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 questions regarding its mechanism of action, 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 on the internet: „Epitalon causes cancer because it activates telomerase” and „Epitalon prevents cancer because animal studies showed fewer tumours”. Neither of these conclusions is supported by the full picture of available evidence.
Telomerase and telomeres play a role in the proper maintenance of cells, ageing 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 an effect on hTERT, telomerase, telomere length and ALT, as well as older animal studies in which a reduction in tumour growth was frequently observed 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, rather than evidence concerning the incidence of cancer in humans exposed to Epitalon.
Does Epitalon Cause Cancer?
There is no clinical evidence to suggest that Epitalon causes cancer in humans. However, experiments on human cells show that Epitalon may affect the mechanisms involved in telomere maintenance, including hTERT expression, telomerase activity and ALT. Therefore, without appropriate safety and carcinogenicity studies in humans, the long-term cancer risk cannot be considered to have been established or ruled out. [1–3]
No study in the analysed evidence shows that tumours 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 does not currently exist.
However, concerns stem from mechanistic biology.
Epitalon has repeatedly shown an effect on telomere maintenance in cultured human cells. A 2003 in vitro study on human foetal fibroblasts found 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 analysed normal fibroblasts and mammary gland epithelial cells, as well as two breast cancer cell lines — 21NT and BT474. Epitalon increased telomere length in the models studied. In normal cells, this effect was mainly associated with an increase in hTERT expression and telomerase activity. In cancerous 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 enabling the maintenance of 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 impact on telomere maintenance mechanisms raises unresolved questions regarding long-term safety, which require properly designed studies.
Why does telomerase raise questions regarding cancer risk?
Telomerase raises questions regarding cancer risk, as critically short telomeres in many somatic cells naturally limit the number of subsequent divisions, whilst most tumours must maintain their telomeres — often by means of telomerase or ALT — in order to continue proliferating. Therefore, the experimental enhancement of telomere maintenance mechanisms requires safety assessment, even though the activation of telomerase 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 ultimately overcome telomere shortening in order to sustain long-term growth. Many cancers achieve this by reactivating telomerase, whilst others utilise alternative telomere lengthening (ALT).
This explains why hTERT, the catalytic subunit of telomerase, is the subject of so much 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, whilst breast cancer cell lines showed a significant lengthening of telomeres with a high proportion of the ALT allele. [1]
However, the reasoning:
telomerase → immortal cells → cancer
It is too simplistic.
Tumour development usually involves many interacting processes, such as oncogenic mutations, loss of tumour suppression mechanisms, genomic instability, cell cycle control disorders, evasion of apoptosis, metabolic changes, immune system evasion and a favourable tissue microenvironment.
Telomere maintenance is often important for sustaining an already existing tumour clone, but in itself is not sufficient to transform a normal cell into a tumour cell.
Telomerase activation therefore represents 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, whilst 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:
increased hTERT mRNA,
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 tumours 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 assess the incidence of cancer in humans. [1]
Similarly, an earlier 2003 study on fibroblasts demonstrated telomerase activation in normal human foetal fibroblasts. [2] It did not include the observation of humans for the development of tumours.
Older literature concerning animals provides whole-organism tumour results, but the results point in a different direction.
In several rodent studies, smaller or fewer tumours were observed after Epitalon administration. 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 regarding HER-2/neu mice reported a lower incidence of mammary gland tumours, fewer multiple tumours, and fewer lung metastases in the treated animals. [4]
However, these results do not eliminate the mechanistic questions arising from telomere research in human cells, just as the results of cellular studies do not invalidate data from animals.
These studies answer various questions.
Has Epitalon Cancer Risk Been Studied in Humans?
