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Lyochem

Cortagen

Khavinson cortical bioregulator tetrapeptide (Ala-Glu-Asp-Pro, AEDP)

≥ 99.0%CAS (verification pending, please confirm via COA)Khavinson Bioregulators

Overview

Cortagen is a Khavinson-class short-peptide bioregulator with the sequence Ala-Glu-Asp-Pro (AEDP), originally isolated as a fraction from Cortexin (the same cerebral-cortex peptide extract that yielded Pinealon). The C-terminal proline of AEDP distinguishes Cortagen from its closely-related sibling tetrapeptides Epitalon (AEDG) and Bronchogen (AEDL), the three share an Ala-Glu-Asp tripeptide core and differ only in the fourth residue, but the single-residue substitution produces dramatically different tissue-selectivity in the Khavinson research framework. Cortagen is studied in CNS, transcriptional-regulation, and neuro-inflammatory research workflows. Lyochem supplies Cortagen as a lyophilized 20 mg vial at ≥99.0% HPLC purity. Sequence verification by LC-MS/MS is particularly important for Cortagen because of the close-mass relationship with Epitalon (AEDG, MW ≈390 Da) and Bronchogen (AEDL, MW ≈432 Da), confusion between sibling tetrapeptides in the family is one of the more common identity issues with Khavinson-class products. The batch COA should explicitly confirm the AEDP sequence.

Who buys this, and why

Khavinson short bioregulators — Admax, Cortagen, Cartalax, Cardiogen, Bronchogen, Crystagen, Prostamax, Vesugen — ship to research labs replicating Russian-school protocols or running comparative tissue-specific peptide-bioregulator studies. The published literature base for this class is concentrated in Russian-language sources; buyers should expect to consult that literature directly for protocol selection. Analytical-packet expectations are the same as any other lyophilised research peptide.

Primary buyer fit: academic and contract research laboratories.

Specifications

CAS
(verification pending, please confirm via COA)
Sequence
AEDP
Purity (HPLC)
≥ 99.0%
Common vial sizes
20 mg
MOQ
On request
Lead time
14–21 days
Storage
-20°C, protect from light

Documentation available on request

  • Lot-specific Certificate of Analysis (CoA)
  • RP-HPLC chromatogram with peak integration
  • ESI-MS identity confirmation (±0.5 Da)
  • Sequence verification by LC-MS/MS
  • Water content by Karl Fischer
  • SDS / MSDS
  • Source-literature pointer (Russian-language references on request)
  • Stability at −20 °C across 12 months
  • Sequence ladder available on request

Regulatory note

Khavinson bioregulator; CAS commonly not registered. Confirm AEDP sequence on batch COA, sibling tetrapeptides (AEDG / AEDL) are close in mass and easily confused.

Frequently asked questions

How is Cortagen related to Cortexin, and why does the distinction matter?

Cortexin is a complex multi-peptide preparation derived from bovine cerebral cortex, approved as a prescription neurological biological in Russia and several Eastern European markets. Cortagen (AEDP) was identified through fractionation of Cortexin as one of the active short-peptide components driving the parent preparation's neurotrophic effects. Distinguishing the two matters operationally: Cortexin is the complex finished biological with regulatory pedigree; Cortagen is a single defined tetrapeptide isolated from that complex preparation, used in research workflows studying the AEDP-specific component in isolation. Buyers should specify whether they want the defined Cortagen tetrapeptide (this SKU) or the complex Cortexin preparation (different SKU) at order placement.

Why is the AEDP sequence distinct from Epitalon's AEDG despite the single-residue difference?

The C-terminal proline in Cortagen (AEDP) versus glycine in Epitalon (AEDG) is a single-residue substitution but produces meaningfully different biophysical and tissue-targeting properties. Proline introduces a rigid kink in the peptide backbone that glycine (the most conformationally flexible amino acid) does not, this changes the molecule's preferred conformation in solution and at the receptor-interaction interface. The tissue-targeting hypothesis within the Khavinson framework is that each tetrapeptide's specific C-terminal residue determines its preferential tissue distribution and gene-expression-modulation profile. The mechanism details remain hypothesized rather than independently confirmed in Western literature, but the biophysical distinction between proline-containing and glycine-containing tetrapeptides is well-established peptide chemistry.

What's the published Khavinson-school research focus for Cortagen specifically?

Cortagen research within the Khavinson framework focuses on cortical-neuron gene-expression effects, transcriptional regulation in neurons, and neuro-inflammatory protection in animal models of cognitive impairment, stroke recovery, and age-related cognitive decline. The reported mechanism hypothesis centers on penetration into neuronal cells and direct interaction with transcriptional machinery (the Khavinson 'bioregulator' framework's central claim across all family members). Published readouts include modulation of cell-cycle markers in cortical neurons, antioxidant-enzyme expression in CNS tissue, and behavioral readouts in rodent cognitive-decline models. As with the rest of the Khavinson framework, this evidence base is concentrated in Russian-language journals.