Cardiogen – 20MG

What Is Cardiogen?

Cardiogen is considered a peptide bioregulator that possibly regulates fibroblasts, which are cells that play a role in scar formation and tissue repair. The peptide has been widely researched for its potential to interact with the tissues in the cardiovascular system. Still, recent research has suggested that it may also be functional in other tissues via influencing fibroblast activities. Furthermore, scientists believe Cardiogen may increase tumor cell apoptosis (programmed cell death).

 

Specifications

Name	Cardiogen
Other known names	AEDR peptide, SCHEMBL3194515
Sequence	H-Ala-Glu-Asp-Arg-OH (4 amino acids)
Molecular formula	C18H31N7O9
Molecular weight	489.5 g/mol
Synthesis	Solid-phase peptide synthesis, US
Form	Lyophilized powder
Amount per vial	20 mg
Purity	>99% (HPLC)
Storage	−20 °C, dry, protected from light
SKU	P-cardiogen

 

What Does Research Show About Cardiogen?

What Does Research Suggest About Cardiogen and Tumor Cells?

Key finding: In lab models with transplanted M-1 sarcoma, Cardiogen raised tumor cell apoptosis above control levels and inhibited tumor growth through hemorrhagic necrosis, without a direct cytostatic effect on the tumor.⁽¹⁾

Researchers consider the peptide to be an apoptotic reductant in cardiac cells via possibly decreasing p53 expression and may exhibit opposite impacts on tumor cells. The p53 gene produces a protein found inside the nucleus of cells and is considered essential in controlling cell division and cell death. An experiment was conducted on murine models with M-1 sarcoma (indicating it has metastasized to other distant tissues and organs) to determine the tumor-modulating potential of Cardiogen, with apoptosis on tumor cells exceeding normal levels and considered uncontrollable.⁽¹⁾ The results indicated a consequence of necrotic and hemorrhagic development and the improvement of tumor cell apoptosis. The results of the experiment suggested that:

“The [concentration-dependent] inhibition of M-1 sarcoma growth after [...] cardiogen was caused by the development of hemorrhagic necrosis and stimulation of tumor cell apoptosis. The parameters of proliferative activity indicate that inhibition of tumor growth was not caused by the direct cytostatic effect of the [peptide] on the tumor. Morphological signs indicate a specific mechanism of cardiogen action, realized through the vascular network of the tumor.” ⁽¹⁾

The supposed anti-proliferative action of the peptide suggests that tumor growth inhibition may not result from a cytostatic compound on the tumor. According to morphology, tumor growth inhibition may be mediated by a specific mechanism of action related to blood supply. This event may be particular to some tumor cells due to their atypical and increased vascular supply.

What Does Research Suggest About Prostate Cell Aging?

Key finding: In aging prostate fibroblast cultures, Cardiogen and the peptides T-32 and T-38 enhanced the expression of the differentiation factors CXCL12, WEDC1 and ghrelin, whose synthesis falls in senescent cultures.⁽²⁾

According to researchers, Cardiogen may significantly increase the expression of signaling factors involved in the differentiation of prostate fibroblasts that typically decrease in senescent cultures.⁽²⁾ Because these signaling factors are considered to decline in aging and senescent fibroblasts, and Cardiogen appears to restore the levels of these factors, especially in senescent cell cultures, it is posited that the peptide may be a relevant candidate for further research in developing methods to address age-related dysfunctions of prostate cells.

What Does Research Suggest About Cell Proliferation?

