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Animal data onlycardiovascularlongevityrecovery

Cardiogen

Myocardium-directed tetrapeptide taken in short courses for cardiac muscle support, usually alongside the vascular bioregulators as the heart half of a Russian cardiovascular protocol.

Also known as Ala-Glu-Asp-Arg, AEDR, heart Cytogen, Cardiogen tetrapeptide, Cardiogen

Animal data onlyRodent or other animal studies. Dose translation to humans is genuinely uncertain.

Aged-rodent and cardiomyocyte-culture work from Khavinson's institute reports improved contractile protein synthesis and mitochondrial markers. There is no human trial, no outcome data, and no independent replication. Anyone selling this as heart medicine is well beyond what the evidence supports.

How it works

Cardiogen is Ala-Glu-Asp-Arg. Khavinson's group reports that it restores protein-synthetic activity in aged cardiomyocyte cultures and improves markers of myocardial contractility and mitochondrial density in aged rodents. The mechanistic claim is the class-standard one: a small charged peptide reaching the nucleus and de-repressing tissue-specific genes, with the arginine residue proposed to drive the DNA groove interaction. Cardiogen has also been described in Russian sources as improving recovery after myocardial ischaemia, but that work is not available in a form a Western reader can evaluate.

Targets: Cardiomyocytes, Contractile protein synthesis, Myocardial mitochondria

Dosing

ProtocolDoseFrequencyRoute
Research-market injectable courseAny time of day.1 mg – 2 mgonce daily for 10 to 20 dayssubcutaneous
Oral capsule courseBefore food.1 mg – 2 mgonce daily for 20 to 30 daysoral
  • · Standard vial-market protocol from a 20 mg vial; no dose-finding data exists.
  • · Chelohart is the corresponding heart Cytomax capsule if you prefer the extract format.

Cycling

Ten to twenty days injectable or a month of capsules, then three to six months off. Two to three courses per year.

Work out your exact syringe units →

Pharmacology

Half-life
Not measured; a free tetrapeptide clears from plasma within minutes.
Onset
Nothing acute. Any effect is framed over a full course.
Routes
subcutaneous, oral, intramuscular
Molecule
Synthetic tetrapeptide
Sequence length
4 amino acids
Molecular weight
489.5 Da

Handling

Diluent
Bacteriostatic water
Typical mix
2 or 3 mL
Vial sizes
20 mg
Lyophilised
Room temperature short term; fridge or freezer long term.
Reconstituted
Refrigerated, use within about 30 days.
Light sensitive
Yes — keep it out of the light

Mixing

20 mg in 2 mL gives 10 mg/mL; 1 mg is 10 units on a U-100 syringe.

Side effects

  • commonInjection-site irritationTransient.
  • commonNo consistent systemic side effects reportedReflects a thin exposure record rather than demonstrated safety.

Do not use if

  • Do not substitute this for actual cardiac care - using an unproven peptide in place of guideline heart failure or ischaemic therapy is the real danger with this compound.
  • Pregnancy and breastfeeding - no data.
  • Active malignancy.

Combining it

  • synergyvesugenHeart plus vessel is the standard Russian cardiovascular Cytogen pairing.
  • synergyss-31Both are aimed at cardiac mitochondria, though elamipretide has vastly better evidence and is doing the real work.

What to monitor

  • · If you have known cardiac disease, keep to your normal cardiology follow-up - echo, BNP and symptom tracking are the meaningful measures, not anything specific to this peptide.
  • · Blood pressure and resting heart rate logged across a course.

Legal status

Not approved for human use in the US, UK or EU; sold as a research chemical or as a supplement capsule in Russia and Eastern Europe.

References

  • Khavinson & Malinin, Gerontological Aspects of Genome Peptide Regulation (Karger monograph) (review)
  • Khavinson, Linkova & Tarnovskaya, short peptides regulate gene expression (preclinical)

Mechanism in depth

Cardiogen has the thinnest verifiable file of the injectable Cytogens, and the two papers I could confirm are not the ones the marketing leans on. Chalisova's group looked at myocardium tissue culture from young and old rats and reported effects on tissue development, comparing the peptide against free amino acids - that is the substrate for the contractile-protein-synthesis claim. The other confirmed paper is stranger and more interesting: Levdik and Knyazkin reported a tumour-modifying effect of cardiogen on M-1 sarcoma in senescent rats. A cardiac peptide with an oncological readout is not what the label suggests, and it is another example of the tissue-specificity doctrine not surviving contact with the primary literature. What I could not verify is anything about mitochondria. The mitochondrial density and myocardial contractility claims that appear throughout vendor copy are not supported by a paper I was able to retrieve, and the arginine-drives-the-DNA-groove-interaction argument is a structural rationalisation from the docking work on the family generally rather than a Cardiogen-specific finding. The honest summary: this is the class mechanism - small charged peptide, no receptor, proposed nuclear entry and chromatin de-repression - applied to heart tissue on the strength of a naming convention and one organotypic culture study.

