The Epitalon peptide (Epithalon; AEDG, Ala-Glu-Asp-Gly) has not been shown to be carcinogenic in humans; however, its effect on telomere maintenance mechanisms raises legitimate mechanistic questions, as a 2025 study on human cells demonstrated telomere elongation not only in normal cells but also in breast cancer cell lines via an alternative telomere elongation pathway (ALT). [1–3]
The relationship between Epitalon and cancer is much more complex than the two commonly encountered claims online: „Epitalon causes cancer because it activates telomerase” and „Epitalon prevents cancer because animal studies have shown fewer tumors.” Neither of these conclusions is supported by the full picture of available evidence.
Telomerase and telomeres play a role in normal cell maintenance, aging processes, stem cell biology, and cancer biology. The mechanism that maintains telomeres is therefore not automatically harmful, but neither is it automatically beneficial. The available literature on Epitalon includes experiments on human cells demonstrating effects on hTERT, telomerase, telomere length, and ALT, as well as older animal studies in which tumor growth was often reduced in specific models, and at least one rat model in which Epitalon did not exhibit an inhibitory effect. [1–8]
Most importantly, these are mechanistic and preclinical results, not evidence regarding the incidence of cancer in humans exposed to Epitalon.
Does Epitalon Cause Cancer?
There is no clinical evidence indicating that Epitalon causes cancer in humans. However, experiments on human cells show that Epitalon may affect telomere maintenance mechanisms, including hTERT expression, telomerase activity, and ALT. Therefore, without adequate safety and carcinogenicity studies in humans, the long-term cancer risk cannot be considered either established or ruled out. [1–3]
None of the studies in the analyzed evidence show that tumors develop more frequently in individuals exposed to Epitalon than in comparable individuals without such exposure.
This matters because the statement „Epitalon causes cancer” would require evidence of an actual increase in cancer incidence in humans, cancer progression, recurrence, or cancer-related mortality. Such evidence currently does not exist.
Concerns, on the other hand, stem from mechanistic biology.
Epitalon has repeatedly demonstrated an effect on the maintenance of telomeres in cultured human cells. A 2003 in vitro study on human fetal fibroblasts found the induction of the catalytic component of telomerase, an increase in telomerase activity, and telomere elongation after exposure to Epithalon. [2]
An in vitro study on human cells conducted in 2025 analyzed normal fibroblasts and mammary gland epithelial cells, as well as two breast cancer cell lines—21NT and BT474. Epitalon increased telomere length in the studied models. In normal cells, this effect was mainly associated with increased hTERT expression and telomerase activity. In cancer cells, significant telomere elongation was accompanied by the activation of an alternative telomere elongation pathway (ALT). [1]
This result is biologically significant because cancer cells require mechanisms to maintain chromosome ends in order to continue unrestricted proliferation.
However, this does not prove oncogenesis.
Breast cancer cell lines were already cancerous prior to exposure to Epitalon. The experiment therefore cannot demonstrate that Epitalon transformed healthy cells into malignant ones or initiated the development of cancer in humans.
The most precise conclusion is:
Epitalon has not been shown to be a carcinogen, but its effect on telomere maintenance mechanisms raises unresolved long-term safety questions that require properly designed studies.
Why Does Telomerase Raise Questions Concerning Cancer Risk?
Telomerase raises questions about cancer risk because critically short telomeres in many somatic cells naturally limit the number of subsequent divisions, whereas most tumors must maintain their telomeres—often using telomerase or ALT — to continue proliferating. Therefore, experimentally enhancing telomere maintenance mechanisms requires safety assessment, even though telomerase activation alone does not cause cancer.
Telomeres are protective DNA-protein structures located at the ends of chromosomes.
With successive cell divisions, telomeres in many somatic cells gradually shorten. When they become critically short, cells can activate a DNA damage response leading to replicative senescence, growth arrest, or apoptosis.
This mechanism may constitute one of the barriers limiting uncontrolled proliferation.
