Cardiogen

Ala-Glu-Asp-Arg, AEDR, "heart tetrapeptide", Khavinson cardiac peptide

Immune & bioregulators

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Summary

Class: Synthetic tetrapeptide (4 amino acids: alanine-glutamate-aspartate-arginine) from the Khavinson "cytogen" family
Mechanism: Proposed to enter cells, bind DNA at gene-promoter regions and nudge expression of genes involved in cardiomyocyte survival and fibroblast activity — shown only in cell and rodent work from one group
Routes studied: Intramuscular and intraperitoneal injection (rodents); oral capsules and sublingual drops (as marketed in Russia; no published pharmacokinetics)
Dose range reported: Rodent studies: roughly 0.1–1 µg/kg to 10 µg/kg injected. Community-reported: 1–2 oral capsules/day in 10–30-day courses, or 5–10 mg/day sublingual. No validated human dose
Half-life: Not characterised. Short peptides of this type are expected to be cleared or degraded within minutes in plasma; whether oral forms reach the heart intact is unknown
Storage: Lyophilised: refrigerate, protect from light. Reconstituted: refrigerate, community practice is use within ~4 weeks. Capsules: room temperature, dry
Regulatory status: Not approved as a medicine anywhere. Sold in Russia as a food supplement ("parapharmaceutical") †. See region table

Doses are as reported in studies or by the community — never recommendations.

1What it is

Cardiogen is one of a series of very short synthetic peptides designed in St Petersburg by Vladimir Khavinson's group at the Institute of Bioregulation and Gerontology. The group first worked with organ extracts (polypeptide "cytomedins" such as Epithalamin and Thymalin), then identified or designed two-to-four-amino-acid sequences that they report reproduce the organ-specific effects. Cardiogen is the heart-targeted member: the tetrapeptide Ala-Glu-Asp-Arg.

It is a synthetic research compound, not a naturally occurring hormone. Nearly all published work comes from the originating group or close collaborators, most of it in Russian-language journals (Bulletin of Experimental Biology and Medicine, Advances in Gerontology) with English abstracts or translations. Independent replication outside that network is, to our knowledge, absent. That is the single most important thing to know when reading any claim about it.

2How it's thought to work

The Khavinson group's unifying hypothesis for all its short peptides is "peptide regulation of gene expression":

The peptides are small and charged enough to pass through cell and nuclear membranes; fluorescence-labelled versions have been shown entering the nucleus of cultured cells (Fedoreyeva 2011).

Once inside, each sequence is proposed to bind preferentially to particular DNA promoter sequences and alter transcription — a kind of sequence-specific epigenetic signal (Khavinson 2014).

For Cardiogen specifically, the group reports effects on cardiomyocyte and fibroblast cultures and on markers of cell proliferation and apoptosis in heart tissue.

A tissue-specificity claim — that AEDR acts on heart and not on, say, lung — rests on the group's own comparative experiments.

Proposed: a tripeptide directed at heart muscle, reported to affect gene expression and tissue repair in animal models. Human evidence is absent.Schematic — not to scale

All of this is mechanism-level, in vitro or rodent. There are no human pharmacodynamic data.

3What the research shows

Cardiomyocyte and cardiac fibroblast biology

Cell-culture work from the originating group reports that Cardiogen changes proliferation and apoptosis markers in heart-derived cells and in ageing cell cultures, in line with their "tissue-specific differentiation" model (Khavinson 2012, Bull Exp Biol Med; Khavinson 2020, Stem Cell Rev Rep). only. [4][6]

Cardiac tissue in ageing rodents

Rodent studies report improved histological and functional indices in aged or stressed heart tissue after Cardiogen courses. Details are mostly in Russian-language reports summarised in the group's reviews (Khavinson & Malinin 2005; Anisimov & Khavinson 2010). Independent replication: none found. [1][2]

Anti-tumour effect in a rodent sarcoma model

The group has reported that Cardiogen slowed growth and increased apoptosis in a transplanted M-1 sarcoma model in rats †. This is sometimes repeated in community discussion as an "anti-cancer" property; it is a single-group rodent finding with no follow-up.

Human outcomes (heart failure, arrhythmia, "cardiac ageing")

No controlled human trial has been published. Russian-language clinical observations of the extract-based predecessors and of Cardiogen as a supplement exist but are uncontrolled and not peer-reviewed in the usual sense. Community reports describe subjective improvements in exercise tolerance or palpitations; these are anecdotal. The literature here is thin, and we have said so rather than pad it.

