Chelohart
Cardiac peptide bioregulator
Chelohart (Cardiac peptide bioregulator) is a longevity & bioregulators research compound. Heart-tissue bioregulator — proposed to normalize protein synthesis and function in cardiomyocytes.
Chelohart quick facts
| Reported research dose (Injectable) | 2mg-5mg (per course) |
| Route | Subq |
| Frequency | 1x Daily · Daily (course) |
| Half-life | ~15-30 min |
| Forms | Injectable, Oral |
| Evidence level | Russian studies; limited |
| Other forms available | Oral — dosed differently |
The 'heart' peptide — targeted cardiac-tissue support, short courses. Aimed at cardiac muscle tissue specifically, which is what separates it from the vascular peptides people run it beside. Course pattern: roughly 10 days on, then off, once or twice a year. To know whether it did anything, take a baseline lipid panel, ApoB and hs-CRP, and re-run at 3 months. Run it as an experiment you measure, not a protocol you trust.
How Chelohart works
Heart-tissue bioregulator — proposed to normalize protein synthesis and function in cardiomyocytes.
Proposed benefits
Researched for mitochondrial and cellular-energy support, tissue-specific bioregulation and healthy-aging pathways.
Where to get Chelohart
Bacteriostatic water is the diluent — sterile water with 0.9% benzyl alcohol, which is what lets a vial be drawn from more than once. It does not come with the vial, and unlike the compound it is bought again every time.
Need bacteriostatic water? Get it at AminoWell USA (my company) → Code CAMERON.
The evidence for Chelohart
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
- The 'natural' extract counterpart to Cardiogen, sold orally for cardiac support. Practical record is thin and largely indistinguishable from Cardiogen's in what users report.
- Beyond that the record is self-reported: community dosing logs are real information about tolerability and almost none about efficacy.
🧪 Theoretical / extrapolated
- A heart-tissue peptide complex proposed to support cardiomyocyte function.
- Two things at once: the mechanism is a real, testable hypothesis with published cell-level work behind it, and essentially all of that work is one group's, unreplicated at scale.
- Where a defined synthetic exists for the same tissue, the extract is the weaker choice on identity grounds alone — Cardiogen's contents are a known sequence, this one's are a process.
What community dosing logs are worth → · 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 Chelohart actually does
Chelohart is not a peptide. It is an extract of calf heart muscle, fractionated by size. The Russian nomenclature separates the two cleanly and the vendor pages never do: a cytomedin or cytomax is the tissue extract, a cytogen is the short synthetic peptide afterwards identified inside it and made in a flask Khavinson 2001. Chelohart is the cytomax of the heart. Cardiogen is the cytogen of the heart. They are sold side by side as though the choice were oral versus injectable.
What that costs, stated as the missing numbers. Cardiogen is C18H31N7O9, 489.50 Da, isoelectric point 4.18, computed charge about −1.06 at pH 7.4. Chelohart has no formula, no mass, no isoelectric point and no charge, because it is not one substance. A certificate of analysis can establish sterility, endotoxin and total peptide content. Nothing in routine use can establish that 2 lots are the same mixture.
And yet this extract has a named molecular readout, which most of them do not. The one indexed study of it reports 2 proteins moving in heart explants: PCNA up and p53 down Ryzhak 2015. PCNA is not a vague activity marker. It is the sliding clamp that holds DNA polymerase delta on the template at a replication fork — a processivity factor, loaded at origins, and its abundance in a tissue is a proliferation index.
Which cell is proliferating is the question this page exists to ask. Adult cardiomyocytes are effectively post-mitotic; they hypertrophy rather than divide. Most nuclei in mammalian myocardium do not belong to myocytes at all — they belong to fibroblasts, endothelial cells, pericytes and resident immune cells. So a rise in PCNA in a lump of heart tissue is, on the ordinary cell biology, most likely the non-myocyte compartment dividing. Proliferating cardiac fibroblasts laying down collagen is the cell biology of fibrosis, and fibrosis is what stiffens a ventricle and impairs its filling. The single published molecular readout for this product, read in the tissue it is named for, points at the cell type you would least want stimulated. No study has co-stained to find out, and no vendor page mentions it.
