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Cardiogen

Cardiac Bioregulatory Tetrapeptide | Cardiovascular & Tissue Repair

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What is Cardiogen?

Cardiogen is a lab-made four-amino-acid peptide (called a bioregulator) developed by Russian researchers to study cardiac tissue in cell cultures and animal models. Published research looks at how it interacts with heart-muscle cells in laboratory settings, with no human clinical trials conducted to date. It's sold here strictly as a research chemical for laboratory study, not for use in people or animals.

Key terms:

Cardiogen is a synthetic tetrapeptide.

Cardiogen (Ala-Glu-Asp-Arg, or AEDR) is a lab-made peptide of four amino acids. It belongs to the bioregulator family developed by Professor Vladimir Khavinson at the St. Petersburg Institute of Bioregulation and Gerontology. Lab work reports that it acts on heart tissue in three ways: it changes how fibroblasts (connective-tissue cells) multiply, it lowers p53 activity so fewer heart-muscle cells self-destruct, and it increases proteins of the cell skeleton and the nuclear matrix. Preclinical studies have looked at cardiac remodeling, recovery from heart-muscle injury, and age-related heart decline. Every published study so far is a cell-culture (in vitro) experiment or an animal model.

Key research areas

  • Direct systemic delivery for cardiac tissue support
  • Established reconstitution protocols
  • Most commonly studied administration route in preclinical research

Researched dosing

This table reflects dosing schedules used in community and preclinical research settings for Cardiogen — presented as research-methodology reference, not usage instructions.

PhaseDoseFrequencyRoute
Standard protocol (community-derived)10mgEvery 3-7 daysSubQ
Higher-dose protocol (community-derived)20mgEvery 3-7 daysSubQ
Extended course (community-derived)10-20mgWeekly for up to 16 weeksSubQ

Commonly cycled 4 weeks on, 12+ weeks off.

How it works

At the cell level, Cardiogen research looks at how the peptide interacts with heart-muscle cells (cardiomyocytes) and supporting tissue cells (fibroblasts) in cultured and animal studies — the terms below are just the biology names for those cell types and processes.

Subcutaneous injection provides systemic distribution allowing AEDR tetrapeptide to reach cardiac tissue and modulate fibroblast proliferation and cardiomyocyte apoptosis pathways

Molecular data

These figures — molecular weight, chain length, sequence — are the chemistry ID researchers use to confirm a Cardiogen sample is the four-amino-acid AEDR sequence it's meant to be.

Weight
489.47 Da
Length
4 amino acids
Type
Tetrapeptide

Ala-Glu-Asp-Arg (AEDR)

Research applications

This section summarizes the research areas — cardiac tissue, cellular health, and longevity pathways — that preclinical studies have looked at for Cardiogen, based entirely on cell-culture and animal-model data, not human trials.

Cardiovascular

Most studied

Preclinical models suggest cardiomyocyte proliferation stimulation and apoptosis suppression through p53 downregulation. Coronary artery ligation mouse models suggest reduced necrotic zones and improved survival outcomes. Stimulates cardiac cell proliferation in both young and aged tissue cultures, potentially addressing age-related cardiovascular deterioration.

Cellular

Well studied

Cellular-level effects on cardiac tissue through modulation of fibroblast proliferation and cardiomyocyte apoptosis pathways.

Longevity

Early research

Potential longevity effects through cardiac tissue support and cellular regeneration based on preclinical data.

Dosage reference

Doses used in research
10–20 mg per dose
Frequency in studies
Every 3-7 days
Handling
Reconstituted solution — research use only; not for administration
Timeline reported in studies
Research protocols typically run 2-4 weeks; effects studied in preclinical models only
Storage
Refrigerate at 2-8°C, use within 30 days after reconstitution
Cycle length
2-4 weeks
Break between cycles
3-6 months between cycles

Interactions

This list shows which other peptides researchers and the community study alongside Cardiogen, and why.

BPC-157 — synergistic TB-500 — synergistic Pinealon — compatible Cartalax — compatible Thymosin Alpha-1 — compatible Epitalon — synergistic Conventional Cardiovascular Medications — compatible Growth Factors (IGF-1, HGH) — compatible

Reconstitution & storage

This is the standard laboratory method for turning freeze-dried Cardiogen powder into a liquid research solution using bacteriostatic water.

  1. Allow vial to reach room temperature (15-20 minutes)
  2. Clean vial top with alcohol swab and allow to dry
  3. Calculate required bacteriostatic water volume using the calculator below
  4. Draw calculated volume of bacteriostatic water into syringe
  5. Inject water slowly down the inside wall of the vial (never directly onto powder)
  6. Gently swirl until powder completely dissolves (never shake)
  7. Solution should be clear - discard if cloudy or contains particles

Lyophilized: Room temperature, use within Stable until expiration date

Reconstituted: 2-8°C, use within 30 days

Open the Cardiogen reconstitution calculator

Quality indicators

These are the checks — powder appearance, solution clarity, lab-report verification — researchers use to confirm a Cardiogen sample is pure and correctly identified before use in a study.

White Lyophilized Powder - Pure Cardiogen appears as white to off-white lyophilized powder or cake

Clear Reconstituted Solution - Properly reconstituted solution should be crystal clear with no particles or cloudiness

Certificate of Analysis - Should include HPLC purity verification (>97%), sequence confirmation (AEDR), and mass spectrometry data

Research Use Only - Cardiogen is not approved for human use - ensure proper research context and documentation

Discolored or Cloudy Solution - Yellow, brown, or cloudy reconstituted solution indicates degradation - do not use

What to expect

This timeline summarizes what animal and cell-culture research reports at each study stage — theoretical research context, not a personal-results promise.

Week 1-2

No significant observable changes expected

Week 2-4

Preclinical research suggests cellular-level effects on cardiac tissue

Long-term

Benefits are theoretical based on animal and in vitro data only

Safety notes

This section covers handling cautions and regulatory notes for Cardiogen — it is not approved for human use by any regulatory agency, and this is research-use-only scope, not medical advice.

  • Not recommended during active cancer due to proliferative effects on fibroblasts
  • Contraindicated in pregnancy and lactation due to absence of safety data
  • Medical supervision recommended
  • Not approved for human use by any regulatory agency
  • All published research is preclinical (animal and in vitro studies)

Regulatory status

  • Not approved by the FDA for any indication.
  • Supplied and described for laboratory research use only — not for human or veterinary use.

Community data

Community Poll

How would you rate your overall experience with this peptide?

1284 votes · Community data

Community Insights

82%reported positive results
68%noticed effects within 2 weeks
91%would recommend to others

Based on data the community reported. Not clinical proof.

References

  1. Mouse embryonic fibroblasts · AEDR treatment · 30 min exposure

    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.

  2. Rat myocardial tissue · Various concentrations · Young (3-month) and old (24-month) tissue cultures

    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.

  3. Senescent rats · Multiple doses · M-1 sarcoma model

    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.