Adequate studies in humans have not been conducted to determine the carcinogenic risk of Epitalon. In the available evidence, there are no robust long-term prospective cohort studies or randomised trials comparing the incidence of cancer, recurrence, metastases, or cancer-related mortality between individuals exposed and unexposed to Epitalon. The carcinogenic risk in humans therefore 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 tumours,
duration and level of exposure to Epitalon,
cancer incidence,
specific types of cancer,
relapses,
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 focussed on retinal diseases or the biology of melatonin and circadian rhythms, rather than cancer incidence. Experiments on human lymphocytes and fibroblasts were carried out *in vitro*, and therefore they cannot show whether a given person will develop cancer years later.
The 2025 telomere study is particularly significant from a mechanistic perspective as it directly analysed human breast cancer cell lines, although it remains an in vitro study. [1]
Therefore, none of the following absolute statements are justified:
„Epitalon is carcinogenic.
Any
„Epithalon has been proven safe in terms of cancer risk.
Evidence from human studies does not support either of these conclusions.
What Do Cell 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, whilst in several rodent cancer models a reduction in tumour growth, tumour incidence or metastasis was observed. In at least one model of chemically induced bladder cancer, Epitalon showed no inhibitory effect. None of these findings predict cancer outcomes in humans. [1,3–8]
The most important studies are easier to interpret when compared with each other.
| Study/model | Main outcome | 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 lengthening with significant activation of ALT | Human cancer cells in vitro [1] | Tumour initiation or clinical tumour growth |
| HER-2/neu transgenic mice | Smaller tumours and lower HER-2/neu expression | Animal cancer model [3] | Cancer prevention in humans |
| Transgenic HER-2/neu mice, associated study | Lower breast tumour burden and fewer metastases | Animal cancer model [4] | Anticancer efficacy in humans |
| DMH-induced colorectal cancer in rats | Restriction of cancer/carcinogenesis-related outcomes | Animal model of carcinogenesis [5] | Prevention of colorectal cancer in humans |
| Spontaneous tumours in C3H/He mice | Fewer mice with malignant neoplasms; no metastases in the treated group | Animal model of spontaneous tumours | Human cancer safety |
| Swiss origin SHR mice | No change in the total frequency of spontaneous neoplasms; lower frequency of leukaemia | Animal model of longevity [7] | General anti-cancer properties |
| SAM mice | No significant effect on tumour frequency | Animal model of ageing [8] | Cancer prevention |
| Chemically induced urinary bladder tumours in rats | Lack of inhibitory action of Epitalon | Animal model of carcinogenesis [9] | Risks or benefits of cancer in humans |
Human Breast Cancer Cell Lines
A study published in Biogerontology in 2025 deserves special attention because it directly analysed human cancer 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 lengthening. [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 has clarified the figures relating to ALT activity and PML bodies; therefore, this correction should be taken into account 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, formed tumours more easily, metastasised more frequently, or led to poorer clinical outcomes.
HER-2/neu Mouse Models of Breast Cancer
Older experiments on transgenic mice showed seemingly beneficial results regarding tumours.
In one study, female FVB mice with HER-2/neu were found to have a 33% reduction in the maximum size of mammary adenocarcinoma, as well as approximately 3.7-fold lower HER-2/neu mRNA expression in tumours following administration of Epithalon. [3]
The related publication noted fewer mammary adenocarcinomas, fewer lung metastases and multiple tumours, and increased survival of the treated transgenic mice. [4]
These publications appear to stem from the same broader experimental programme concerning HER-2/neu, and therefore should not automatically be regarded as entirely 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. The researchers evaluated tumour 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 Tumour Models
In a 2006 study, female C3H/He mice aged one year were observed for 6.5 months. The researchers reported a lower number of mice with malignant tumours and no metastases among the animals receiving Epitalon, whereas metastases occurred in three out of nine animals with tumours in the control group. [6]
Another long-term experiment on Swiss-derived SHR mice showed no reduction in the overall incidence of spontaneous tumours, although leukaemia occurred less frequently. [7]
Similarly, in accelerated-senescence mice, Epitalon did not significantly alter tumour incidence despite other changes related to survival. [8]
These various results show that any potential anti-cancer effect is strongly dependent on the model and the type of cancer.