Cancer cells face the same problem. A malignant cell that divides repeatedly must eventually overcome telomere shortening to sustain long-term growth. Many cancers achieve this by reactivating telomerase, while others utilize alternative telomere lengthening (ALT).
This explains why hTERT, the catalytic subunit of telomerase, is of such great interest in oncology.
Epitalon complicates this issue, as studies on human cells have shown an increase in hTERT expression and telomere length. In a 2025 study, normal cells exhibited greater functional telomerase activity, while breast cancer cell lines showed significant telomere elongation with a high proportion of the ALT allele. [1]
However, the reasoning:
telomerase → immortal cells → cancer
It is too simplistic.
Tumor development typically involves multiple interacting processes, such as oncogenic mutations, loss of tumor suppression mechanisms, genomic instability, cell cycle control defects, evasion of apoptosis, metabolic alterations, immune evasion, and a supportive tissue microenvironment.
Telomere maintenance is often important for sustaining an already existing tumor clone, but in itself it is not sufficient to transform a normal cell into a cancer cell.
Telomerase activation is therefore a theoretical and mechanistic safety question, rather than proof of carcinogenicity.
What is the Difference Between Telomerase Activity and Cancer Outcomes?
Telomerase activity is a molecular measure, whereas a cancer-related outcome refers to the development, progression, recurrence, metastasis, or cancer-related mortality. The finding that Epitalon alters telomerase activity or ALT in cultured cells does not allow us to determine whether it increases, decreases, or has no effect on cancer risk in living humans.
This distinction is of fundamental importance.
The mechanistic endpoint informs researchers about what is happening to the molecular pathway.
Examples include:
hTERT mRNA increase,
the change in telomerase enzymatic activity,
telomere lengthening,
or an increase in ALT markers.
The cancer outcome, on the other hand, concerns whether organisms actually develop more or fewer cancers, whether tumors grow faster, whether metastases form, and whether cancer-related survival changes.
The 2025 study by Al-Dulaimi measured the first category of outcomes. It did not evaluate the incidence of cancer in humans. [1]
Similarly, an earlier fibroblast study from 2003 demonstrated telomerase activation in normal human fetal fibroblasts. [2] It did not include human monitoring for tumor development.
Older literature on animals provides whole-organism tumor results, but the findings point in a different direction.
In several studies on rodents, smaller or fewer tumors were observed after the administration of Epitalon. For example, Epithalon reduced the maximum size of breast adenocarcinoma and the expression of HER-2/neu in transgenic mice carrying the HER-2/neu oncogene. [3]
Another publication concerning HER-2/neu mice reported a lower incidence of mammary gland tumors, fewer multiple tumors, and fewer lung metastases in the treated animals. [4]
However, these results do not eliminate the mechanistic questions arising from telomere studies in human cells, just as the results of cell studies do not invalidate data from animals.
These studies answer various questions.
Has Epitalon Cancer Risk Been Studied in Humans?
No adequate studies have been conducted in humans to determine the cancer risk of Epitalon. The available evidence lacks robust long-term prospective cohort studies or randomized trials comparing cancer incidence, recurrence, metastasis, or cancer-related mortality between individuals exposed and unexposed to Epitalon. Therefore, the carcinogenic risk in humans remains unknown.
This is the biggest gap in the available evidence.
To correctly determine whether Epitalon affects cancer risk in humans, researchers would need long-term data including clinically relevant outcomes.
Such research should include:
baseline cancer risk,
Age,
family history,
tobacco smoking and other carcinogenic exposures,
pre-existing tumors,
duration and level of exposure to Epitalon,
cancer incidence,
specific types of cancer,
recurrences,
progression,
metastases,
and cancer-related mortality.
None of the available clinical publications regarding Epitalon contain such a dataset.
Available human studies are also poorly suited to answer this question.
