Cardiogen

Ala-Glu-Asp-Arg (cardiac bioregulator)

Cardiogen (Ala-Glu-Asp-Arg (cardiac bioregulator)) is a longevity & bioregulators research compound. Khavinson cardiac bioregulator — proposed to normalize protein synthesis and gene expression in heart-muscle and vascular tissue.

How Cardiogen works

Khavinson cardiac bioregulator — proposed to normalize protein synthesis and gene expression in heart-muscle and vascular tissue.

Proposed benefits

Researched for mitochondrial and cellular-energy support, tissue-specific bioregulation and healthy-aging pathways.

Where to get Cardiogen

The evidence for Cardiogen

Graded by what exists behind each claim.

Human clinical evidence

• The human record is Soviet and post-Soviet clinical work — real patients and real endpoints, published in Russian and rarely replicated to Western standards.

📊 Correlative data

• Used in Russian cardiology practice as an adjunct and in the community for cardiac support with age. Typically run in courses alongside Vesugen or Ventfort on the reasoning that muscle and vessel are separate targets.

🧪 Theoretical / extrapolated

• Ala-Glu-Asp-Arg — a defined tetrapeptide targeting cardiomyocytes, proposed to normalize protein synthesis in heart muscle.
• The shared claim across the Khavinson series: peptides this short are proposed to enter the cell nucleus and bind promoter regions of DNA, shifting tissue-specific gene expression.
• Cardiac muscle is largely post-mitotic, which makes it an unusually reasonable target for a gene-expression argument — you cannot replace those cells, so maintaining function in existing ones is the only available strategy.

How to read the Soviet clinical series → · The Khavinson series, in full →

How to read these tiers: they say how much human evidence exists, not how well something works — and ✗ flags harm, never a disappointing trial. How the evidence tiers work →

What Cardiogen actually does

Cardiogen is Ala-Glu-Asp-Arg. Four residues, formula C18H31N7O9, average mass 489.50 Da, isoelectric point 4.18, computed net charge about −1.06 at blood pH. Two structural facts about it are worth more than everything written on the vendor pages combined.

Fact one: this is Pinealon with an alanine stuck on the front. Pinealon is Glu-Asp-Arg. Cardiogen is Ala-Glu-Asp-Arg. The difference is 1 alanine residue, 71.08 Da, and the same relationship runs through the rest of the catalog: Chonluten (Glu-Asp-Gly) and Epitalon (Ala-Glu-Asp-Gly); Ovagen (Glu-Asp-Leu) and Bronchogen (Ala-Glu-Asp-Leu). Three pairs, each differing by a single N-terminal alanine, each pair sold for two entirely different organs — brain and heart, pineal and lung, liver and lung. Either that one alanine redirects a molecule from one organ to another, which would be a remarkable and highly specific claim, or the organ assignments are not coming from the chemistry at all. Nobody in this market states the pattern, and the pattern is visible from the sequences alone.

Fact two: the arginine makes this the most plausible DNA binder in the family and the least plausible tissue-specific one. Arginine's guanidinium group is the single most common DNA-contacting side chain in structural biology, because it makes paired hydrogen bonds to guanine and salt bridges to the phosphate backbone. The systematic search this group published for structural motifs that let peptides bind double-stranded DNA is the place that logic is worked out Kolchina 2019. Arginine is also why this peptide's computed charge is only −1.06 while the purely acidic members of the set sit near −2.06 — the positive guanidinium cancels one of the carboxylates. So it is less repelled by the phosphate backbone than its siblings. The problem is that arginine-to-guanine contact is the most generic interaction in nucleic acid chemistry. It is what makes binding likely and specificity unlikely, at the same time and for the same reason.

What the group itself claims. The 2021 gene-expression review reports AEDR among the peptides that bind fluorescently tagged histone proteins H1, H2B, H3 and H4 Khavinson 2021 — that is the proposed route from a peptide in the cytoplasm to a promoter in the nucleus. Note what it is not: it is not a report of AEDR regulating any named cardiac gene. The related peptide EDR has a developed mechanistic literature of its own, and that literature is about neurons and Alzheimer's disease Khavinson 2021, not about cardiomyocytes.

Cell, rodent, human — and where it stops

Say the count first. 0 randomized human trials, 0 controlled human trials, 0 human data of any kind. What this compound does have is 3 indexed Russian-language papers, and they are more interesting than anything on a vendor page.

