinical. The best-documented findings are a mouse cardiac transcriptome study, rat models of chronic brain ischemia and ischemic preconditioning where Cortagen limited lipid peroxidation and aided behavioral recovery, and work on tetrapeptide effects on free-radical processes. The 2004 microarray paper states in its introduction that Cortagen showed a therapeutic effect on posttraumatic peripheral nerve recovery in humans, but that is a background assertion pointing at other work rather than data reported in the paper, and the underlying human study could not be located. No randomized controlled trial of Cortagen exists in any language, and no Western replication has been published as of 2026.[1][2][3][4]

📄This section cites 4 peer-reviewed sources. View all references →
§ 04b

Evidence grading

Each claimed benefit is graded by the strength of available evidence. Grades reflect study quality, not effect size.

insufficient
Promotes peripheral nerve regenerationAsserted as background in Anisimov 2004 but not measured there, and the underlying study could not be located. The previously printed figure of a 40% increase in regenerating fibers at 10 mcg/kg IM had no source and has been removed
preliminary
Alters gene expression in vivoAnisimov Neuro Endocrinol Lett 2004: female CBA mice, 5 daily injections, cardiac cDNA microarray. 234 clones matching 110 genes changed. This is mouse heart tissue, not brain and not human cells
preliminary
Neuroprotection in brain ischemiaZarubina Eksp Klin Farmakol 2011 and Bull Exp Biol Med 2016: rats with chronic brain ischemia and ischemic preconditioning. Rodent only
insufficient
Post-stroke neurological recovery in humansNo human study of Cortagen in stroke was located

Strong = multiple RCTs · Moderate = limited trials or observational · Preliminary = animal or in vitro only · Insufficient = anecdotal or no published data

§ 05

Side effects

Limited human safety data
Injection site reactions
Headache (anecdotal)
No significant toxicity observed in preclinical studies

Side effects vary by individual. This is not an exhaustive list. Report unusual symptoms to a healthcare professional.

§ 06

Common stacks

Peptides commonly paired with Cortagen for synergistic effects.

§ 08

Sourcing & access

Research compound

Cortagen is classified as a research compound. Regulatory status varies by jurisdiction. Always verify current legal status and source from vendors providing third-party certificates of analysis (COA).

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Frequently asked questions

Cortagen is a synthetic tetrapeptide (AEDP) from Professor Vladimir Khavinson's bioregulator family, studied primarily for neuroprotection, peripheral nerve regeneration, and restoration of cortical function in aging. It is classified as a research compound and is not FDA-approved.

Cortagen is proposed to act as an epigenetic regulator that enters cells and interacts with DNA to modulate transcription. The supporting measurement is a microarray study in mouse heart, where 5 days of injections changed expression of 110 genes. Note that this was cardiac tissue in mice, not brain tissue and not human cells, so it establishes that the peptide does something to gene expression rather than showing a specific neurological mechanism.

Human safety data is essentially absent. No toxicology study or human trial of Cortagen was located. Anecdotally reported side effects include injection site reactions and headache. The evidence base is Russian-language rodent work without independent replication.

No human dose has been established by any published study. Supplier material quotes 1 to 5 mg subcutaneously daily in cycles, but no trial tested that range and there is no human pharmacokinetic data for the peptide. The intranasal figures previously listed here had no source and have been removed.

§ 10

Research references

  1. Elucidation of the effect of brain cortex tetrapeptide Cortagen on gene expression in mouse heart by microarrayAnisimov SV, Khavinson VKh, Anisimov VNNeuro Endocrinol Lett, 2004PubMed
  2. [Cortexin and cortagen as correcting agents in functional and metabolic disorders in the brain in chronic ischemia] (Russian-language; rats)Zarubina IV, Shabanov PDEksp Klin Farmakol, 2011PubMed
  3. Neuroprotective Effects of Peptides during Ischemic PreconditioningZarubina IV, Shabanov PDBull Exp Biol Med, 2016PubMed
  4. Effects of bioactive tetrapeptides on free-radical processesKozina LSBull Exp Biol Med, 2007PubMed
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