What usually goes wrong

Substitution, and here it can kill someone. Heart failure and ischaemic heart disease have therapies - ACE inhibitors or ARNIs, beta blockers, SGLT2 inhibitors, mineralocorticoid antagonists - with mortality reductions demonstrated in tens of thousands of randomised patients. Cardiogen has an organotypic rat myocardium culture. Anyone deferring or reducing guideline therapy to run peptide courses is trading proven survival benefit for a naming convention. Second, the mitochondrial claims are unverified: I could not retrieve a study demonstrating mitochondrial density or contractility changes with this peptide, so treat that language as vendor copy. Third, the same microgram-versus-milligram dose gap as the rest of the class.

Bloodwork worth running

MarkerWhenWhy it matters
NT-proBNPBaseline and three months later if you have known cardiac disease. Not indicated in a healthy person.If someone is taking a cardiac peptide because they have actual heart disease, this is the number that reflects ventricular wall stress and it is the one a cardiologist will act on. It is also the marker that will make it obvious that a peptide changed nothing.Act if: A rising NT-proBNP, or any value above roughly 125 pg/mL in someone under 75 with symptoms, means you need cardiology, not another course.
hs-troponinBaseline in anyone with cardiovascular risk. Not for routine course monitoring.Baseline hs-troponin is a genuine risk marker in asymptomatic people and it is the test that catches ongoing myocardial injury. Nothing about Cardiogen is expected to move it.Act if: Any detectable rise with chest symptoms is an emergency and has nothing to do with peptides.
Lipid panel with ApoB, plus a seven-day home blood pressure averageBaseline and at your normal clinical interval.These are the modifiable drivers of the disease Cardiogen claims to address. Measuring them is how you find out whether you are treating the actual problem or a story about the actual problem.Act if: ApoB above about 100 mg/dL or a home average above 135/85 mmHg in someone with cardiac risk means evidence-based therapy, not a research peptide.

Pharmacokinetics

Metabolism
Aminopeptidase cleavage to alanine, glutamate, aspartate and arginine.
Elimination
Renal filtration of fragments.

Receptor targets

  • Myocardial tissue in organotypic cultureNo binding data

    Reported effects on the development of myocardium tissue culture from young and old rats. This is the substrate for the contractile-protein claim and it is a dish.

  • M-1 sarcoma in senescent rats

    Reported tumour-modifying effect - an off-label oncological finding that further undermines the idea that these peptides act only on their named tissue.

  • No identified receptorNone published

    No receptor. No binding constant. No mitochondrial target I could verify.

What to expect, and when

Nothing acute and nothing perceptible at any point. Days one to twenty: injection-site irritation only. Weeks four to twelve: if you are tracking blood pressure and resting heart rate properly, this is where a change would show, and no change is the expected result. Anything you feel is either another compound in the stack or expectation. If you develop chest pain, breathlessness or palpitations during a course, that is a cardiac event to be investigated, not a peptide side effect to be waited out.

Stacking and comparisons

Cardiogen plus Vesugen is the standard Russian cardiovascular pairing and is convention, not tested synergy. Cardiogen plus Chelohart is duplication - Chelohart is the heart Cytomax extract. The stack that shows up in longevity protocols is with elamipretide (SS-31), and the framing there should be honest: elamipretide is a mitochondria-targeted tetrapeptide with completed clinical trials in primary mitochondrial myopathy and Barth syndrome, real cardiolipin binding, and a defined mechanism. If those two are in a stack together and anything changes, elamipretide is the reason.

Against elamipretide (SS-31): not comparable. Elamipretide binds cardiolipin, has a defined mitochondrial mechanism and has been through registrational trials. Against Vesugen: Vesugen has a more specific in vitro dataset - endothelin-1, connexins, sirtuin-1 - than Cardiogen has for heart tissue. Against Chelohart: the synthetic at least has defined chemistry. Against guideline heart failure therapy: there is no comparison to make, and framing it as one is the mistake that causes harm with this compound.

Rough cost

$35–$110/month. One 20 mg vial per ten- to twenty-day course. Indicative research-chemical pricing, not verified against vendor listings in this session.

Genuinely uncertain

  • The Ala-Glu-Asp-Arg sequence is what the Khavinson literature and vendor material state, but Cardiogen has no PubMed supplementary-concept record giving the sequence, so I could not verify it independently. Flagged as unverified.
  • No pharmacokinetic data of any kind.
  • I could not verify any study demonstrating mitochondrial density, mitochondrial function or contractility changes with this peptide despite those claims being standard in vendor material.
  • No human data of any kind - no trial, no case series, no bloodwork study.
  • The verified in vivo result is an oncological one in sarcoma-bearing senescent rats, not a cardiac one.
  • Oral absorption of the intact tetrapeptide has never been demonstrated.
  • Cost figures are indicative research-chemical estimates and were not verified against live vendor listings in this session.

Papers