Chelohart Dosage Chart, Schedule & Reconstitution Protocol

Mechanism of Action (MOA)

Chelohart is a "Cytomax," a natural peptide preparation rather than a single synthetic molecule. It consists of a low-molecular-weight complex of peptide fractions (marketed as Peptide Complex A-14) isolated and purified from the cardiac muscle tissue of young animals, typically calves, using the extraction-and-filtration technology developed within Vladimir Khavinson's bioregulation program at the St. Petersburg Institute of Bioregulation and Gerontology; the resulting peptides are generally under 5 kDa and are processed to remove foreign DNA and high-molecular-weight protein [5]. This distinguishes Chelohart from Cardiogen, the synthetic single tetrapeptide (Ala-Glu-Asp-Arg) marketed for the same cardiac indication.\n\nThe proposed mechanism is shared across the Khavinson bioregulator (cytomedin and cytogen) family: these short peptides are thought to be small enough to enter the cytoplasm and nucleus of target cells, where they bind specific sequences in gene promoter regions and modulate transcription of a tissue-appropriate set of genes, rather than acting on a cell-surface receptor [1][3]. Fluorescence-labeled Khavinson peptides have been shown to penetrate the nucleus and nucleolus of cultured cells and to bind defined DNA oligonucleotides in vitro, and independent reviews classify these di- to tetrapeptides as endogenous epigenetic-style modulators that can influence DNA methylation and gene expression [3][4]. For a cardiac-tissue complex such as Chelohart, the marketed rationale is that the peptides act selectively on cardiomyocytes to normalize myocardial metabolism and energy production, support intracellular protein synthesis, and regulate cell renewal, with the broader cardiovascular peptide literature framing this in terms of slowing senescence-associated changes and inflammaging in heart and vessel-wall cells [2].\n\nIt must be emphasized that this mechanism is largely hypothesized from the broader bioregulator program and animal or in-vitro work; there are no published controlled human pharmacology studies of Chelohart itself, and the in-vivo evidence originates predominantly from a single research lineage [1][2].\n\nPharmacokinetics have not been formally characterized for Chelohart. As a mixture of short, unmodified peptides it would be expected to undergo extensive gastrointestinal and plasma proteolysis, so oral bioavailability of intact peptides is low and the free-peptide plasma half-life is presumed to be on the order of minutes. In the Khavinson framework, any lasting effect is attributed to downstream changes in gene expression that persist after the peptide fragments are cleared, which is the rationale for short, pulsed courses rather than continuous dosing [5].\n\nIn practice Chelohart is taken orally: 1-2 capsules (10 mg each) one to two times daily with meals, about 10-20 mg/day, for a 30-day course repeated every 3-6 months. The once-daily subcutaneous reconstitution described on this page is purely an educational modeling convention used across this site; reconstituting a 20 mg vial in 2 mL of bacteriostatic water gives 10 mg/mL, so a 1-2 mg reference dose is 10-20 units on a U-100 syringe. The injectable figures are not a validated route for Chelohart and are not a potency conversion of the oral capsule dose. Chelohart remains an unapproved supplement and research peptide, and all dosing here is reference information only, not therapeutic guidance [6][7].