NOT FOR HUMAN CONSUMPTION

Cardiogen is most commonly described in the peptide-bioregulator ecosystem as an ultrashort tetrapeptide with the sequence H-Ala-Glu-Asp-Arg-OH (AEDR), positioned as a cardiac tissue bioregulator. 

Core concept
Cardiogen is not framed as a classic receptor agonist drug. It’s proposed to enter cells and influence gene expression / DNA-associated processes, with particular focus on cardiac repair/adaptation pathways (often via fibroblast/cardiomyocyte biology in models).

Regulatory status
As commonly sold in “bioregulator / research peptide” channels, Cardiogen is not an FDA/EMA-approved medicine(no drug-label-grade indications/safety/PK).

1) Additional benefits now under investigation (Cardiogen/AEDR-centered)

Evidence quality note: The most solidly citable material is mechanistic/review framing and biochemical interaction claims; robust, widely indexed human outcome RCTs (hard CV endpoints) for Cardiogen itself are not clearly established from the above sources.

2) Molecular mechanism of action

2.1 “Pharmacodynamics” framing (typical)

• Intracellular/nuclear interaction paradigm: ultrashort peptides are proposed to enter nuclei/nucleoli and interact with DNA/nucleosome machinery, affecting transcription and DNA repair processes.

• AEDR-specific DNA processing modulation: AEDR is described as influencing DNA hydrolysis via endonuclease systems (enzyme-mediated mechanism proposed).

2.2 Down-stream biology (conceptual map)

3) Pharmacokinetics (PK)

There is no authoritative drug-label PK for Cardiogen in common research/bioregulator commerce. As an unmodified tetrapeptide, systemic exposure would generally be expected to be route/formulation dependent and subject to rapid peptidase degradation, making formal PK/PD bridging critical for any clinical translation claims.

4) Pre-clinical and clinical evidence

4.1 Mechanistic / preclinical (stronger)

• Reviews of peptide gene regulation describe ultrashort peptides (including AEDR) as capable of modulating DNA processing and gene expression pathways.

• Secondary summaries describe effects on cardiac tissue repair biology (often emphasizing fibroblast targets).

4.2 Human clinical evidence (weaker / unclear)

From the retrieved sources here, high-quality, widely indexed human trials showing meaningful clinical outcomes (e.g., EF improvement in HF, post-MI remodeling endpoints, MACE reduction) are not clearly established for Cardiogen itself.

5) Emerging clinical interests

6) Safety and tolerability

High-certainty statement: Cardiogen in typical “research/bioregulator” channels does not come with an FDA/EMA-style safety label, so contraindications/interactions/monitoring are not defined to drug standards.

Practical risk drivers:

• Identity/purity/sterility variability across suppliers (especially given sequence inconsistency in the market).

• Immunologic/local reactions are possible with peptides; true rates unknown without regulated pharmacovigilance.

7) Regulatory landscape

• Generally positioned as research / bioregulator material rather than an approved therapeutic with standardized indications.

8) Future directions (what would validate claims)

1. Sequence + GMP standardization (AEDR confirmed by MS/HPLC; impurities and stability defined).

2. Human PK/PD bridging (exposure, tissue distribution, biomarker engagement).

3. Controlled clinical trials in defined indications (post-MI remodeling, HF biomarkers/imaging endpoints), plus long-term safety datasets.

Selected references

• AEDR definition and general Cardiogen description:

• Peptide gene-expression / nuclear interaction framework (systematic review):

• DNA hydrolysis modulation mention including AEDR among ultrashort peptides:

• Marketplace inconsistency example (different “Cardiogen” sequence claimed)