In explant culture, and this is the tissue-specificity experiment the whole catalog rests on. Organotypic culture of explants from heart, lung, prostate and pancreas taken from 3-week-old and 18-month-old rats, with cardiogen, bronchogen, prostamax and pancragen applied at 0.05 ng/mL; the report is a stimulating effect in the appropriate tissue cultures against control explants in all groups Zakutskiĭ 2006. Read the title and then read the abstract again: it says the effect appeared in appropriate tissue, and it does not say whether any peptide was ever applied to a non-matching tissue. That cross arm — cardiogen on lung, bronchogen on heart — is the entire content of the word 'specific', and this paper does not report it.

In myocardial tissue specifically, and here the number is startling. Myocardial explants from 3-month and 24-month-old rats, cardiogen at 10^-12 M — a picomolar concentration — against 20 individual amino acids run as comparators Chalisova 2009. 7 of the 20 amino acids stimulated proliferation in young tissue and only 2 still did in old tissue; cardiogen stimulated proliferation in both. The mechanistic readout is the part nobody quotes: immunohistochemistry showed decreased p53 protein under cardiogen, which the authors read as inhibition of apoptosis in the myocardium.

And in a tumor model, where the same molecule does the opposite. Rats with transplanted M-1 sarcoma, cardiogen injected: tumor cell apoptosis higher than control in every experimental group, dose-dependent inhibition of sarcoma growth through hemorrhagic necrosis, and explicitly not a direct cytostatic effect — the authors attribute it to the tumor's vascular network Levdik 2009. Put the last two paragraphs side by side and the page has a real problem to think about rather than a slogan: p53 down and apoptosis suppressed in heart muscle, apoptosis driven up in tumor tissue, from the same peptide, in the same species, reported in the same 2 years. Both cannot be a general property of the molecule; at least one of them is a property of the tissue it was in, and nobody has said which.

The cell-level record beyond that is 1 line in a review: it binds histones Khavinson 2021. No named cardiac gene is credited to it anywhere.

What the class contributes, and where it stops. The transport case is that PEPT1, PEPT2, LAT1 and LAT2 carry these molecules into cells, with a described substrate range of di- and tripeptides Khavinson 2022; AEDR has 4 residues, so it is outside that range, and the 2023 assessment that scored 26 of these peptides against those carriers was docking against all 8,400 possible di- and tripeptides with no measured uptake in any cell Khavinson 2023. The DNA case is a structural argument about motifs Kolchina 2019, and the nuclear entry it presupposes was demonstrated in HeLa cells Fedoreyeva 2011 rather than in a cardiomyocyte. The human case for the family as a whole comes from an independent systematic review that pooled 24 randomized trials over 2,245 participants on cognitive endpoints, rated risk of bias moderate to high and certainty low to very low, and contains no cardiac arm at all Alsulaimani 2021.

The obstacles, and they are specific rather than generic. (1) Every animal result is in explanted tissue or in a transplanted tumor, and neither is a working heart. An explant is cut off from blood supply, innervation and load; a beating heart under afterload is a different system, and no study has measured contractile function, ejection fraction or infarct size. (2) The concentration that worked in culture, 10^-12 M, was applied directly to tissue; nothing published says what concentration reaches myocardium after an injection in any species. (3) 4 residues sits outside the di- and tripeptide substrate range described for PEPT1, PEPT2, LAT1 and LAT2 Khavinson 2022, and the 2023 scoring of 26 peptides against those carriers was docking with no cellular uptake measured Khavinson 2023. (4) The tissue-specificity paper does not report the cross-tissue arm Zakutskiĭ 2006. (5) Its nearest structural relative, the same sequence minus 1 alanine, is sold for the brain and has a developed neurological literature Khavinson 2021 — and no experiment has ever put the 2 side by side.

And the comparison that matters is not to another peptide. Cardiovascular risk is the most heavily studied area in medicine. Lowering apolipoprotein B, treating blood pressure and stopping smoking are supported by randomized trials with mortality endpoints and effect sizes measured in the tens of thousands of participants. This compound has 0. That gap is the honest context for every decision about it, and it is a gap of evidence rather than a claim that the molecule does nothing.

Cardiogen pharmacokinetics — how much of it actually gets in

The catalog says ‘Short’. Here is what has to be true behind that word.

What degrades it. A free N-terminal alanine is an aminopeptidase N substrate, and aminopeptidase N is abundant on vascular endothelium — the exact surface a subcutaneous dose has to cross to reach the circulation. Nothing on this molecule slows that down: no acetyl cap, no D-amino acid, no C-terminal amide, no ring. For an unmodified 4-residue peptide the expected plasma residence is minutes, and there are 0 published pharmacokinetic measurements for it in any species to check that expectation against.

