Cardiogen
Research OnlyA synthetic tripeptide (Ala-Glu-Asp, AED) developed by Russian scientist Vladimir Khavinson and marketed as a cardiac "bioregulator." Despite that marketing, no PubMed-indexed study has examined AED in heart, cardiomyocyte, or myocardial tissue. The only published AED research is in vitro and non-cardiac — anti-aging gene-expression effects in cultured stem cells, fibroblasts, kidney and immune cells. No human or animal data and no regulatory approval anywhere.
AED · Ala-Glu-Asp · Cardiac tripeptide
Preclinical evidence only
- Preclinical
- 67%
- Clinical
- 0%
Based on 9 cited sources
Demonstrated effect magnitude — not a recommendation or safety claim.
Research depth: only in-vitro cell-culture data exists for AED (Ala-Glu-Asp), all in NON-cardiac tissue (stem cells, fibroblasts, kidney, thymocytes); no cardiac human or animal studies, no RCTs. Mechanism: AED penetrates cells and binds DNA minor groove (docking + gene-expression readout) but lacks knockout/in-vivo confirmation. Plausibility: cardioprotection is a large leap from generic non-cardiac gene-expression effects. Global coverage: AED replicated by an independent Italian group (Russia + Italy), modest volume, no regulatory approval. Community experience: negligible documented use. Effectiveness: not-established (no clinical efficacy data and no meaningful community effect signal). NOTE: all 8 cardiac PMIDs in this dossier are fabricated/mismatched and were excluded; no cardiac-specific AED study exists on PubMed.
Cardiogen is sold as a heart-specific peptide, but no published study has ever examined its AED (Ala-Glu-Asp) tripeptide in cardiac tissue. Every PubMed-indexed AED study is an in-vitro experiment in non-cardiac cells, focused on anti-aging gene expression. The heart framing is a marketing position, not an evidence-based one.
No PubMed-indexed study has examined Cardiogen’s AED tripeptide in heart, cardiomyocyte, or myocardial models. Published AED research is limited to in-vitro work in non-cardiac cells (stem cells, fibroblasts, kidney and immune cells). Claims of cardioprotection, anti-fibrotic, antioxidant, or cardiac-regenerative effects are not supported by any study.
How It Works (Simplified)
The genuinely studied mechanisms of AED are general and non-cardiac:
AED is proposed to enter cells and bind specific DNA sequences (the minor groove) — the general Khavinson “bioregulator” mechanism. Demonstrated in cultured non-cardiac cells.
In cultured stem cells, fibroblasts and renal cells, short peptides including AED have been reported to shift aging-related genes (e.g. IGF1, FOXO1, TERT) and senescence markers (p16, p21, p53, SIRT-6).
Cell-culture studies report effects on stem-cell differentiation (including neuronal) and tissue-renewal processes — entirely outside any cardiac context.
No study demonstrates antioxidant, anti-fibrotic, ischemia-protective, or regenerative effects in heart tissue. The cardiac mechanism is hypothetical.
Key context: Khavinson’s bioregulation theory proposes that short peptides penetrate cells and bind DNA to regulate gene expression in a tissue-specific way. For AED, the published evidence covers only non-cardiac cells, and the body of work is small — mostly from Khavinson-affiliated Russian groups, with some independent in-vitro replication by an Italian group. The “cardiac” designation is a product label, not a tested indication.
Important Limitations
- No published study has examined AED in cardiac, cardiomyocyte, or myocardial tissue
- No animal studies and no human studies of any kind — all evidence is in vitro (cell culture)
- No randomized controlled trials; not approved by any regulator
- Most research comes from Khavinson-affiliated Russian groups; a minority is independent (Italian) in-vitro replication of the broader peptide class
- AED is usually studied as one of several short peptides, not in isolation
- The proposed cell-penetration / DNA-binding mechanism lacks knockout or in-vivo confirmation
- Pharmacokinetics, bioavailability, and any clinical effect in humans are unknown
- Should never replace evidence-based cardiac care
Net effect.Demonstrated only in non-cardiac cultured cells (stem cells, fibroblasts, kidney, immune cells). No cardiac, animal, or human data.
Good Signs (7 indicators)
Warning Signs (5 indicators)
Bad Signs (7 indicators)
For Research Evaluation Only
These quality indicators are general guidelines based on typical peptide characteristics. Professional laboratory testing (HPLC, mass spectrometry) provides definitive quality verification. This checklist is for initial visual evaluation only.
Epithalon
CompatibleBoth are synthetic Khavinson "bioregulator" peptides studied only in vitro for gene-expression/anti-aging effects. No interaction or combination studies exist; any pairing is theoretical.
Thymalin
CompatibleBoth come from the Russian Khavinson peptide-bioregulator program. No interaction or combination studies exist; co-use is not supported by evidence.
Research Note: Interaction data is based on published literature, mechanistic understanding, and theoretical considerations. Most peptide combinations lack direct clinical study. This information is for educational purposes only and does not constitute medical advice. Always consult qualified healthcare providers.
Key Studies Cited
Full reference list available on request. All citations link to PubMed for verification.
This dossier synthesizes available evidence from peer-reviewed literature, regulatory documents, and clinical trial registries. Evidence strength ratings follow a modified GRADE approach.
For complete methodology details, see our Methodology page.
Important Disclaimer
This dossier is for educational purposes only and does not constitute medical advice. Always consult a qualified healthcare provider before making health decisions.
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