The family's chromatin claim cannot be tested on a mixture. The mechanism offered for the whole catalog is that ultrashort peptides reach the nucleus and engage DNA and histone-modified chromatin Khavinson 2021. That claim has real biophysics behind it — fluorescein-labeled peptides were tracked into HeLa nuclei and their binding preferences measured against defined oligonucleotides Fedoreyeva 2011. Every molecule in that experiment had a known sequence. You cannot label a mixture and learn which component went where, so for Chelohart the mechanism is not unsupported — it is untestable in its current form, which is a different and worse problem.
Cell, rodent, human — and where it stops
One paper. Searched by name against NCBI PubTator3 on 4 September 2026, ‘Chelohart’ returns exactly 1 indexed record. Here is what is in it, because it is better than its obscurity suggests.
The one study. 7 polypeptide preparations extracted from calf tissues — Cortexin from brain cortex, Epinorm from pineal, Ventvil from liver, Prostatilen from prostate, Thymalin from thymus, Chelohart from heart, Chondrolux from cartilage — applied to organotypic explant cultures of the matching tissue from young and old rats, across 0.01 to 100 ng/mL Ryzhak 2015. Growth was stimulated in the 20–50 ng/mL band. PCNA rose and p53 fell in cortex, pineal, liver, prostate, heart and cartilage; Thymalin additionally raised CD5 and CD20, the B-cell differentiation markers. Each extract was applied to its own tissue. As with the synthetic arm of this catalog, the mismatched pairs were not run, so ‘selective activity’ here means it worked on its own tissue and not it failed on somebody else’s.
Now put the extract and the synthetic on the same axis. Nobody has, and it is one line of arithmetic. Cardiogen stimulated proliferation in myocardial explants at 10−12 M Chalisova 2009. At 489.50 Da that concentration is 0.00049 ng/mL. Chelohart needed 20–50 ng/mL in the same kind of assay. The extract therefore requires roughly 40,000 to 100,000 times more material by mass than the peptide sold as its active principle. Against the other published cardiogen concentration, 0.05 ng/mL in the 2006 organotypic series, the gap is still 400- to 1,000-fold.
What that number actually bounds, which is the useful part. If every bit of Chelohart's activity came from an AEDR-type peptide inside it, the extract would only need to contain 1 part in 40,000 of it — 0.0025% by mass — to explain the result. So the published data are entirely consistent with the extract being 99.99% inert carrier. They are equally consistent with the extract working through something else that has never been named. Those are 2 completely different products and no experiment distinguishes them.
Rodent, in a living animal: none under this name. Human: none. The human evidence people attach to the heart extract belongs to different preparations from different organs — the thymus and pineal series injected into 266 elderly subjects over 6 to 8 years Khavinson 2003. The independent view of the family pooled 24 randomized trials over 2,245 participants, rated the risk of bias moderate to high and the certainty low to very low, and its endpoints were cognitive Alsulaimani 2021. There is no cardiac arm anywhere in it.
The obstacles, in the order that matters. (1) Identity. You cannot compute a dose, predict a marker or compare 2 vendors for a substance with no composition. (2) An explant is not a heart. It has no coronary perfusion, no innervation and no afterload, and it is cut, which is itself a wound-healing stimulus — the exact stimulus that recruits fibroblasts. (3) The comparison that would settle the category — extract against synthetic, same plate, same day — has existed as an obvious experiment since the 2002 series that put Cortexin, Epithalamin, Hepalin and Thymalin alongside Cortagen, Epitalon, Livagen and Vilon in one culture system Khavinson 2002. That paper's abstract states the effects were concentration-dependent and does not report the concentrations, so the ratio it contains cannot be read from the record.
Chelohart pharmacokinetics — how much of it actually gets in
Start with the card, because the card is wrong in an instructive way. The Vault lists a half-life of about 15 to 30 minutes for this product. A mixture cannot have a half-life. Each component has its own, they differ by orders of magnitude, and the number that would describe the preparation is a distribution nobody has measured. What makes it worth pointing at is the direction of the error: the defined tetrapeptide next to it on the shelf is listed only as ‘Short’. The extract has been given the more precise figure, and it is the one for which no such figure can exist.