Earlier reports focused on retinal diseases or the biology of melatonin and the circadian rhythm, rather than the incidence of tumors. Experiments on human lymphocytes and fibroblasts were performed outside the organism, so they cannot show whether a given person will develop a tumor years later.
The 2025 telomere study is particularly significant from a mechanistic standpoint because it directly analyzed human breast cancer cell lines, but it remains an in vitro study. [1]
Therefore, none of the following absolute statements are justified:
„Epitalon is carcinogenic.
I
„The safety of Epitalon in terms of cancer risk has been proven.
Evidence from human studies does not support either of these conclusions.
What Do Cell Studies and Animal Studies Show?
Cell-based and animal studies present a mixed, context-dependent picture. Epitalon lengthened telomeres via ALT in human breast cancer cell lines, while in several rodent cancer models, a reduction in tumor growth, tumor incidence, or metastasis was observed. In at least one model of chemically induced bladder cancer, Epitalon showed no inhibitory effect. None of these results predict cancer outcomes in humans. [1,3–8]
The most important studies are easier to interpret when compared with each other.
| Study/model | Main result | Level of evidence | What it does not prove |
|---|---|---|---|
| Normal human fibroblasts, 2003 | Telomerase activation and telomere lengthening | Human cells in vitro [2] | Cancer risks in humans |
| Breast cancer cells 21NT and BT474, 2025 | Telomere elongation with significant activation of ALT | Human cancer cells in vitro [1] | Tumor initiation or clinical tumor growth |
| HER-2/neu transgenic mice | Smaller tumors and lower HER-2/neu expression | Animal cancer model [3] | Cancer prevention in humans |
| HER-2/neu transgenic mice, related study | Lower breast cancer burden and fewer metastases | Animal tumor model [4] | Anticancer efficacy in humans |
| DMH-induced colorectal cancer in rats | Limitation of cancer/carcinogenesis-related results | Animal model of carcinogenesis [5] | Prevention of colorectal cancer in humans |
| Spontaneous tumors in C3H/He mice | Fewer mice with malignant tumors; no metastases in the treated group | Animal model of spontaneous tumors [6] | Human cancer safety |
| SHR mice of Swiss origin | No change in the total frequency of spontaneous tumors; lower frequency of leukemia | Animal model of longevity [7] | General anticancer |
| SAM mice | No significant effect on cancer incidence | Animal model of aging [8] | Cancer prevention |
| Chemically induced urinary bladder tumors in rats | Epitalon inhibitory effect | Animal model of carcinogenesis [9] | Human cancer risks or benefits |
Human Breast Cancer Cell Lines
A study published in Biogerontology in 2025 deserves special attention because it directly analyzed human cancer-derived cells.
For four days, researchers exposed the 21NT and BT474 breast cancer cell lines to various concentrations of Epitalon. Under several experimental conditions, the telomeres underwent significant elongation. [1]
The amount of hTERT mRNA also increased.
However, the functional enzymatic activity of telomerase in cancer cell lines did not increase significantly in proportion to hTERT transcription. Instead, the researchers observed increased ALT activity and elevated levels of PML bodies associated with ALT. [1]
The revised version of the publication clarified the figures regarding ALT activity and PML bodies; therefore, this correction should be considered alongside the original publication when interpreting the experimental details. [10]
This is a significant finding requiring caution, as it shows that Epitalon can affect the telomere maintenance mechanism in malignant cells.
However, the experiment did not show that the cells became more invasive, more readily formed tumors, metastasized more frequently, or led to worse clinical outcomes.
HER-2/neu Mouse Models of Breast Cancer
Older experiments on transgenic mice showed seemingly favorable results regarding tumors.
In one study, female FVB mice with HER-2/neu were found to have a 33% reduction in the maximum size of mammary adenocarcinomas, as well as approximately 3.7-fold lower HER-2/neu mRNA expression in tumors following administration of Epithalon. [3]
The related publication noted fewer mammary adenocarcinomas, fewer lung metastases and multiple tumors, and increased survival of the treated transgenic mice. [4]
These publications appear to stem from the same broader experimental program concerning HER-2/neu, and therefore should not automatically be treated as completely independent replications.
