Cardiogen
Cardiac Bioregulatory Tetrapeptide | Cardiovascular & Tissue Repair
Cardiogen (Ala-Glu-Asp-Arg / AEDR) is a synthetic tetrapeptide bioregulator developed by Professor Vladimir Khavinson at the St. Petersburg Institute of Bioregulation and Gerontology. It targets cardiac tissue through modulation of fibroblast proliferation, suppression of cardiomyocyte apoptosis via p53 downregulation, and upregulation of cytoskeletal and nuclear matrix proteins. Preclinical research has explored its potential in cardiac remodeling, myocardial injury recovery, and age-related cardiovascular decline. All published studies to date are based on in vitro experiments and animal models.
Daily dose
10-20mg
Frequency
Every 3-7 days
Cycle length
2-4 weeks
Storage
2-8°C
Key benefits
Cardiac tissue support, fibroblast proliferation, cardiomyocyte protection, cytoskeletal protein upregulation
How it works
Tetrapeptide that stimulates expression of cytoskeletal proteins (actin, vimentin, tubulin) and nuclear matrix proteins (lamin A, lamin C) in fibroblasts, while suppressing apoptosis in cardiomyocytes via p53 downregulation
Dosage protocols
Goal
Standard Injectable (Community-Derived)
Dose
10-20mg · Every 3-7 days
Route
SubQ
Goal
Oral Capsule Protocol
Dose
2 capsules (200mcg) · 1-2x daily before meals
Route
Oral
Goal
Oral Intensive Protocol
Dose
2 capsules (200mcg) · Twice daily before meals for 1 month
Route
Oral
Research indications
cardiovascular
cellular
anti Aging
Administration
Interactions
Safety notes
Not approved for human use by any regulatory agency (FDA, EMA)
All published research is preclinical - based on in vitro and animal studies only
Russian pharmaceutical capsule form available as dietary supplement in CIS countries
Side effects are reported as rare in Russian clinical experience when properly sourced
Not recommended during active cancer due to fibroblast proliferative effects
Contraindicated in pregnancy and lactation due to absence of safety data
Can be combined with conventional cardiovascular medications per Russian protocols
Research studies
Cytoskeletal and Nuclear Matrix Protein Expression (2012)
Mouse embryonic fibroblasts | AEDR treatment | 30 min exposure | 2-5x protein upregulation
Tetrapeptide H-Ala-Glu-Asp-Arg-OH enhanced expression of cytoskeletal proteins (actin, tubulin, vimentin) by 2-5 times and nuclear matrix proteins (lamin A, lamin C) by 2-3 times in cultured mouse embryonic fibroblasts, establishing the mechanism for its cardioprotective activity.
View study →Myocardial Tissue Culture in Young and Old Rats (2009)
Rat myocardial tissue | Young (3-month) and old (24-month) | Various concentrations | Proliferation stimulation
Cardiogen demonstrated significant stimulating effect on cell proliferation in myocardial tissue from both young and old rats. Immunohistochemical analysis showed decreased p53 protein expression, indicating inhibition of apoptosis in cardiac tissue.
View study →Tumor-Modifying Effect on M-1 Sarcoma (2009)
Senescent rats | M-1 sarcoma model | Multiple doses | Dose-dependent tumor inhibition
Dose-dependent inhibition of M-1 sarcoma growth through hemorrhagic necrosis and stimulation of tumor cell apoptosis. Mechanism operated through disruption of tumor vascular network rather than direct cytostatic effects.
View study →Tissue-Specific Bioregulator Effects in Organotypic Culture (2006)
Rats (young 3-week and aged 18-month) | Heart, lung, prostate, pancreatic tissue | 0.05 ng/ml | Tissue-specific stimulation
Cardiogen, alongside other Khavinson peptides (bronchogen, prostamax, pancragen), showed tissue-specific stimulating effects on heart tissue cultures at 0.05 ng/ml, confirming organ-selective bioregulatory activity in both young and aged rats.
View study →Fibroblast Signaling Factor Expression in Aging (2010)
Human prostate fibroblasts | Cell aging model | Peptide treatment | Enhanced CXCL12, WEDC1, ghrelin
Cardiogen and related peptides enhanced expression of signaling factors (CXCL12, WEDC1, ghrelin) in aging fibroblasts, with treated older cultures achieving expression rates comparable to young controls. Demonstrates potential for age-correction at the cellular level.
View study →Coronary Artery Ligation Mouse Model
Mouse | Coronary artery ligation | AEDR treatment | Threefold mortality reduction
Experimental myocardial injury model using coronary artery ligation showed a threefold reduction in mortality in AEDR-treated groups versus controls, with potential reduction in necrotic zones. The cardioprotective activity is attributed to activated synthesis of cytoskeletal and nuclear matrix proteins.
View study →