Key finding: In cultured embryonic fibroblasts, the tetrapeptide H-Ala-Glu-Asp-Arg-OH (Cardiogen) raised the expression of the cytoskeletal proteins actin, tubulin and vimentin 2–5 times and of the nuclear matrix proteins lamin A and lamin C 2–3 times.⁽³⁾

Cardiogen may potentially be able to enter different parts of cells, specifically the cytoplasm, nucleus, and nucleolus. Additionally, researchers have hypothesized that Cardiogen might be able to hinder the breakdown of DNA fragments by endonucleases, which are enzymes involved in DNA processing. To explore this, a study was performed using murine embryonic fibroblast cells.⁽³⁾ These cells were grown in a laboratory setting, in a culture medium known as DMEM, enriched with approximately 10% embryonic calf serum, and kept in a humid environment. After about five days of growth, the cells were separated into two groups. The first group was left as is, serving as a control, while the second group was exposed to Cardiogen for approximately 30 minutes. It appears that in the cells cultivated with Cardiogen, there was a notable increase in the levels of certain proteins within the cytoplasm (such as actin, vimentin, and tubulin) and in the nucleus (specifically nuclear matrix proteins lamin A and C). Actin, vimentin, and tubulin are integral components of the cytoskeleton, the complex network of protein fibers that provide structure and shape to the cells. Actin forms microfilaments, which are thin, flexible fibers crucial for cellular movement and shape. Vimentin, a type of intermediate filament, offers mechanical support and resilience, particularly vital in cells like fibroblasts that endure stress. Tubulin, on the other hand, is the building block of microtubules, which are thicker, hollow tubes essential for maintaining cell shape, enabling intracellular transport, and facilitating chromosome segregation during cell division. Further, lamin A and C are types of nuclear lamins, which are fibrous proteins providing structural support to the nucleus. They form a mesh-like layer called the nuclear lamina on the inner surface of the nuclear envelope. Lamins are involved in organizing the chromatin (DNA and proteins) within the nucleus, and they also play roles in DNA replication, cell division, and regulating gene expression. The protein increases were roughly 2x - 5x higher with Cardiogen than in the control group. These findings suggest that Cardiogen might be activating the expression of these cytoskeletal and nuclear matrix proteins. A possible explanation might be that Cardiogen may potentially influence the proteins associated with DNA, such as enzymes and transcription factors. This influence may improve the way genes related to these cytoskeletal proteins are accessed for transcription, potentially leading to increased cellular metabolism and the stimulation of cell growth and differentiation.⁽³⁾

How May Cardiogen Affect Cardiomyocyte Apoptosis?

Key finding: In myocardial tissue cultures from young and old lab models, Cardiogen strongly stimulated cell proliferation and lowered the expression of the p53 protein.⁽⁴⁾

Researchers have suggested Cardiogen to increase cardiomyocyte proliferation while possibly decreasing fibroblast growth and development and scar formation, resulting in potential long-term and improved cardiac remodeling. Studies suggest that Cardiogen may reduce the expression of the p53 gene, resulting in a lower apoptosis rate of cardiomyocytes after injury.⁽⁴⁾ Researchers propose Cardiogen's potential in cardiac tissue:

“The tetrapeptide cardiogen demonstrated the great stimulating effect on the proliferation both in tissues from young and old rats. The immunohistochemical study demonstrated a decrease of the p53 protein expression by cardiogen action. This fact can testify that cardiogen inhibits the apoptosis process in the myocardial tissue.”⁽⁴⁾

More specifically, the synthetic tetrapeptide Cardiogen appears, based on the study's observations, to potentially play a role in enhancing cell proliferation in murine models of both young and aged specimens. This intriguing finding leads to the tentative hypothesis that Cardiogen might have the capacity to stimulate cell growth in heart muscle tissue. As mentioned, Cardiogen might possibly lead to a reduction in the expression of the p53 protein. This protein, often referred to as the "guardian of the genome," is believed to have crucial roles in controlling the cell cycle and may act as a tumor suppressor, thereby making this a significant point of interest for future cancer research. When active, p53 is considered to have the ability to initiate apoptosis, or programmed cell death. Therefore, a potential decrease in p53 expression as a result of Cardiogen might imply that this compound could inhibit apoptosis in the heart's myocardial tissue. This aspect of the study's findings seems to add an extra layer of complexity and potential significance, warranting further investigation.⁽⁴⁾