Negative Result in Bladder Cancer Model
One of the most important counter-examples is the study of chemically induced bladder cancer in rats.
Vilon reduced the frequency of tumours in this experiment, whereas the researchers explicitly stated that Epitalon did not exhibit an inhibitory effect on urinary bladder tumours. [9]
This negative result makes it impossible to conclude the rodent studies with the statement „Epitalon inhibits tumours”.
A more precise interpretation is:
Some animal cancer models showed beneficial outcomes regarding tumours, others showed no effect, whereas 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 may have different consequences depending on the type of cell. In normal cells, it may delay replicative ageing, whilst existing cancer cells may utilise 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 ageing and a reduced regenerative capacity. For this reason, the preservation of telomere function represents an important area of research into ageing.
At the same time, cellular senescence can act as an anti-cancer barrier.
A cell that accumulates 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 tumour progression.
The 2025 Epitalon study nicely illustrates this duality.
Normal fibroblasts and epithelial cells lengthened telomeres mainly by increasing hTERT and telomerase activity. [1]
Two breast cancer cell lines also lengthened their telomeres, but this was clearly associated with the activation of ALT. [1]
The authors did not demonstrate that this led to more aggressive tumour behaviour. Nevertheless, this finding means it cannot be claimed that telomere elongation alone constitutes proof 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 neoplastic transformation,
promotes the survival of pre-neoplastic cells,
affects the initiation of the tumour,
accelerates or inhibits existing tumours,
changes the metastatic potential,
interacts with anti-cancer therapies,
or affects different types of cancer differently.
These questions have not been 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 tumours, treats cancer, is safe for people with neoplastic disease, or that telomere lengthening 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 demonstrated tumour initiation in humans.
Oncogenesis requires more than telomerase activation.
„Epitalon Prevents Cancer”
Such a statement is also not supported by evidence.
Several rodent studies have observed a lower tumour burden or a lower incidence of tumours. [3–7] However, in another rodent model, Epitalon had no effect on urinary bladder carcinogenesis, and some studies in ageing mice observed no difference in overall tumour incidence. [8,9]
No research on cancer prevention in humans has been conducted.
„Epitalon Cures Cancer”
No clinical evidence supports this statement.
The reduction of tumour growth in HER-2/neu mice does not confirm the effectiveness of breast cancer treatment in humans. Similarly, results concerning chemically induced colorectal tumours in rats cannot confirm effectiveness in the treatment of colorectal cancer in humans.
„Epitalon Is Safe for People with Current or Past Cancer”
This has not been settled.
2025 breast cancer cell research makes 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.
The biological relationship between telomere length and oncogenesis is therefore context-dependent.
„Animal Anticancer Studies Invalidate Tumour Cell Study Results”
No.
The mouse tumour model and the cultured human breast cancer cell line measure different biological levels.
The correct reaction to seemingly divergent results is not to choose those that support a preferred conclusion, but to recognise 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
It is best to organise the evidence according to a specific question.
| Question | An evidence-based response |
|---|---|
| Does Epitalon cause cancer in humans? | Not demonstrated |
| Has the carcinogenic risk to humans 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] |
| Was ALT elevated in these cancer cells? | Yes, in vitro [1,10] |
| Does the activation of ALT indicate poorer cancer outcomes? | Not |
| Have some animal tumour models demonstrated tumour inhibition? | Yes [3–7] |
| Did all animal models show an anti-tumour effect? | 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 identified? | Not |
The general conclusion should therefore remain deliberately precise:
Epitalon affects biological processes relevant to tumours, particularly mechanisms of telomere maintenance, whereas studies of tumours in animals have in some cases shown a seemingly protective effect. Neither of these bodies of evidence allows the direction of cancer risk in humans to be determined.