Colorectal Carcinogenesis
Epitalon has also been studied in DMH-induced colorectal cancer models in rats.
In one study, 80 male rats were divided into groups receiving Epitalon at various stages of chemically induced carcinogenesis. Researchers evaluated tumor proliferation, the adjacent mucosa, and apoptosis, noting an inhibitory effect in several treatment conditions. [5]
Again, this is a chemically induced model in rodents, not evidence regarding human colorectal cancer.
Spontaneous Tumor Models
In a 2006 study, female C3H/He mice of one year of age were observed for 6.5 months. The researchers reported a lower number of mice with malignant tumors and no metastases among the animals receiving Epitalon, whereas metastases occurred in three out of nine animals with tumors in the control group. [6]
Another long-term experiment on Swiss-derived SHR mice showed no decrease in the overall incidence of spontaneous tumors, although leukemia was less frequent. [7]
Similarly, in accelerated-senescence mice, Epitalon did not significantly alter the incidence of tumors despite other changes related to survival. [8]
These various results show that the potential anticancer effect is strongly dependent on the model and type of cancer.
Negative Result in Bladder Cancer Model
One of the most important counterexamples is the study of chemically induced bladder cancer in rats.
Vilon reduced the incidence of tumors in this experiment, whereas the researchers explicitly stated that Epitalon did not exhibit an inhibitory effect against urinary bladder tumors. [9]
This negative result makes it impossible to conclude the rodent studies with the statement that „Epitalon inhibits tumors.”.
A more precise interpretation is:
Some animal tumor models showed beneficial tumor outcomes, others showed no effect, while contemporary studies on human cancer cells indicate potentially significant changes in the biology of telomere maintenance.
Can It Be Assumed That Telomere Lengthening Is Safe?
No. It cannot be automatically assumed that telomere lengthening is beneficial or safe, as telomere maintenance can have different consequences depending on the cell type. In normal cells, it may delay replicative aging, whereas existing cancer cells may use telomerase or ALT to sustain further proliferation. The long-term clinical significance of Epitalon’s effect on telomeres therefore remains uncertain.
Telomeres are often portrayed in such a way that their greater length always means younger, and thus healthier, cells.
Biology is more complex.
In normally dividing cells, very short telomeres can contribute to cellular senescence and reduced regenerative capacity. Therefore, preserving telomere function represents an important area of research on aging.
At the same time, cellular senescence can act as an anti-cancer barrier.
A cell accumulating dangerous molecular changes may eventually stop dividing. If such a cell acquires mechanisms allowing for unlimited replication, this can become one of the elements of tumor progression.
A 2025 Epitalon study illustrates this duality well.
Normal fibroblasts and epithelial cells elongated telomeres mainly by increasing hTERT and telomerase activity. [1]
Two breast cancer cell lines also lengthened their telomeres, but with a clear contribution from ALT activation. [1]
The authors did not demonstrate that this led to more aggressive tumor behavior. Nevertheless, this result makes it impossible to claim that telomere elongation alone constitutes evidence of safety or rejuvenation.
It would be equally incorrect to state that telomere lengthening automatically leads to cancer.
A proper risk assessment would require determining whether Epitalon:
alters the frequency of malignant transformation,
promotes the survival of pre-neoplastic cells,
influences tumor initiation,
accelerates or inhibits existing tumors,
changes the metastatic potential,
interacts with anticancer therapies,
or affects different types of cancer differently.
These questions were not answered in human studies.
What Conclusions Should Not Be Drawn from Mechanistic Studies?
Mechanistic studies on Epitalon cannot prove that the peptide causes cancer, prevents tumors, cures cancer, is safe for individuals with cancer, or that telomere elongation is beneficial. Cellular and molecular results serve to generate biological hypotheses, whereas clinical conclusions require human outcome data, which are currently lacking.
