Cardiogen Research, Specifications & Scientific Information

Introduction

Cardiogen is the cardiac member of the Khavinson bioregulator series — Ala-Glu-Asp-Arg, four residues, 489 daltons — and the first thing a reader needs about it is that its name belongs to two other things as well.

A PubChem search for "Cardiogen" returns L-carnitine, compound identifier 10917, which is not a peptide and has nothing to do with this compound. CardioGen-82 is a rubidium-82 generator used in cardiac positron emission tomography, a radiopharmaceutical device with its own recall history and its own trial records. Search the bare name in a trial register or a regulatory database and the results belong to the radiopharmaceutical. The peptide is reached only by structure: H-Ala-Glu-Asp-Arg-OH, PubChem compound identifier 11583989.

Beyond the name, the record is small. One rat tumour study, one organotypic explant study in cardiac tissue, one cytoskeletal protein study in fibroblasts, and two appearances in multi-peptide comparisons. The family's shared limitations apply in full and are stated once: all of it from the St Petersburg Institute of Bioregulation and Gerontology and its collaborators, some in Russian, group sizes unstated in the indexed abstracts, no clinical report of any design, and no independent replication. The strongest primary paper on this sequence does not even use the trade name — it calls the compound H-Ala-Glu-Asp-Arg-OH throughout.

What Is Cardiogen?

A synthetic tetrapeptide with free termini, AEDR in single-letter code: L-alanyl-L-alpha-glutamyl-L-alpha-aspartyl-L-arginine.

Structurally it belongs to the Ala-Glu-Asp family: Epitalon closes with glycine, Bronchogen with leucine, Cortagen with proline, Cartalax with nothing at all, and this one with arginine. Arginine is the most strongly basic residue in the standard set, and it is the only one in this molecule — a fact that does real work in the chemistry section below.

Within the series it is assigned to cardiac tissue, and two experiments are consistent with that assignment. In organotypic culture, explants of heart, lung, prostate and pancreas from 3-week-old and 18-month-old rats each responded to their own matched peptide at 0.05 ng/ml ^[5]. And in a separate study explants of cardiac tissue from 3- and 24-month-old rats were exposed to twenty individual amino acids and to this tetrapeptide, with the tetrapeptide producing a larger stimulatory effect than any of the amino acids in both age groups ^[3].

The peptide has not been approved by the U.S. Food and Drug Administration for any indication. No marketing application for it is on record in the United States, and no study of it appears on ClinicalTrials.gov under its sequence.

Cardiogen Specifications

The name is ambiguous outside this literature and the ambiguity has to be handled before the identifiers make sense. A PubChem name search for "Cardiogen" returns L-carnitine, compound identifier 10917, which is an entirely unrelated substance; "CardioGen-82" is separately a trade name for a rubidium-82 generator used in cardiac PET imaging. The peptide is reached by structure, not by name: H-Ala-Glu-Asp-Arg-OH is PubChem compound identifier 11583989, formula C18H31N7O9, average mass 489.48 g/mol. No CAS registry number and no FDA/NCATS unique ingredient identifier resolve for the peptide, so both fields are published as unknown rather than estimated. The identification of the trade name with the sequence comes from the originating group's own reviews, which list Cardiogen as AEDR; the strongest primary paper on the molecule refers to it only as H-Ala-Glu-Asp-Arg-OH and never uses the trade name at all.

Values that a public register does not carry are shown as not publicly characterised rather than estimated. Identifiers are reference values; the certificate of analysis supplied with a laboratory order is the record for a given lot.

How Does Cardiogen Work?

Not established. No receptor has been identified, none is proposed, and the specification table shows primary target, receptor family and agonist status as not publicly characterised.

The structural-protein account. The most specific result for this sequence is a protein-expression one, and its logic runs backwards from a claim rather than forwards from a measurement. In cultured mouse embryonic fibroblasts the tetrapeptide raised expression of the cytoskeletal proteins actin, tubulin and vimentin by two- to five-fold and of the nuclear matrix proteins lamin A and lamin C by two- to three-fold. The paper's conclusion is that the previously reported cardioprotective activity of the tetrapeptide is determined by this capacity to activate structural protein synthesis, which stimulates proliferation and reduces apoptosis ^[1].

Two things are worth separating there. The measurement — several-fold increases in five named structural proteins in a defined cell line — is concrete and, as reported, large. The conclusion is an explanation offered for a cardioprotective effect that the paper itself does not demonstrate and does not cite a source for. The fibroblasts used are mouse embryonic, not cardiac.

The tumour result points somewhere else entirely. In the rat sarcoma work described below, the authors' conclusion is that the compound acts through the tumour's vascular network and explicitly not by a direct cytostatic effect on the tumour cells ^[2]. A vascular mode of action and a cytoskeletal protein synthesis mode of action are not incompatible, but nothing published connects them, and the two papers do not cite one another's mechanism.