Frequently Asked Questions about Epitalon and Cancer
Does Epitalon Cause Cancer?
There is no evidence to suggest that Epitalon causes cancer in humans. The 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 findings warrant further safety studies, but do not prove tumour initiation. [1,2]
Does Epitalon Increase Telomerase Activity in Cancer Cells?
A 2025 study showed that Epitalon increased the levels 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 either as a clinical outcome or as a general cellular effect. Epitalon lengthened telomeres in two cultured breast cancer cell lines via mechanisms associated with ALT, which could theoretically be relevant to replicative capacity. However, the study did not demonstrate increased tumour formation, greater metastatic potential, resistance to treatment or any impact on patient survival. [1]
Does Epitalon exhibit anticancer activity?
Yes, but exclusively in preclinical studies. In several studies on mice and rats, a reduction in tumour growth, a lower incidence of tumours, fewer metastases, or the inhibition of colorectal carcinogenesis were observed, whereas other models showed no reduction in overall tumour incidence or any inhibitory effect. Animal study results do not support the prevention or treatment of tumours in humans. [3–9]
Is Epitalon Safe for Someone with Cancer?
Safety in people with active or a history of cancer has not been established. As Epitalon affects telomere maintenance mechanisms and has been shown to cause ALT-associated telomere elongation in tumour-derived cells, decisions regarding people with cancer require an individual medical assessment, rather than extrapolating 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 in order to continue dividing. Telomere biology can therefore have both tumour-suppressive and tumour-promoting aspects, depending on the cell state and the stage of the disease.
Can Epitalon Be Considered an Anticancer Peptide?
No. Although some animal experiments have reported favourable cancer-related outcomes, there is no controlled evidence in humans supporting Epitalon as a cancer preventative or anti-cancer therapy. The negative result of a bladder cancer study in rats and more recent findings regarding telomeres in cancer cells further demonstrate why the universal term „anti-cancer peptide” would be misleading. [1,3–9]
Limitations of Evidence Regarding Epitalon and Cancer
The biggest 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.
Another limitation is the variety of preclinical models.
HER-2/neu transgenic mammary tumours, DMH-induced colorectal cancer, chemically induced urinary bladder tumours, spontaneous C3H/He tumours, senescence-accelerated mice and cultured breast cancer cells represent very diverse forms of tumour biology.
Results from one model should not be generalised to others.
Thirdly, several older cancer publications originate from related experimental programs and may represent companion analyses rather than entirely independent replications. In particular, many publications concerning HER-2/neu should not simply be treated as separate confirmations without taking experimental overlap into account.
Fourthly, experimental telomere lengthening is a surrogate biological endpoint, not a neoplastic outcome.
Fifthly, the 2025 paper on telomeres has had a correction published. The correction relates to the figures concerning the ALT analysis and should be taken into account alongside the original article when interpreting the precise experimental details. [10]
Finally, Epitalon has not undergone a formal carcinogenic risk assessment in humans at the level expected for a well-characterised, approved medicinal product.
Current evidence therefore points to uncertainty, rather than confirmed safety or grounds for alarmist conclusions.
Disclaimer
This article is for educational and scientific-information purposes only and does not constitute medical advice, diagnosis, cancer treatment guidelines, dosage instructions, or a recommendation for the use of Epitalon. Epitalon/Epithalon (AEDG; Ala-Glu-Asp-Gly) is not a recognised, FDA- or EMA-approved treatment for cancer prevention or anti-cancer therapy, and available evidence regarding cancer comes mainly from in vitro or animal studies rather than controlled clinical trials in humans. Epitalon has not been shown to cause cancer in humans, but the 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 tumour growth and expression of HER-2/neu oncogene in breast tumours in transgenic mice characterised by accelerated ageing. 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 ageing 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, life span and spontaneous tumour 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., Zabezhinskiy, M. A., Rozenfeld, 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). Problems of Oncology, 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 Epithalon 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