Several frequently repeated conclusions go beyond the available evidence.
„Epitalon Causes Cancer Because It Activates Telomerase”
Such a statement is not supported by evidence.
Epitalon activated telomerase in cultured normal human cells and affected telomere maintenance mechanisms in cancer cells. [1,2] Neither of these experiments showed tumor initiation in humans.
Oncogenesis requires more than telomerase activation.
„Epithalon Prevents Cancer”
This statement is also not supported by evidence.
Several studies in rodents have observed a lower tumor burden or a lower incidence of tumors. [3–7] However, in another rodent model, Epitalon had no effect on urinary bladder carcinogenesis, and some studies in aging mice observed no difference in overall tumor incidence. [8,9]
No human cancer prevention study has been conducted.
„Epitalon Cures Cancer”
No clinical evidence supports this statement.
The reduction of tumor growth in HER-2/neu mice does not confirm the efficacy of treatment for breast cancer in humans. Similarly, results concerning chemically induced colorectal tumors in rats cannot confirm efficacy in the treatment of colorectal cancer in humans.
„Epitalon Is Safe for People with Current or Past Cancer”
It has not been determined.
Breast cancer cell research results from 2025 make this a particularly important unresolved question. [1]
There are no controlled human trial data determining how Epitalon affects active cancer, remaining cancer cells, anti-cancer therapies, or the risk of recurrence.
„Longer Telomeres Mean Lower Cancer Risk”
Not necessarily.
Telomere dysfunction can contribute to genomic instability, but stable telomere maintenance can also enable existing malignant cells to continue proliferating.
Therefore, the biological relationship between telomere length and oncogenesis is context-dependent.
„Animal Cancer Studies Invalidate Cancer Cell Study Results”
No.
A mouse tumor model and a cultured human breast cancer cell line measure different biological levels.
The proper reaction to seemingly divergent results is not to select those that support a preferred conclusion, but to recognize that the effect of Epitalon may strongly depend on the tissue, genetic background, type of cancer, stage of carcinogenesis, and experimental conditions.
How to Interpret Evidence Regarding Epitalon and Cancer?
Evidence is best organized by specific question.
| Question | Evidence-based answer |
|---|---|
| Does Epitalon cause cancer in humans? | Not demonstrated |
| Has the human carcinogenic risk been adequately studied? | Not |
| Does Epitalon affect telomerase? | Yes, in cultured normal human cells [1,2] |
| Does Epitalon affect hTERT? | Yes, it has been demonstrated in vitro [1,2] |
| Can Epitalon lengthen telomeres in cancer cells? | Yes, in two breast cancer cell lines [1] |
| Did ALT levels increase in these cancer cells? | Yes, in vitro [1,10] |
| Does ALT activation indicate poorer cancer outcomes? | Not |
| Have some animal cancer models demonstrated tumor inhibition? | Yes [3–7] |
| Did all animal models show anti-tumor activity? | No [8,9] |
| Does Epitalon prevent cancer in humans? | Not demonstrated |
| Does Epitalon cure cancer in humans? | Not demonstrated |
| Has the safety of Epitalon been proven in cancer patients? | Not |
| Have the long-term oncological consequences been understood? | Not |
Therefore, the general conclusion should remain deliberately precise:
Epitalon affects biological processes relevant to tumors, particularly telomere maintenance mechanisms, while animal tumor studies have in some cases shown a seemingly protective effect. Neither of these lines of evidence allows for determining the direction of cancer risk in humans.
Frequently Asked Questions About Epitalon and Cancer
Does Epitalon Cause Cancer?
There is no evidence to suggest that Epitalon causes cancer in humans. Concerns are theoretical and mechanistic in nature, as Epitalon increased hTERT, telomerase-related activity, and telomere length in cultured cells, and a 2025 study demonstrated telomere lengthening associated with the ALT variant in two already malignant breast cancer cell lines. These results warrant further safety studies but do not prove tumor initiation. [1,2]
Does Epitalon Increase Telomerase Activity in Cancer Cells?