What degrades it. Swallowed, it meets gastric acid at roughly pH 1.5–3.5 and pepsin, then pancreatic trypsin, chymotrypsin and elastase, then the brush-border aminopeptidases. Injected, it skips all of that and meets plasma and endothelial peptidases instead. The only named route across an enterocyte for material this small is PEPT1, whose described substrate range is di- and tripeptides Khavinson 2022. An extract cut by molecular-weight filtration is, by construction, mostly species longer than 3 residues.
The point that is specific to an extract sold both ways, and it is the most useful paragraph on this page. For a defined peptide, oral versus injectable is a question about how much arrives. For a mixture it is a question about what arrives. The gut is a size-selective and sequence-selective filter: it destroys the long components preferentially and passes a biased subset. So the material reaching blood after a capsule is a different mixture from the material reaching blood after an injection of the same vial. A person moving between the 2 forms is not adjusting a dose. They are changing compound. The catalog quotes one band, 2–5 mg per course, for both routes, and no published figure exists that would let anybody correct it in either direction.
And the exposure that has never been measured at all. There are 0 biodistribution studies for this preparation, so whether any of it reaches myocardium after a subcutaneous injection is assumed on every page that sells it, including this one until the sentence you are reading.
What would have to be true, and how you would know it was not
Three predictions. Two of them say the product should fail a test, which is the direction that carries information here.
1. TGF-beta1 should not fall, and it may rise. This is the prediction the mechanism section forces. If the published readout is a proliferative signal in a tissue whose dividing cells are fibroblasts, the matching circulating marker is the principal fibrogenic cytokine, and the honest expectation is no fall. Draw it before a course and at 3 months. A drop would be evidence against the fibroblast reading and would be the most interesting result anybody could produce on this compound. A rise would be a reason to stop.
2. ESR and hs-CRP should not move. Nothing in the published record predicts a systemic anti-inflammatory effect from a heart extract. ESR is on this list rather than hs-CRP alone because it tracks a slower inflammatory state and a 10–20 day course sits inside hs-CRP's own week-to-week noise. Retest at 3 months. Flat is the prediction; flat is also what a person should expect to find.
3. Watch the CBC differential, specifically the eosinophils. This is not an inflammation question, it is an immunogenicity question, and it is the one readout on this page that could plausibly move. Repeated subcutaneous injection of a foreign-species tissue protein preparation is the textbook setting for sensitization. Baseline CBC with differential, repeat at 3 and 6 months, and treat a climbing eosinophil count together with worsening injection-site reactions as a reason to stop rather than a curiosity.
What nobody has tested yet
Five experiments. The first costs one culture plate.
1. Nobody has run the extract against its own synthetic on the same plate. Chelohart and Cardiogen, same myocardial explants, same day, dose-response across 6 log units. The output is a single number — the potency ratio — and that number decides whether the extract is a dilute source of the peptide or a different agent wearing the same organ label. Every reagent is commercially available and the assay is the one both papers already used Ryzhak 2015 Chalisova 2009.
2. Nobody has put a vial through a mass spectrometer. Liquid chromatography with tandem MS on one lot would answer 2 questions at once: what is in it, and does it contain Ala-Glu-Asp-Arg at all. The potency arithmetic above predicts at least 1 part in 40,000 if the ‘natural counterpart’ framing is true. A result of zero would end that framing permanently.
3. Nobody has asked which cell divided. The PCNA result is a stain. Adding a second stain to the same slides — cardiac troponin T or alpha-actinin for myocytes, vimentin or CD31 for the rest — turns an ambiguous proliferation signal into either a regeneration finding or a fibrosis finding. This is 2 antibodies and an afternoon, and 11 years after the original study it is still unpublished.
4. Nobody has applied it to the wrong tissue. The 2015 series gave each of 7 extracts its own matching explant Ryzhak 2015. Adding Chelohart to prostate and cartilage explants, in the same experiment, is what would turn tissue selectivity from a description of the study design into a property of the preparation.
5. No human heart has ever been imaged before and after a course. If the fibroblast reading is right, the endpoint it predicts is diastolic: E/e′ and left atrial volume index on a standard echocardiogram, before a course and 6 months after. Echocardiography is 40 years old, widely available and non-invasive, and there is no such measurement for this compound or for any other member of its family.
Chelohart — its own safety story, not its class's
The class block is written for injectable peptides in general. Four things here are not general.