The oral barrier, which is why this one is not sold as a capsule. A swallowed tetrapeptide meets gastric acid, then pancreatic proteases, then brush-border peptidases, and the only named route across the enterocyte is PEPT1, whose described substrate range is di- and tripeptides Khavinson 2022. Anything crossing would then face hepatic first-pass extraction. No oral bioavailability figure has ever been published for this molecule, so the only honest move is to bound it: even at a generous 1 in 10 surviving, an oral course and a subcutaneous course would differ roughly 10x in delivered material, and nothing published could distinguish a 10x gap from a 1,000x one.

The injectable route, and what it does and does not buy. Subcutaneous injection removes the gut and the first-pass liver from the problem, which is a real advantage over the oral products in this catalog. It does not remove plasma peptidases, and it does not answer the question that actually matters here, which is whether any of the dose reaches cardiac tissue. 0 biodistribution studies exist for this compound or for any other member of the family, so tissue delivery is assumed on every page that sells it, including the ones that sound most technical.

What would have to be true, and how you would know it was not

Three predictions. The first two say what should not happen, which on this compound is the informative direction.

1. ApoB will not move, and that is the number that decides cardiac risk. There is no proposed mechanism by which a 4-residue peptide changes hepatic apolipoprotein B secretion or LDL receptor activity. This site retests ApoB every 3 to 6 months after an intervention, so draw it before and after a course and expect a flat line. If it falls, look at what else changed — diet, weight, alcohol, a statin dose — before crediting the peptide. This prediction argues against the product and it is the one most worth running, because a person taking a cardiac peptide while their ApoB sits high has bought a story instead of a risk reduction.

2. Lp(a) will not move either, and you only need to measure it once. Lipoprotein(a) is genetically set and this site's own guidance is that once in a lifetime is sufficient unless kidney or thyroid status changes markedly. It is on this page because a high Lp(a) is the single most common unmeasured reason a person has cardiac risk they do not know about, and a course of an unstudied peptide is a poor substitute for finding that out.

3. Where a real effect could hide, if there is one. The family-level claim is about gene expression in aging tissue, and the closest circulating markers a person can actually order are hs-CRP, retested at 3 months on this site, and fibrinogen, retested every 6 to 12 months when elevated. Neither is cardiac-specific and neither would prove anything on its own — but a course that moved neither, alongside an unmoved ApoB, would mean the compound produced no measurable change in anything a person can test, which is a conclusion worth being able to state. High-sensitivity troponin is deliberately not on that list: it is a marker of myocardial injury ordered on physician direction, not a wellness readout, and a self-ordered troponin is far more likely to generate an alarm than an insight.

What nobody has tested yet

Five experiments. The first is the one that would tell you whether this entire catalog means anything.

1. Nobody has compared Ala-Glu-Asp-Arg with Glu-Asp-Arg head-to-head. These two products differ by 1 alanine and are sold for the heart and the brain respectively. Put both on the same cells — cardiomyocytes and neurons, 1 experiment, 1 readout — and the tissue-specificity claim that justifies selling a catalog of separate organ products either survives or does not. The reagents cost almost nothing, both peptides are commercially available, and in 20 years nobody has published it. This is the single most informative unrun experiment in this category.

2. Nobody has measured whether it reaches the heart. A labeled biodistribution study in rodents, counts per gram of tissue in heart, brain, liver, kidney and plasma at 5 timepoints, is standard and old. Every organ-specific claim in this catalog depends on the answer and no member of the family has one.

3. Nobody has run the cross-tissue arm of the experiment that already exists. The 2006 organotypic study applied 4 peptides to their 4 matching tissues Zakutskiĭ 2006. Adding the mismatched pairs to the same protocol — cardiogen on lung explants, bronchogen on heart explants — is the same rats, the same culture technique and the same readout, and it is the difference between 'stimulates its own tissue' and 'stimulates tissue'. 20 years later it is still unpublished.

4. Nobody has tested the arginine hypothesis against a control. If arginine is what lets these peptides contact DNA, then Ala-Glu-Asp-Arg and a version with the arginine replaced by lysine or by glutamine should differ measurably in a DNA melting or electrophoretic mobility shift assay. That is a first-year experiment and it would put a number on the mechanism this whole family is sold on Kolchina 2019.

5. No cardiac endpoint of any kind has been collected in a person. Not an echocardiogram, not a resting heart rate, not heart-rate variability from a wrist device that millions of people already own. A group running a course with continuous heart-rate variability logging would produce the first human cardiac dataset that exists for this molecule, and the equipment is already on their wrist.

Cardiogen — its own safety story, not its class's

The class block is generic to injectable peptides. Two things here are not.