4Reported side effects and interactions

Literature-reported

No adverse effects reported in rodent or cell studies; no human safety data in the peer-reviewed literature. The group describes its short peptides as non-toxic and non-immunogenic at the doses used.

Community-reported

Very few reports; occasional mentions of mild headache or "feeling wired" in the first days of a course. Most reports describe no noticeable effect at all.

Theoretical. A compound proposed to alter transcription in cardiac cells could in principle affect heart rhythm or remodelling in either direction; nothing has been measured. Any effect on tumour cell apoptosis cuts both ways and is untested in humans.

Interactions. None established. Nothing is known about combination with cardiac medicines (beta-blockers, antiarrhythmics, anticoagulants), and the absence of data is not the same as safety.

Markers researchers commonly monitor

No compound-specific markers are established in any human literature. Markers members commonly discuss, with rationale:

Marker	Why it's watched
Resting ECG and heart-rate variability (wearable)	the compound targets the heart; a baseline rhythm record is the minimum sensible check.
Blood pressure and resting heart rate	cheap, daily, and directly relevant to the claimed organ.
NT-proBNP	the standard blood marker of cardiac strain; only meaningful if there is a clinical reason to check it.
hs-CRP	general inflammation; the group's rationale often invokes "anti-inflammatory" effects.
CBC and CMP	general baseline for any compound with no human safety data.

Free for everyone. Safety information is never behind a paywall.

5Reconstitution and handling

Injectable versions are typically supplied as powder in 10–20 mg vials; oral capsules and sublingual drops are the forms the originating group sells in Russia. For lyophilised vials, with , swirl gently, protect from light. Tetrapeptides are relatively stable but should still be refrigerated once in solution.

Open in calculator, pre-loaded →

6Commonly studied alongside

Other Khavinson bioregulators — Vesugen (vascular), Epitalon (#13, pineal), Vilon, Thymogen — usually in the group's "course" protocols combining two or three tissue peptides. In the community it is sometimes discussed with Epitalon and with MOTS-c in "longevity stacks"; no study of any combination exists.

Informational cross-links. Not stack recommendations.

7Regulatory status by region

Region	Status (checked —)
United States	Not FDA-approved. Not on the FDA 2023 Category 2 compounding list to our knowledge †. Not a permitted dietary supplement ingredient
European Union	Not authorised as a medicine; not a permitted novel food/supplement ingredient
United Kingdom	Not licensed
Australia	Not approved; peptides for injection fall under prescription-only scheduling †
South Africa	Not registered with SAHPRA
Sport (WADA)	Not specifically named. As a non-approved substance it would fall under S0 †

8Open questions

Does any Cardiogen reach cardiac tissue intact after oral or sublingual use? No pharmacokinetic data exist.
Can the reported DNA-binding and gene-expression effects be replicated by an independent laboratory?
Is there any human outcome — even a surrogate marker — that moves with the compound?

9References

1Khavinson VKh, Malinin VV (2005). Gerontological Aspects of Genome Peptide Regulation. Karger, Basel. DOI
2Anisimov VN, Khavinson VKh (2010). Peptide bioregulation of aging: results and prospects. Biogerontology. PubMed · DOI
3Fedoreyeva LI, Kireev II, Khavinson VKh, Vanyushin BF (2011). Penetration of short fluorescence-labeled peptides into the nucleus in HeLa cells and in vitro specific interaction of the peptides with deoxyribooligonucleotides and DNA. Biochemistry (Moscow). PubMed · DOI
4Khavinson VKh, Linkova NS, Polyakova VO, Kheifets OV, Tarnovskaya SI, Kvetnoy IM (2012). Peptides tissue-specifically stimulate cell differentiation during their aging. Bull Exp Biol Med. PubMed · DOI
5Khavinson VKh, Solov'ev AYu, Tarnovskaya SI, Linkova NS (2014). Mechanism of biological activity of short peptides: cell penetration and epigenetic regulation of gene expression. Biology Bulletin Reviews. DOI
6Khavinson V, Linkova N, Diatlova A, Trofimova S (2020). Peptide regulation of cell differentiation. Stem Cell Rev Rep. PubMed · DOI
7Khavinson VKh, Popovich IG, Linkova NS, Mironova ES, Ilina AR (2021). Peptide regulation of gene expression: a systematic review. Molecules. PubMed · DOI

† Being confirmed by our reviewers against current sources.

10Community

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Self-reported side effects Phase 2

Not enough data yet. 0 of the 50 members needed have logged this compound for 4+ weeks. We don't show anything below 50, so no one can be identified.

11Page history

26 Oct 2026Profile published — awaiting medical review

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