Cardiogen

Also known as: AEDR, Ala-Glu-Asp-Arg

Evidence: Preclinical

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Overview

Khavinson-series synthetic tetrapeptide (AEDR) for heart tissue; studied in rat myocardial explants and mouse fibroblasts, where it raised proliferation and cytoskeletal proteins.

Cardiogen is a synthetic tetrapeptide (AEDR, Ala-Glu-Asp-Arg) from the St. Petersburg Institute of Bioregulation and Gerontology, listed as a cardioprotector; the source cited for that label is a US patent, not a study (Khavinson 2022). Published work is in tissue culture and rats: at 10^-12 M it stimulated proliferation and lowered p53 in myocardial explants from young and old rats (Chalisova 2009), raised actin, tubulin, vimentin and lamins A and C 2 to 5 fold in mouse embryonic fibroblasts (Khavinson 2012), and slowed transplanted M-1 sarcoma growth in old rats through tumor necrosis and apoptosis (Levdik 2009). No study in a heart disease model and no human trial has been published.

Benefits

Myocardial explant cell proliferation and lower p53 (rat tissue culture), cytoskeletal and nuclear matrix protein synthesis (mouse cells in vitro), slowed M-1 sarcoma growth (rat)

Dosing reference

Research dose: 200 to 1000 mcg daily: vendor/community range, no published human dose
Range: 200 to 1000 mcg, 1x daily

Sold as oral capsules and as lyophilized powder for injection. Published work used 10^-12 M in tissue culture (Chalisova 2009); no in vivo dose for a heart indication has been published. Community protocols run 10 to 20 day courses two or three times a year; no study compared schedules.

Mechanism

Proposed, from cell culture only. The peptide raised synthesis of cytoskeletal proteins (actin, tubulin, vimentin) and nuclear matrix proteins (lamin A, lamin C) in mouse embryonic fibroblasts, which the authors link to more proliferation and less apoptosis (Khavinson 2012). In rat myocardial explants it lowered p53 expression (Chalisova 2009). Its effect on sarcoma growth appeared to act through tumor blood vessels rather than direct cytotoxicity (Levdik 2009). Gene regulation by direct DNA binding is the developing group's hypothesis, not an established mechanism.

Evidence

Preclinical: animal or in vitro data only

At 10^-12 M, stimulated proliferation and lowered p53 in myocardial explant cultures from 3 and 24 month old rats (Chalisova et al., 2009)
Raised actin, tubulin and vimentin 2 to 5 fold and lamins A and C 2 to 3 fold in mouse embryonic fibroblasts (Khavinson et al., 2012)
Dose-dependently slowed transplanted M-1 sarcoma in old rats via hemorrhagic necrosis and apoptosis, not direct cytostasis (Levdik et al., 2009)
At 0.05 ng/mL, stimulated growth of rat heart explants in organotypic culture, alongside other tissue peptides (Zakutskii et al., 2006)
Human-trial status: no published human study of any design

References

Side effects

No controlled safety study has been published in any species, and the animal and cell studies, almost all from the developing institute, were not designed to detect harm. The rat sarcoma study reports effects on tumor vasculature that have not been followed up for safety (Levdik 2009). Commonly reported (anecdotal): injection-site irritation with injectable forms; oral capsules draw few complaints.

Storage

Storage: Room temperature
Lyophilized: 24+ months

Pharmacology

Half-life: No published pharmacokinetic data in any species
Bioavailability: Not measured in any species. Docking predicts transport by LAT1 and PEPT1 (Khavinson 2022)
Molecular weight: 489.48 Da
Sequence: AEDR (Ala-Glu-Asp-Arg)