F tier · safety concern
The cardiac claim rests on a single 2012 experiment in cultured mouse embryonic fibroblasts showing increased cytoskeletal and nuclear-matrix protein expression, plus later narrative reviews by the same authors; there is no animal cardiac outcome study, no human data, and no registered trial.
Cardiogen
Cardiogen is a synthetic tetrapeptide (AEDR) from Khavinson's St Petersburg group, marketed as a cardiovascular 'bioregulator'. The primary published finding is a 2–5-fold rise in actin, tubulin, vimentin, lamin A and lamin C expression in cultured mouse embryonic fibroblasts, from which cardioprotection is inferred. No cardiac functional endpoint has been measured in any species, and no human study exists.
// we supply this one
available as a research reagent
≥ 98% HPLC · lyophilised powder · batch certificate published. Grade F above is our own and is not adjusted because we stock it.
the explanation
Cardiogen is a four-amino-acid peptide sold as a 'heart' peptide. The main published experiment measured proteins in mouse cells growing in a dish — not in a heart, and not in a person. The cardiovascular claim is an inference from that one cell experiment, repeated in later review articles by the same authors.
regulatory status
No medicinal approval anywhere; research reagent
Cardiogen has no marketing authorisation as a medicine in the UK, EU, or US, and there is no MHRA, EMA, or FDA record for it. A ClinicalTrials.gov query returns no registered study of Cardiogen or AEDR. In Russia it is distributed within the consumer 'Cytogens' peptide product line linked to Khavinson's institute rather than as a registered medicine, and we could not verify any Russian medicines-register entry; notably, the group's own 2014 review of clinical results for its peptide bioregulators does not include Cardiogen. Supplied in the UK as a research reagent only, not for human consumption.
how it works · proposed mechanism
Cardiogen is proposed to work like the rest of the family — cell entry, nuclear localisation, and tissue-specific gene regulation — with arginine at the C-terminus assigned responsibility for cardiac targeting. The supporting data are structural-protein expression changes in a non-cardiac cell type. The mechanistic story is therefore built on a proxy readout.
Cytoskeletal protein upregulation
In cultured mouse embryonic fibroblasts, AEDR increased actin, tubulin and vimentin expression roughly 2–5-fold. The authors interpret enhanced cytoskeletal synthesis as a mechanism for maintaining contractile-cell integrity, but fibroblasts are not cardiomyocytes and no contractile function was measured.
Nuclear matrix and lamin A/C
Lamin A and lamin C expression rose about 2–3-fold in the same system, which the authors link to nuclear stability and reduced apoptosis. Lamin biology is genuinely relevant to cardiac disease, but an expression change in fibroblast culture is a long way from a cardioprotective effect.
Proposed anti-senescence and inflammaging role
A 2023 review from the same institute positions AEDR as a regulator of molecules involved in the cardiovascular senescence-associated secretory phenotype. This is an authorial framing of prior in vitro work rather than new experimental evidence.
Assumed C-terminal organ specificity
Across the family, the terminal residue is claimed to determine which organ's genes are engaged — hence AEDR for heart, AEDL for lung, AEDP for cortex. The rule is asserted from within-group comparisons and has not been validated by any independent laboratory.
what’s reported
evidence shape
5 sourcesThe composition of the cited literature by study type. This describes the shape of the evidence, not its quality — and it does not by itself set the grade.
⚠ the catch
The entire cardiovascular case for Cardiogen is one 2012 cell-culture paper in a Russian translated journal, in mouse embryonic fibroblasts rather than cardiac cells, reporting protein-expression changes rather than any functional outcome. Everything since is review-level restatement by the same institute, which makes the literature look larger than it is without adding evidence. No animal model of cardiac injury, no haemodynamic endpoint, no human data, and no registered trial exist. Even basic chemistry is unresolved: unlike its siblings, AEDR has no verifiable PubChem record or CAS number we could confirm, so purity and identity claims from suppliers cannot be checked against a public reference. For a compound marketed for the highest-stakes organ system, that is the thinnest possible foundation.
key published findings
- ClinicalTrials.gov contains no registered study of Cardiogen or AEDR (verified by registry query).
- The sequence Ala-Glu-Asp-Arg is confirmed in the primary literature: Bulletin of Experimental Biology and Medicine 2012, 'Tetrapeptide H-Ala-Glu-Asp-Arg-OH Stimulates Expression of Cytoskeletal and Nuclear Matrix Proteins'.
- That study used cultured mouse embryonic fibroblasts and measured protein expression only — no cardiac cell type, no functional cardiac endpoint.
- Later positioning of AEDR against cardiovascular senescence and inflammaging (Cells, 2023) is by the same St Petersburg authors and is review-level, not experimental.
- The originating group's own 2014 review of clinical results does not list Cardiogen among the bioregulators with clinical data.
- No PubChem compound record, molecular formula, molar mass, or CAS number for AEDR could be verified; a name search for 'cardiogen' in PubChem resolves to an unrelated compound, and CardioGen-82 (a rubidium-82 generator) is a separate FDA-approved product that pollutes literature searches.
limitations of the evidence
- One primary experimental paper carries the whole compound; the rest of the literature is reviews by the same group.
- Single-originator evidence base: St Petersburg Institute of Bioregulation and Gerontology plus Pavlov Institute of Physiology, with no independent replication located.
- Primary work published in a Russian translated journal (Bulletin of Experimental Biology and Medicine) with limited external scrutiny.
- Chemistry unverifiable — formula, molar mass and CAS left null rather than computed, so supplier identity claims cannot be independently checked.
- Name collision with CardioGen-82, an unrelated FDA-approved rubidium-82 PET generator, makes both literature and registry searching error-prone.
- Sources are shared with the other Khavinson bioregulators in this index, since these compounds share one common body of literature; the shared reviews are not independent support.
documented safety signals
- No documented safety signals, and equally no published human safety data, no toxicology accessible to us, and no adverse-event surveillance.
- Absence of reported harm reflects absence of monitored human exposure.
- Identity risk is a safety issue in itself: with no verifiable public chemical reference record, material sold as 'Cardiogen' cannot be checked against an authoritative standard.
identity
| full name | Cardiogen (Ala-Glu-Asp-Arg, AEDR) |
| category | Other |
| modality | peptide |
| sequence | Ala-Glu-Asp-Arg (AEDR) |
laboratory handling
| storage | Lyophilised powder is stored desiccated at -20 °C and protected from light. Once reconstituted, laboratory practice is refrigeration at 2-8 °C for short-term use, or aliquoting and freezing to avoid repeated freeze-thaw cycles. Handling information only; this compound has no approved human use. |
| solubility | Short hydrophilic peptide, readily soluble in sterile or bacteriostatic water and in dilute aqueous buffer. Lot-specific solubility is stated on the certificate of analysis. |
Handling information describes laboratory practice for a research reagent. It is not a preparation guide for use in humans.
the receipts
5 citedClinicalTrials.gov, US National Library of Medicine · 2026 · official
Cells · 2023 · review
Advances in Gerontology (English translation of Uspekhi Gerontologii, Russian) · 2014 · review
Bulletin of Experimental Biology and Medicine (Russian translated journal) · 2012 · preclinical
Molecules · 2021 · systematic review
others in Other