Chelohart

What it is

The Khavinson school distinguishes two product families. The Cytogens are synthetic short peptides of two to four amino acids, precisely defined and chemically manufactured. The Cytomaxes are natural peptide complexes, that is, mixtures of many peptides obtained from the organs of young animals. Chelohart belongs to the second group: a polypeptide complex from the heart tissue of calves.

Vendors list Chelohart under the code A-14, as a capsule and as drops for use under the tongue. In some lists the code A-6 appears by mistake; it belongs to Vladonix, the thymus preparation of the same line.

The distinction from Cardiogen is important. Cardiogen is the synthetic tetrapeptide Ala-Glu-Asp-Arg, which, according to the group’s own review, was found by mass spectrometry in the polypeptide complex of the heart. Chelohart is thus, in a sense, the starting material, and Cardiogen a single isolated component. The two names are often mixed up in the trade.

How it is supposed to work

According to the theory of bioregulation, every organ contains its own signaling peptides that control the reading of tissue-specific genes. With age these signals are said to decline, and an extract from young tissue is supposed to replace them. For Chelohart this means: heart muscle cells are supposed to maintain their metabolism, their renewal and their resilience for longer.

Part of this is measurable in tissue culture. In the 2015 study, Chelohart stimulated the growth of heart tissue from young and old rats alike. PCNA, a marker of cell division, rose, and p53 fell, a protein that sends cells into arrest or programmed death. This fits the picture of cell renewal, but it is not a measure of a heart’s pumping capacity.

The background: heart peptide extracts since the 1980s

Long before today’s capsules, the group around Khavinson studied a heart peptide preparation from bovine hearts, called Cordialin or Cardiolin in the papers. The findings from 1987 to 1993 are all animal experiments, but they show a comprehensible mechanism.

In 25 rats with an artificially induced infarction, cell damage in the border zone was lower under Cardiolin 6 hours after the vessel occlusion, and after 24 hours there was a trend toward normalization. In heart muscle cells under oxygen deficiency, the extract improved the energy balance: more ATP and glycogen in the heart muscle, a more favorable pathway of energy production. It protected heart muscle cells from a poison used in industry and agriculture, and in single-cell measurements the heart peptides activated ATP-dependent potassium channels of the heart muscle cells.

In 2000, the group tested several such organ extracts, called cytomedins by the group, together in tissue cultures of internal organs of young rats. Alongside Cortexin and Epithalamin from the brain and Thymalin from the thymus, Cordialin from the heart was included, and all of them stimulated the growth of the tissue pieces. This paper is the bridge between the early infarction experiments and the 2015 study in which Chelohart appears for the first time under its current name.

Whether today’s Chelohart is identical to this preparation cannot be determined from the literature. The origin is similar, the name is not.

What the studies show

Seven organ extracts in tissue culture (2015)

Ryzhak and colleagues compared polypeptide complexes from calf tissues, including Chelohart from the heart, on the matching tissue cultures of young and old rats. All of them stimulated the growth of their tissue, with more PCNA and less p53. The endpoint was the growth of the tissue pieces, not the function of a heart.

Cardiolin in the infarction model (1989)

Khlystov and colleagues studied 25 rats with experimental infarction. After 6 hours, the damage to the heart muscle cells in the border zone was smaller under the extract and the mitochondria worked more efficiently; after 24 hours there was a trend toward normalization, while the damage in untreated animals became irreversible.

Cordialin in acute ischemia (1990)

Pavlenko and colleagues found fewer deaths on the first day and longer survival of the cells in the ischemic zone. Later, however, the damaged zone healed more slowly and scar formation was delayed. The authors therefore recommended use only on the first day of infarction.

Dose and effect in the isolated heart (1992)

In the same line of research, low concentrations of the heart peptides improved the contraction of isolated hearts after ischemia. High concentrations, by contrast, inhibited contraction and cellular respiration, all the more strongly the more severe the ischemia was.

Where the data stop

There is not a single published study of Chelohart in humans and no entry in public trial registries. Vendors write that efficacy was determined in clinical studies, but name no publication that could be checked. The claim that the preparation was very well tolerated in Russian studies therefore cannot be substantiated. A higher mitochondrial density in the heart muscle, as is occasionally advertised, was not found in any paper either; what is documented is a better energy efficiency of the mitochondria under the predecessor preparation in animal experiments.

The older animal data are also not one-sided. Under Cordialin the infarcted area healed more slowly, lipid peroxidation rose when blood flow was restored, and high concentrations slowed the heart muscle. Whether these findings apply to today’s product is as open as for the favorable ones. And whether a peptide mixture reaches the heart in an effective form at all after being swallowed has never been measured.

Status, approval and legal

Chelohart is not an approved medicine in Germany or the EU. As a dietary supplement it would require authorization under the Novel Food Regulation (EU) 2015/2283, which does not exist. It is offered by online retailers as a capsule or sublingual preparation. It is not listed by name on the World Anti-Doping Agency’s prohibited list, but as a non-approved substance it falls under group S0 and is banned in sport at all times.

Safety

There are no safety data in humans. From the animal experiments with the predecessor preparation, delayed scar formation after infarction, lipid peroxidation on reperfusion and an inhibition of the heart muscle at high concentrations are known. How well an extract from bovine tissue is tolerated, for example with regard to allergic reactions, has not been studied for Chelohart. Interactions with beta-blockers, anticoagulants, antiarrhythmics or heart failure medications are unknown. Anyone who has heart disease or has had an infarction discusses any supplement with their cardiologist and does not replace any prescribed therapy. There are no data for pregnancy and breastfeeding.

Sources

• Ryzhak et al., Adv Gerontol 2015 – polypeptides from calf tissues, including Chelohart, in tissue cultures from young and old rats
• Khlystov et al., Arkh Patol 1989 – Cardiolin and the border zone of experimental infarction
• Pavlenko et al., Biull Eksp Biol Med 1990 – heart peptide preparation in acute ischemia
• Pavlenko et al., Biull Eksp Biol Med 1992 – dose and effect of heart peptides
• Pavlenko et al., Patol Fiziol Eksp Ter 1992 – Cordialin and energy metabolism of heart muscle cells
• Babenko et al., Biull Eksp Biol Med 1992 – cardiopeptides activate ATP-sensitive potassium channels
• Bakhrizina et al., Patol Fiziol Eksp Ter 1992 – Cordialin against toxic heart muscle damage
• Khavinson et al., Cells 2022 – AEDR in the polypeptide complex of the heart (review)
• ClinicalTrials.gov – search for Chelohart without a registered study
• NADA – Prohibited List 2026, informational German translation (group S0)