A 2025 study showed that Epitalon increased the amount of hTERT mRNA in the 21NT and BT474 breast cancer cell lines, but this did not lead to a corresponding significant increase in functional telomerase activity. Instead, telomere lengthening in these cells was largely associated with increased ALT activity. This demonstrates that hTERT expression, telomerase activity, and telomere lengthening are not equivalent endpoints. [1]
Can Epitalon Make Cancer Cells Live Longer?
This was not established as either a clinical outcome or a general cellular effect. Epitalon lengthened telomeres in two cultured breast cancer cell lines through mechanisms associated with ALT, which theoretically may be relevant to replicative capacity. However, the study did not show increased tumor formation, greater metastatic potential, resistance to treatment, or an effect on patient survival. [1]
Does Epitalon Exhibit Anticancer Effects?
Yes, but exclusively in preclinical studies. In several studies on mice and rats, a reduction in tumor growth, a lower incidence of tumors, fewer metastases, or inhibition of colorectal carcinogenesis were observed, while other models showed no reduction in overall tumor incidence or any inhibitory effect. Animal study results do not support the prevention or treatment of tumors in humans. [3–9]
Is Epitalon Safe for a Person with Cancer?
Safety in individuals with active or a history of cancer has not been established. Because Epitalon affects telomere maintenance mechanisms and has been shown to cause ALT-associated telomere lengthening in cancer-derived cells, decisions regarding individuals with cancer require an individual medical evaluation, rather than extrapolation from animal study results or online claims. [1]
Do Longer Telomeres Prevent Cancer?
Not necessarily. Critically short telomeres can contribute to genomic instability, but malignant cells also require telomere-maintaining mechanisms to continue dividing. Telomere biology can therefore have both tumor-suppressive and tumor-promoting aspects, depending on the cell state and the stage of the disease.
Can Epitalon Be Considered an Anticancer Peptide?
No. Although several animal experiments have reported beneficial results related to tumors, there is no controlled human evidence confirming Epitalon as a cancer preventive or anti-cancer therapy. The negative result of a bladder cancer study in rats and newer findings regarding telomeres in cancer cells further demonstrate why the universal term „anti-cancer peptide” would be misleading. [1,3–9]
Evidence Limitations Regarding Epitalon and Cancer
The greatest limitation is the lack of direct data on cancer outcomes in humans.
Cancers develop over a long period of time, which is why even reassuring data on short-term tolerance would not be sufficient to confirm carcinogenic safety.
The second limitation is the diversity of preclinical models.
HER-2/neu transgenic mammary tumors, DMH-induced colorectal cancer, chemically induced urinary bladder tumors, spontaneous C3H/He tumors, senescence-accelerated mice, and cultured breast cancer cells represent very different forms of cancer biology.
Results from one model should not be generalized to others.
Third, several older cancer publications stem from related experimental programs and may represent companion analyses rather than entirely independent replications. In particular, many publications regarding HER-2/neu should not simply be treated as separate confirmations without considering experimental overlap.
Fourth, experimental telomere lengthening is a surrogate biological endpoint, not a neoplastic outcome.
Fifth, the 2025 publication on telomeres has a published correction. The correction concerns the figures related to the ALT analysis and should be considered together with the original article when interpreting the precise experimental details. [10]
Finally, Epitalon has not undergone a formal human carcinogenic risk assessment at the level expected for a well-characterized, approved medicinal product.
Current evidence therefore points to uncertainty, rather than confirmed safety or a basis for alarmist conclusions.