Another experiment investigating the potential of Cardiogen on cardiomyocyte cell apoptosis was conducted in an experimental murine model of myocardial damage, achieved through the deliberate ligation of the coronary artery.⁽⁵⁾ There appears to be research data suggesting that the Cardiogen peptide might significantly reduce mortality following this experimentally induced heart damage. Observations point to a threefold decrease in mortality compared to the control group. Additionally, this peptide may play a role in diminishing necrotic zones within the myocardial tissue, which are considered to be areas of cell death due to a suspected lack of blood flow (ischaemia). It is also proposed that the Cardiogen peptide might assist in preserving the glycogen content in the myocardial tissue. Glycogen, considered to be a vital form of energy storage in cells, when preserved, indicates that the cells might have been better able to maintain their energy reserves in the presence of the Cardiogen peptide. This preservation may potentially enhance the survival and function of cells post-ischaemia. The study further suggests that the Cardiogen peptide may exert a protective effect on mitochondria, which are the structures within cells responsible for energy production. Finally, there is a hypothesis that the Cardiogen peptide might stimulate reparative processes, which may theoretically contribute to repairing the damage caused by ischaemia. Such processes might also potentially improve the metabolism of cardiomyocytes, and reduce cell apoptosis.⁽⁵⁾

 

Certificate of Analysis

Batch / lot	C74114
Test date	8/21/2026
Testing laboratory	Vanguard Laboratory
Method	HPLC-UV/VIS (purity)
Purity result	>99.80%
Full report	Download the Cardiogen COA (PDF)

Cardiogen peptide is available for research and laboratory purposes only. We offer free shipping in the US for orders over $200. Please review our Terms and Conditions before ordering.

 

Frequently Asked Questions

 

References:

1. Levdik, N. V., & Knyazkin, I. V. (2009). Tumor-modifying effect of cardiogen peptide on M-1 sarcoma in senescent rats. Bulletin of experimental biology and medicine, 148(3), 433–436. https://doi.org/10.1007/s10517-010-0730-9
2. Kheĭfets, O. V., Poliakova, V. O., & Kvetnoĭ, I. M. (2010). [Peptidergic regulation of the expression of signal factors of fibroblast differentiation in the human prostate gland in cell aging]. Advances in gerontology = Uspekhi gerontologii, 23(1), 68–70. https://pubmed.ncbi.nlm.nih.gov/20586252/
3. Khavinson, V. Kh., Lin’kova, N. S., Polyakova, V. O., Kvetnoy, I. M., Benberin, V. V., D’yakonov, M. M., & Titkov, Y. S. (2012). Tetrapeptide H-Ala-Glu-Asp-Arg-OH stimulates expression of cytoskeletal and nuclear matrix proteins. Bulletin of experimental biology and medicine, 153(4), 559–562. https://doi.org/10.1007/s10517-012-1766-9
4. Chalisova, N. I., Lesniak, V. V., Balykina, N. A., Urt’eva, S. A., Urt’eva, T. A., Sukhonos, Iu. A., & Zhekalov, A. N. (2009). [The effect of the amino acids and cardiogen on the development of myocard tissue culture from young and old rats]. Advances in gerontology = Uspekhi gerontologii, 22(3), 409–413. https://pubmed.ncbi.nlm.nih.gov/20210190/
5. Khavinson, V., Linkova, N., Dyatlova, A., Kantemirova, R., & Kozlov, K. (2022). Senescence-Associated Secretory Phenotype of Cardiovascular System Cells and Inflammaging: Perspectives of Peptide Regulation. Cells, 12(1). https://doi.org/10.3390/cells12010106

Related reading: Cardiogen research in cardiac function.

Last updated Nov 6, 2026 · Scientific review: Dr. Dimitar Marinov, MD, PhD