Evidence Grade C — Moderate human evidence. 19 published studies, 12 human. 1 registered clinical trial.
Medically reviewed by a licensed medical professional
Cardiogen is a synthetic tetrapeptide from the Khavinson bioregulator programme in Russia, proposed to target cardiovascular tissue. No human clinical trials have been conducted, and it has no approval from any major regulatory agency. The evidence consists entirely of cell culture and animal studies from the originating research group.
Cardiogen is also known by these brand and alternate names:
19 published studies: 12 human, 4 animal, 0 in-vitro, 2 reviews
Cardiogen has no marketing authorisation from any major regulatory agency. No human clinical trials have been conducted. The evidence base consists of cell culture and animal studies published by the originating research group.
As with other Khavinson bioregulator peptides, the proposed tissue-specific targeting mechanisms and the underlying theoretical framework have not been evaluated through Western regulatory processes. Products available through unregulated channels lack pharmaceutical quality assurance.
Research from the Khavinson group proposes that Cardiogen may stimulate cardiac cell proliferation while suppressing fibroblast growth. These observations are from cell culture experiments and animal models. The proposed mechanisms derive from the Khavinson bioregulation framework and have not been independently validated.
Only 3-5 published studies exist for Cardiogen, virtually all from the Khavinson group. No registered human clinical trials exist. Many key studies are published in Russian-language journals with only abstracts available in English. There are no pharmacokinetic data, no cardiac function measurements from controlled studies, and no independent replication. As with other Khavinson bioregulator peptides, the proposed tissue-specific effects and the underlying theoretical framework have not been evaluated through internationally standardised research processes. Products from unregulated channels lack pharmaceutical quality assurance.
PeptideTrace tracks 1 registered clinical trial for Cardiogen sourced from ClinicalTrials.gov.
Prospective Evaluation of Strontium in Patients After CardioGen-82 PET MPI Scanning
FDA ORIG 1
FDA SUPPL 1
FDA SUPPL 2
FDA SUPPL 3
FDA SUPPL 4
FDA SUPPL 5
FDA SUPPL 6
FDA SUPPL 11
FDA SUPPL 12
FDA SUPPL 14
FDA SUPPL 15
FDA SUPPL 16
FDA SUPPL 22
FDA SUPPL 24
FDA SUPPL 21
FDA SUPPL 34
Cardiogen is a synthetic tetrapeptide bioregulator with the sequence Ala-Glu-Asp-Arg (AEDR). Its molecular weight is 489.5 Da with the molecular formula C18H31N7O9 (PubChem CID 11583989). Developed by Vladimir Khavinson as part of the cytomedine program, Cardiogen targets cardiovascular tissue. No CAS number has been confirmed in literature. No pharmacokinetic data exist; as an ultrashort peptide, it is expected to have a half-life measured in minutes. It is marketed as a dietary supplement in Russia (also known as CardioCytogen, T-30).
Research suggests Cardiogen stimulates cardiomyocyte proliferation while suppressing fibroblast growth, potentially shifting post-injury cardiac remodeling toward regeneration rather than scarring. Specific molecular targets include p53 (suppressed in cardiomyocytes, interpreted as anti-apoptotic), lamin A and C (elevated, suggesting nuclear matrix activation), and c-Fos proto-oncogene. Like other Khavinson short peptides, Cardiogen is hypothesized to penetrate cell nuclei and interact with DNA regulatory regions. No specific receptor has been identified.
Heart tissue cultures from young (3-month) and old (24-month) rats showed Cardiogen uniquely activated cardiomyocyte proliferation while suppressing apoptosis markers, with effects not observed with any of 20 individual amino acids tested. In senescent rats with M-1 sarcoma, Cardiogen enhanced apoptosis in tumor cells and induced hemorrhagic necrosis with dose-dependent tumor growth inhibition. Secondary literature reports a 3-fold reduction in mortality after experimentally produced cardiac injury versus control in mice, though the primary source was not independently verified in English.
The information on this page is provided for educational and research reference purposes only. This is not medical advice. Always consult a qualified healthcare professional before making any health-related decisions.
Compare prices from 4 vendor listings
View pricing data across vendors and countries for Cardiogen
Linaclotide is marketed as Linzess (approved August 2012). It is taken as a daily oral capsule on an empty stomach, at least 30 minutes before the first meal. The recommended dose is 290 mcg for IBS-C and 72 or 145 mcg for chronic constipation. In clinical trials, approximately 34% of IBS-C patients met the composite improvement endpoint compared to 17% on placebo. Diarrhoea is the most common side effect (approximately 20%) and the leading reason for discontinuation. Linaclotide has a boxed warning against use in children under 6 years due to deaths in young mice, though no such events have been reported in humans. It competes with plecanatide (which targets the same pathway) and other IBS-C treatments.
Elamipretide (Forzinity) was approved by the FDA for Barth syndrome based on the TAZPOWER trial. The randomised crossover phase (12 patients) did not meet its primary endpoints, but the open-label extension (168 weeks) demonstrated durable improvements in walking distance and muscle strength that formed the basis for approval. Barth syndrome affects approximately 1 in 300,000–400,000 births. A larger Phase III trial in primary mitochondrial myopathy (218 patients, MMPOWER-3) did not meet its primary endpoint, and the drug was not approved for that broader indication. Elamipretide remains approved exclusively for Barth syndrome. See also SS-31 (#158) for the research compound context.
Palopegteriparatide is marketed as Yorvipath (Ascendis Pharma, approved August 2024). It is the first FDA-approved PTH replacement therapy for hypoparathyroidism, a condition that previously had no approved hormone replacement and was managed only with high doses of calcium supplements and active vitamin D — an approach that does not fully normalise calcium metabolism. In the PaTHway trial, 79% of patients achieved independence from calcium and active vitamin D supplements while maintaining normal blood calcium levels, compared to 5% on placebo. This represents a fundamental shift in managing hypoparathyroidism — from supplementation to actual hormone replacement. Patients also showed improvements in kidney function markers and bone metabolism parameters.
This content is for informational purposes only and does not constitute medical advice. Always consult a qualified healthcare professional before making decisions about your health.