Disclaimer
This article is for educational and scientific-informational purposes only and does not constitute medical advice, diagnosis, cancer treatment guidelines, dosage instructions, or recommendations for the use of Epitalon. Epitalon/Epithalon (AEDG; Ala-Glu-Asp-Gly) is not a recognized, FDA- or EMA-approved treatment for cancer prevention or anti-cancer therapy, and available evidence regarding cancer comes primarily from in vitro or animal studies rather than controlled human clinical trials. Epitalon has not been shown to cause cancer in humans, but its long-term carcinogenic risk in humans has also not been adequately established.
References
[1] Al-Dulaimi, S., Thomas, R., Matta, S., & Roberts, T. (2025). Epitalon increases telomere length in human cell lines through telomerase upregulation or ALT activity. Biogerontology, 26(5), 178. https://doi.org/10.1007/s10522-025-10315-x
[2] Khavinson, V. K., Bondarev, I. E., & Butyugov, A. A. (2003). Epithalon peptide induces telomerase activity and telomere elongation in human somatic cells. Bulletin of Experimental Biology and Medicine, 135(6), 590–592. https://doi.org/10.1023/A:1025493705728
[3] Anisimov, V. N., Khavinson, V. K., Alimova, I. N., Provinciali, M., Mancini, R., & Franceschi, C. (2002). Epithalon inhibits tumor growth and expression of HER-2/neu oncogene in breast tumors in transgenic mice characterized by accelerated aging. Bulletin of Experimental Biology and Medicine, 133(2), 167–170. https://doi.org/10.1023/A:1015555023692
[4] Anisimov, V. N., Khavinson, V. K., Alimova, I. N., Semchenko, A. V., & Yashin, A. I. (2002). Epithalon decelerates aging and suppresses development of breast adenocarcinomas in transgenic HER-2/neu mice. Bulletin of Experimental Biology and Medicine, 134(2), 187–190. https://doi.org/10.1023/A:1021104819170
[5] Anisimov, V. N., Khavinson, V. K., Popovich, I. G., & Zabezhinski, M. A. (2002). Inhibitory effect of peptide Epitalon on colon carcinogenesis induced by 1,2-dimethylhydrazine in rats. Cancer Letters, 183(1), 1–8. https://doi.org/10.1016/S0304-3835(02)00090-3
[6] Kossoy, G., Anisimov, V. N., Ben-Hur, H., Kossoy, N., & Zusman, I. (2006). Effect of the synthetic pineal peptide Epitalon on spontaneous carcinogenesis in female C3H/He mice. In Vivo, 20(2), 253–257. https://pubmed.ncbi.nlm.nih.gov/16634527/
[7] Anisimov, V. N., Khavinson, V. K., Popovich, I. G., Zabezhinski, M. A., Alimova, I. N., Rosenfeld, S. V., Zavarzina, N. Y., Semenchenko, A. V., & Yashin, A. I. (2003). Effect of Epitalon on biomarkers of aging, lifespan, and spontaneous tumor incidence in female Swiss-derived SHR mice. Biogerontology, 4(4), 193–202. https://doi.org/10.1023/A:1025114230714
[8] Anisimov, V. N., Popovich, I. G., Zabezhinskiĭ, M. A., Rozenfel’d, S. V., Khavinson, V. K., Semenchenko, A. V., & Iashin, A. I. (2005). Effect of Epitalon and melatonin on life span and spontaneous carcinogenesis in senescence-accelerated mice (SAM). Voprosy Onkologii, 51(1), 93–98. https://pubmed.ncbi.nlm.nih.gov/15909815/
[9] Pliss, G. B., Mel’nikov, A. S., Malinin, V. V., & Khavinson, V. K. (2001). Effect of Vilon and Epithalone on induction and growth of induced bladder neoplasms in rats. Voprosy Onkologii, 47(5), 601–607. https://pubmed.ncbi.nlm.nih.gov/11785104/
[10] Al-Dulaimi, S., Thomas, R., Matta, S., & Roberts, T. (2025). Correction: Epitalon increases telomere length in human cell lines through telomerase upregulation or ALT activity. Biogerontology, 27(1), 1. https://doi.org/10.1007/s10522-025-10326-8