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Professor Peptides
Research compound

Cortagen

Also known as Cortagen · Ala-Glu-Asp-Pro · AEDP · AEDP peptide

Ala-Glu-Asp-Pro tetrapeptide studied for chromatin effects; marketed for neuroprotection

Last reviewed · Educational reference — not medical advice.

NCAEDP4 residuesN → C
  • Small / Pro
  • Hydrophobic
  • Polar
  • Acidic
  • Basic
Primary sequence, N → C, by residue class.
Formula
C17H26N4O9
Molecular weight
430.4 g/mol
Half-life
Not characterised in published pharmacokinetic studies
Route
Subcutaneous or intramuscular in the source literature
CAS
335591-03-2
PubChem
18439621 (opens in new tab)
Status
Research compound — short peptide bioregulator
Sequence
AEDP
Mechanism
Reported to induce deheterochromatinisation of condensed chromatin and activate ribosomal gene synthesis in aged cells, selectively at particular chromosome regions. Proposed neuroprotective action is by epigenetic regulation; no receptor or neural mechanism has been demonstrated.
01

Overview

Cortagen is the synthetic tetrapeptide Ala-Glu-Asp-Pro (AEDP). PubChem lists Cortagen under CID 18439621 with formula C17H26N4O9 and CAS 335591-03-2, which matches the formula computed from AEDP exactly. The 2023 chromatin study names it independently as "Ala-Glu-Asp-Pro - Cortagen".

This identity matters, because it is a point where vendor listings contradict each other: some sources assign the AEDP sequence to Cardiogen instead. The chemistry and the literature both place AEDP with Cortagen.

The published evidence is chromatin work. In the four-peptide comparison in lymphocytes from 75–88-year-old donors, Cortagen produced deheterochromatinisation of total heterochromatin and activated ribosomal gene synthesis, while — like the other three peptides tested — leaving pericentromeric structural heterochromatin intact, and acting selectively on specific chromosome regions.

Cortagen is marketed as a brain cortex and spinal cord bioregulator for neuroprotection and cognitive decline. The peptide family as a whole has been reviewed as a candidate class for Alzheimer's disease on epigenetic grounds, but that review proposes a hypothesis; it does not report a Cortagen trial. No indexed study measures cognition after Cortagen administration.

Research areasChromatin remodelling in ageingNeuroepigeneticsUltrashort peptides in neurodegenerationPeptide regulation of gene expression
02

What the evidence shows

Separated by study type
HumanClinical trials and human studies
No controlled clinical trials and no cognitive endpoint measured. Human-derived evidence is ex vivo chromatin work on lymphocytes from 75–88-year-old donors.
AnimalRodent and other animal models
No independently replicated animal outcome data in the indexed literature.
In vitroCell and tissue studies
Induced deheterochromatinisation of total heterochromatin and activation of ribosomal genes in aged-donor lymphocytes, with a selective effect on specific chromosome regions and no decondensation of pericentromeric structural heterochromatin.
03

Key studies & findings

2 studies
  1. 1

    Ala-Glu-Asp-Pro (Cortagen) induced deheterochromatinisation and activated ribosomal gene synthesis in lymphocytes from 75–88-year-old donors, acting selectively on defined chromosome regions.

    2023Georgian Medical News, 2023

  2. 2

    Ultrashort peptides of this class have been reviewed as candidate neuroprotective agents in Alzheimer's disease via epigenetic mechanisms — a proposed hypothesis, not trial evidence for any individual peptide.

    2022International Journal of Molecular Sciences, 2022 (opens in new tab)

04

Benefits & effects

2 documented

  • Deheterochromatinisation of condensed chromatin in aged cells

    Verified

  • Ribosomal gene activation in aged lymphocytes

    Verified
05

Side effects & safety

1 reported

Safety noteResearch compound for laboratory use only. No regulatory safety review, no established human safety database, and no controlled toxicology data in the public literature.

Recorded in the cited literature No controlled human safety data exist for this compound.

  • Marketed cognitive/neuroprotective claims are unsupported by indexed research

    unknown
06

Limitations & open questions

Nearly all published work on this compound originates from a single research programme (the St Petersburg Institute of Bioregulation and Gerontology, Khavinson group) and its collaborators. Independent replication outside that network is sparse to non-existent, sample sizes are small, and much of the source literature is published in Russian-language journals with limited peer-review transparency. Effects reported in cell culture and in aged-donor lymphocytes have not been shown to produce clinical outcomes in controlled human trials. Specific to Cortagen: the neuroprotective and cognitive positioning rests on a review that proposes ultrashort peptides as a candidate class for neurodegeneration, not on any study measuring cognition, neuronal survival, or a neurological endpoint after Cortagen administration.

07

Pharmacology

Cortagen is the tetrapeptide Ala-Glu-Asp-Pro (C17H26N4O9, MW 430.4, CAS 335591-03-2, PubChem CID 18439621). The PubChem formula matches the formula computed from the sequence. No published human pharmacokinetic data exist.

08

Frequently asked questions

Is Cortagen AEDP or is that Cardiogen?

AEDP is Cortagen. PubChem CID 18439621 lists Cortagen as C17H26N4O9 with CAS 335591-03-2 — matching Ala-Glu-Asp-Pro exactly — and the 2023 chromatin paper names it as Ala-Glu-Asp-Pro-Cortagen. Vendor listings that assign AEDP to Cardiogen are incorrect.

Does Cortagen protect the brain?

There is no study measuring any neurological or cognitive endpoint after Cortagen administration. The neuroprotective framing comes from a review proposing this peptide class as a research direction in Alzheimer's disease.

What was actually measured in the Cortagen studies?

Chromatin condensation state in lymphocytes from elderly donors, using differential scanning calorimetry, ribosomal gene activity staining, C-heterochromatin polymorphism and sister chromatid exchange.

09

Citations

3 sources
  1. 1
    Epigenetic modification under the influence of peptide bioregulators on the "old" chromatinLezhava T, Jokhadze T, Monaselidze J, Buadze T, Gaiozishvili M, et al. (2023)
  2. 2
    Neuroepigenetic Mechanisms of Action of Ultrashort Peptides in Alzheimer's Disease (opens in new tab)Ilina A, Khavinson V, Linkova N, Petukhov M (2022) · doi:10.3390/ijms23084259
  3. 3
    Peptide Regulation of Gene Expression: A Systematic Review (opens in new tab)Khavinson VKh, Popovich IG, Linkova NS, Mironova ES, Ilina AR (2021) · doi:10.3390/molecules26227053