1. The direction of the only published molecular result is not obviously the direction you want. p53 down and PCNA up Ryzhak 2015 reads as rejuvenation on a sales page. In myocardium it more plausibly describes the non-myocyte compartment proliferating, and p53 is the tumor suppressor whose job is to stop damaged cells dividing. This is not a report of harm — no such report exists — it is the specific open question this compound carries, and it is invisible everywhere it is sold. Anyone with a history of cancer, or with known cardiac fibrosis, is weighing an unanswered question rather than a known risk.
2. Bovine tissue injected repeatedly is a sensitization question, not a toxicity question. The synthetic peptides in this catalog are built from reagents; this one is made from an animal. The failure mode for a foreign-species protein preparation given in repeated courses is an immune response to it, and it announces itself as an injection site that gets angrier over a course rather than calmer, sometimes with itching or a rash away from the site. Stop and get it looked at rather than pushing through — a reaction that is escalating course on course is the pattern that matters.
3. The oral and the injectable form are not interchangeable, and the catalog's single dose band implies they are. Since the gut filters a mixture rather than merely reducing it, switching routes changes what you are taking, not how much. Nobody can state the correction because nobody has published the composition of either exposure.
4. Read the empty adverse-event column correctly. With 1 indexed study, run in rat explants, and 0 people ever dosed under observation, no channel has existed through which a side effect could have been counted. The zero describes how little has been looked at rather than what was found — and the practical harm on this page remains the months a person can spend on an unmeasured injection while a blood pressure cuff, an ApoB and a conversation about smoking go unused.
Sources read for this page
- Ryzhak AP, Chalisova NI, Lin'kova NS, Khalimov RI, Ryzhak GA, Zhekalov AN. [Polypeptides influence on tissue cell cultures regeneration of various age rats]. Advances in Gerontology 2015;28(1):97-103 [Russian] · PMID 26390619
- 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
- Khavinson VK. Tissue-specific effects of peptides. Bulletin of Experimental Biology and Medicine 2001;132(2):807-808 · PMID 11713572
- Khavinson VKh, Malinin VV, Chalisova NI, Grigor'ev EI. [Tissue-specific action of peptides in tissue culture of rats of various ages]. Advances in Gerontology 2002;9:95-100 [Russian] · PMID 12096446
- 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 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 VKh, Popovich IG, Linkova NS, Mironova ES, Ilina AR. Peptide Regulation of Gene Expression: A Systematic Review. Molecules 2021;26(22):7053 · PMID 34834147
- Khavinson VKh, Morozov VG. Peptides of pineal gland and thymus prolong human life. Neuro Endocrinology Letters 2003;24(3-4):233–240 · PMID 14523363
- 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
Chelohart — safety, predicted from mechanism
Predicted from mechanism, not from a human safety trial. How that reasoning works →
What the mechanism predicts
Derived from the molecule, not a trial.
- These are short peptide fragments of organ extracts, and the honest starting point is that the mechanism itself is not established in a way that lets anyone predict harm precisely. The proposal is gene-regulatory — short peptides binding DNA and modulating transcription in a tissue-specific way. If that is what they do, the theoretical concern is influencing transcription in tissue you were not aiming at.
- In practice the doses are tiny, the peptides are short, and they are degraded quickly — which is also the argument that they may do very little at all. Those two possibilities are the same uncertainty viewed from opposite ends, and you should hold both.
What has actually been reported
- Decades of Russian clinical use with a strikingly clean tolerability record — injection-site reactions and little else reported.
- That record comes almost entirely from one research school, is largely unreplicated outside it, and safety data from a group with an interest in the outcome is worth less than the same data from a skeptic. This is not an accusation; it is how evidence weighting works.
How to reduce the risk
Same mechanism as the prediction.
- Follow the course printed on the label rather than running continuously. These are the one class in the Vault where a duration is STATED rather than inferred, and it is typically 10–20 days repeated a few times a year. Read the box.
- Run one at a time. They are cheap and it is tempting to stack six. If something changes, a stack of six tells you nothing about which one did it — and given the evidence base, attribution is the entire value of your own experiment.