Histone binding. The tetrapeptide is one of six reported to bind FITC-labelled wheat histones H1, H2B, H3 and H4 and their complexes with deoxyribooligonucleotides, with binding depending on the histone and on the peptide's primary structure ^[4]. That is the series' general nucleic-acid hypothesis, tested on purified components.

No pharmacokinetic dataset exists for this compound in any species.

Preclinical Research on Cardiogen

Animal research

M-1 sarcoma in senescent rats

Senescent rats carrying transplanted M-1 sarcoma received injections of the peptide ^[2].

Reported results. Apoptosis of tumour cells was higher than control in every experimental group. Inhibition of tumour growth varied with the amount administered and was attributed to haemorrhagic necrosis together with stimulated apoptosis.

The explicit negative. Measurements of proliferative activity indicated that the inhibition was not caused by a direct cytostatic effect of the compound on the tumour. The authors read the morphological signs as pointing to a specific mechanism acting through the tumour's vascular network.

How to read it. The negative finding is the most valuable part of the paper: it rules out the simplest explanation and narrows the claim, which is the opposite of what a promotional account would do. Against that, the indexed abstract states no group sizes, no randomisation, no blinding of the histological scoring, and no statistical tests; haemorrhagic necrosis in a rapidly growing transplanted tumour is also a common non-specific finding; and a single transplantable tumour line in one rat strain from one laboratory supports very little on its own.

Findings in this section were obtained in rats. Nothing in them establishes anything about humans.

Cardiogen Mechanism of Action

In vitro research

Cytoskeletal and nuclear matrix proteins. In cultured mouse embryonic fibroblasts, actin, tubulin and vimentin rose two- to five-fold and lamin A and lamin C two- to three-fold after exposure ^[1]. The lamin result is the more interesting half: lamins A and C form the nuclear lamina, and their levels are a recognised correlate of nuclear mechanical integrity and of cellular senescence, so a change there is a plausible connection to the ageing claims made across this series. It is also a single measurement in a single non-cardiac cell type.

Organotypic cardiac explants against twenty amino acids. Explants of cardiac tissue from 3- and 24-month-old rats were exposed at 10⁻¹² M. Seven of twenty individual amino acids stimulated proliferation in explants from young animals, but only two did so in explants from old animals. The tetrapeptide stimulated proliferation strongly in both age groups, and immunohistochemistry showed decreased p53 expression, which the authors read as inhibition of apoptosis ^[3].

The comparison against twenty free amino acids is the useful design feature here, and it is unusual in this literature. If a short peptide were acting only as a source of its constituent residues, a mixture of those residues should reproduce its effect; the reported failure of most individual amino acids to do so in aged tissue is at least consistent with the peptide doing something the residues alone do not. A mixture of the four constituent residues at matched concentration would be the sharper control, and it was not run.

Tissue-matched explants. Cardiac explants from young and old rats responded at 0.05 ng/ml alongside three sibling peptides in lung, prostate and pancreas ^[5].

Histone binding. Reported among six peptides against four wheat histone classes and their oligonucleotide complexes ^[4].

Everything in this section was observed in cultured cells, excised tissue or on purified proteins. None of it establishes anything about an intact animal, and none of it about a person.

What Is Cardiogen Being Researched For?

• Cytoskeletal and nuclear matrix protein synthesis — the actin, tubulin, vimentin and lamin measurements ^[1].
• Cardiac tissue proliferation in ageing — organotypic explants against an amino acid panel ^{[3, 5]}.
• Tumour vasculature and apoptosis — the transplantable sarcoma model ^[2].
• Peptide–histone interaction — binding to four histone classes ^[4].
• Cardiovascular cell senescence — proposed, in a review, as a regulator of molecules forming the senescence-associated secretory phenotype ^[6].

None of that is research into, or evidence about, research-grade material supplied for laboratory use.

Current Research Status

Status as of September 22, 2026. This block is rendered from maintained fields, not from prose, so it cannot go stale in one place and stay current in another.

Cardiogen vs Related Compounds

L-carnitine and CardioGen-82

Neither is this compound and neither is related to it. L-carnitine is what a PubChem name search for "Cardiogen" returns; CardioGen-82 is a rubidium-82 generator for cardiac imaging. A name collision three ways is a practical hazard for anyone searching registers, and it is the reason this page gives the structure everywhere the name appears.