The dangerous failure on this page is substitution, not toxicity. Chest pain on exertion, breathlessness that is new, ankle swelling, palpitations with lightheadedness, and a blood pressure nobody has measured in a year are all situations where the cost of a peptide course is the time it takes. Cardiac medicine has randomized evidence with mortality endpoints; this compound has 0 human studies. The relevant harm is what happens during the months somebody spends on an unstudied injection instead of a lipid panel, an ApoB, a blood pressure cuff and a conversation about smoking.

The stacking issue this page owns. This site's own catalog notes that Cardiogen and Chelohart are aimed at the same tissue, and people commonly run Cardiogen with Vesugen or Ventfort on the theory that muscle and vessel are separate targets. There is no published evidence that any of those combinations behaves differently from any one of them alone, and no interaction study exists for any pair. Running 3 unstudied compounds at once does not triple the information you get; it makes any change impossible to attribute, which is the practical harm.

The finding that belongs in a safety section and has never been put in one. The myocardial culture work reports that cardiogen lowers p53 protein expression and, on the authors' own reading, inhibits apoptosis in that tissue Chalisova 2009. p53 is the cell's principal tumor suppressor and apoptosis is how a damaged cell is removed; suppressing both is the direction you want in a heart cell you are trying to keep, and it is the opposite of the direction you want anywhere a cell has acquired damage. The counterweight is real and comes from the same group: in rats carrying M-1 sarcoma, cardiogen increased tumor cell apoptosis and slowed growth through hemorrhagic necrosis rather than by a cytostatic effect Levdik 2009. So the published record contains 1 result pointing each way, both in rats, neither replicated, and 0 studies of either effect in a person. That is not a reason for alarm and it is not a reason for comfort. It is the specific open question this compound carries, it is invisible on every page that sells it, and anyone with a history of cancer should weigh it before a course rather than after.

What 0 reported adverse events means. It means there has never been a trial arm in which one could have been recorded. It is not a safety finding, and the honest version of the sentence is that nothing is known in either direction for this specific sequence.

Sources read for this page

• Chalisova NI, 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 2009 · PMID 20210190
• Levdik NV, et al. Tumor-modifying effect of cardiogen peptide on M-1 sarcoma in senescent rats. Bulletin of Experimental Biology and Medicine 2009 · PMID 20396706
• Zakutskiĭ AN, et al. The tissue-specific effect of synthetic peptides-biologic regulators in organotypic tissues culture in young and old rats. Advances in Gerontology 2006 · PMID 17152728
• Fedoreyeva LI, et al. 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) 2011;76(11):1210–1219 · PMID 22117547
• Khavinson VKh, Popovich IG, Linkova NS, Mironova ES, Ilina AR. Peptide Regulation of Gene Expression: A Systematic Review. Molecules 2021;26(22):7053 · PMID 34834147
• Kolchina N, Khavinson V, Linkova N, Yakimov A, Baitin D, Afanasyeva A, Petukhov M. Systematic search for structural motifs of peptide binding to double-stranded DNA. Nucleic Acids Research 2019;47(20):10553–10563 · PMID 31598715
• Khavinson V, Linkova N, Kozhevnikova E, Trofimova S. EDR Peptide: Possible Mechanism of Gene Expression and Protein Synthesis Regulation Involved in the Pathogenesis of Alzheimer's Disease. Molecules 2021;26(1):159 · PMID 33396470
• Khavinson V, Linkova N, Kozhevnikova E, Dyatlova A, Petukhov M. Transport of Biologically Active Ultrashort Peptides Using POT and LAT Carriers. International Journal of Molecular Sciences 2022;23(14):7733 · PMID 35887081
• Khavinson VK, Linkova NS, Rudskoy AI, Petukhov MG. Feasibility of Transport of 26 Biologically Active Ultrashort Peptides via LAT and PEPT Family Transporters. Biomolecules 2023;13(3):552 · PMID 36979488
• Alsulaimani RA, Quinn TJ (independent — not the Khavinson group). The efficacy and safety of animal-derived nootropics in cognitive disorders: Systematic review and meta-analysis. Cerebral Circulation – Cognition and Behavior 2021;2:100012 · PMID 36324709

Cardiogen — safety, predicted from mechanism

Cardiogen — interference & stacking

Bloodwork to run alongside Cardiogen

Baseline first, then again at 8–12 weeks.

The Longevity Baseline panel covers these in one order — 13 markers, $219.10 with the discount applied.

Check results you already have → · All 103 markers A–Z

Cardiogen — frequently asked questions

Cardiogen inside a finished plan

One arm of 1 Protocol Blueprint, free to read in full.

What Cardiogen is used for

Cardiogen appears under 2 goals in the goal router.

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