- Decide your endpoint before you start, and make it a marker or a measurable symptom rather than a feeling. With a compound class this under-evidenced, an unfalsifiable endpoint means you will conclude it worked no matter what happened.
- Buy from a source that publishes third-party testing. Where the molecule itself is uncertain, identity and purity are the only variables you can actually control.
What it does to your bloodwork
A fact about the assay.
- Test the ORGAN, not the peptide. A thymic peptide is judged on immune markers, a pineal one on sleep and IGF-1, a vascular one on lipids and inflammatory markers. There is no assay for the compound itself.
Don't run this if
- Pregnancy — not because of a specific finding, but because nobody has studied it and the mechanism claim is transcriptional.
- Active malignancy, on the same reasoning as any tissue-growth signal: unproven, mechanistically arguable, and not worth finding out.
The honest unknown
- Essentially everything a skeptic would want: independent replication, pharmacokinetics, and whether the oral forms survive digestion at all. Unproven is not the same as ineffective — but here it is a large unproven.
Not medical advice. If you take prescription medication or have a diagnosed condition, check this with a pharmacist or doctor.
Chelohart — interference & stacking
Predicted from mechanism, not from an interaction study. How mechanism-predicted claims are made →
What Chelohart moves on your bloodwork
Expected direction, not a measured one.
- Comprehensive Metabolic Panel (CMP) — ◆ worth watching
These are short peptide fragments given in microgram amounts and there is no mechanism predicting a specific marker shift. Listing markers here would be padding.
What to do: Test the organ system the bioregulator is aimed at, not a generic panel — that is the only measurement that would tell you anything.
The evidence base here is almost entirely one research group's, largely in Russian, and rarely replicated independently. That is the single most important thing to know before running a course, and it is more useful than any interaction list.
- How to work up to it, and when not to
- When to take it, and why that window
- Cycle length
- Time off between cycles
- Fasted or fed, and when in the day
- Needle gauge and injection site
- How the forms differ in dose
- Coach Cam's personal notes
- Which compounds push the same lever, and why the dose adds up faster than people count
- What blunts it — the stacks that waste your money
- What compounds the risk, so a side effect arrives sooner than any one of them suggests
- Coach Cam's read on running it alongside the rest of your protocol
Everything above is free and stays free. Skool is where it becomes a plan — Chelohart in an order, with the rest of what you're running.
Unlock in Skool — $10/mo →Bloodwork to run alongside Chelohart
Baseline first, then again at 8–12 weeks.
| Marker | What it’s watching for |
|---|---|
| hs-CRP (High-Sensitivity C-Reactive Protein) | Chronic low-grade inflammation is the process most of these target |
| ApoB (Apolipoprotein B) | Counts the particles that actually cause plaque, unlike LDL-C |
| HbA1c (Hemoglobin A1c) | Glycation, which is the other half of the ageing story |
| Comprehensive Metabolic Panel (CMP) | Liver and kidney — the two organs that clear everything you take |
| Complete Blood Count (CBC) with Differential | The cheapest broad screen there is |
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
Chelohart — frequently asked questions
What is Chelohart?
Chelohart (Cardiac peptide bioregulator) is a longevity & bioregulators research compound. Heart-tissue bioregulator — proposed to normalize protein synthesis and function in cardiomyocytes.
Is the full Chelohart protocol on this page?
The reported research dose is on this page, along with how Chelohart works and the evidence behind it. The protocol — how to work up to it, frequency, cycle length, time off, what not to stack it with and Coach Cam's notes — is inside Skool.
What is the half-life of Chelohart?
Chelohart has an approximate half-life of ~15-30 min, which is part of what determines how often it's dosed.
What forms does Chelohart come in?
Chelohart is available as: Injectable, Oral.
What's the evidence behind Chelohart?
Current evidence level: Russian studies; limited. Chelohart is offered for research purposes only and is not an approved medicine.
Chelohart inside a finished plan
One arm of 1 Protocol Blueprint, free to read in full.
What Chelohart is used for
Chelohart appears under 2 goals in the goal router.
Related Longevity & Bioregulators compounds
Where this goes next
Chelohart is the cardiac & vascular arm of this plan. The page above is the free breakdown of one compound; the plan it belongs to — the dosing, the order to correct things in, the week-by-week schedule and what to retest — is a lesson inside Skool.