Epitalon, Bronchogen, Cortagen and Cartalax :: The other members of the Ala-Glu-Asp family, closing with glycine, leucine, proline and nothing respectively. This one closes with arginine, the only basic residue among them, which makes it the least anionic of the group — and the group's premise is that these single terminal differences assign each to a different organ. Vesugen :: The other cardiovascular-positioned peptide of the series, Lys-Glu-Asp. The 2022 senescence review discusses the two together as candidate regulators in cardiovascular cells ^[6], which is the only place they appear side by side.

Evidentiary position

Not approved by the U.S. Food and Drug Administration, no registered trial, no clinical report of any design, and a primary record of five papers from one programme.

No comparison of effect between these compounds is made on this page.

Chemical & Molecular Characteristics

Arginine changes the charge balance and nothing else does. Alanine, glutamate and aspartate contribute no basic groups. Arginine's guanidinium side chain is the most strongly basic in the standard set, with a pKa around 12.5, so it remains protonated across the entire physiological range and well beyond. Set against the glutamate side chain, the aspartate side chain and the C-terminal carboxyl, this gives a molecule with two cationic centres — the guanidinium and the N-terminal amine — and three anionic ones. It is the least net-negative member of the Ala-Glu-Asp family, and it is the only one with a permanently charged cationic group. For a series whose proposed mechanism involves approaching DNA, a polyanion, that difference is not trivial and has never been tested against its siblings directly.

Arginine also complicates the analysis. Guanidinium groups adsorb to silica and to residual free silanols on reversed-phase columns, which can cause peak tailing that is easily mistaken for an impurity or for poor synthesis. Ion-pairing conditions change retention substantially. And arginine-containing peptides are prone to residual protecting-group adducts from synthesis, which appear as small mass shifts rather than as separate peaks.

No aromatic residue, so no absorbance at 280 nm. Quantification relies on peptide-bond absorbance near 214 nm, where buffers and solvents also absorb.

Aspartate and glutamate bring isomers of identical mass. Both residues undergo alpha/beta and alpha/gamma rearrangement under thermal and acidic stress, giving species with the same formula and mass as the intended compound. Mass spectrometry confirms composition, not connectivity.

Two register fields are empty and one is a trap. No CAS registry number and no FDA/NCATS unique ingredient identifier resolve for this peptide, and they are shown as unknown above. The PubChem compound identifier, 11583989, is reached by structure. Any identifier obtained by searching the trade name belongs to a different substance — a point worth checking against a certificate of analysis that cites a registry number for material sold under this name.

Frequently Asked Questions

Scientific References

1. Khavinson VKh, Lin'kova NS, Polyakova VO, et al.. Tetrapeptide H-Ala-Glu-Asp-Arg-OH stimulates expression of cytoskeletal and nuclear matrix proteins Bulletin of experimental biology and medicine; 2012. PMID 22977870 doi:10.1007/s10517-012-1766-9
2. Levdik NV, Knyazkin IV. Tumor-modifying effect of cardiogen peptide on M-1 sarcoma in senescent rats Bulletin of experimental biology and medicine; 2009. PMID 20396706 doi:10.1007/s10517-010-0730-9
3. Chalisova NI, Lesniak VV, Balykina NA, et al.. [The effect of the amino acids and cardiogen on the development of myocard tissue culture from young and old rats] Advances in gerontology = Uspekhi gerontologii; 2009. PMID 20210190
4. Fedoreyeva LI, Smirnova TA, Kolomijtseva GY, et al.. Interaction of short peptides with FITC-labeled wheat histones and their complexes with deoxyribooligonucleotides Biochemistry. Biokhimiia; 2013. PMID 23581987 doi:10.1134/S0006297913020053
5. Zakutskiĭ AN, Chalisova NI, Ryzhak GA, et al.. [The tissue-specific effect of synthetic peptides-biologic regulators in organotypic tissues culture in young and old rats] Advances in gerontology = Uspekhi gerontologii; 2006. PMID 17152728
6. Khavinson V, Linkova N, Dyatlova A, et al.. Senescence-Associated Secretory Phenotype of Cardiovascular System Cells and Inflammaging: Perspectives of Peptide Regulation Cells; 2022. PMID 36611900 doi:10.3390/cells12010106
7. Khavinson V, Linkova N, Kozhevnikova E, et al.. Transport of Biologically Active Ultrashort Peptides Using POT and LAT Carriers International journal of molecular sciences; 2022. PMID 35887081 doi:10.3390/ijms23147733

Every identifier above is resolved against PubMed, Crossref or ClinicalTrials.gov at build time, and the title returned by the register is compared with the title stored here. A page does not publish if a reference fails to resolve.

Research-Use Information

For in vitro research use only. This material is a laboratory reagent. It is not a drug, food, dietary supplement, or cosmetic and is not for human or veterinary use, including ingestion, injection, or any other administration. No information on this page describes or implies any effect in humans or animals. Sold only to researchers under our Terms of Sale.