Telomir Pharmaceuticals Announces New Findings in a Prostate Cancer Model Demonstrating Telomir-1 Also Resets DNA Methylation of Tumor Suppressor Genes Implicated in Two of the Most Persistent Challenges in Oncology-Metastasis and Treatment Resistance
Findings show that Telomir-1 restores the body's natural tumor suppressor defenses by reversing abnormal DNA methylation of MASPIN and RASSF1A - genes that help block invasion, limit metastasis, and improve chemotherapy responsiveness in aggressive …
Findings show that Telomir-1 restores the body's natural tumor suppressor defenses by reversing abnormal DNA methylation of MASPIN and RASSF1A - genes that help block invasion, limit metastasis, and improve chemotherapy responsiveness in aggressive prostate cancer models.
MIAMI, FLORIDA / ACCESS Newswire / October 7, 2025 / Telomir Pharmaceuticals, Inc. (NASDAQ:TELO) ("Telomir" or the "Company"), a preclinical-stage biotechnology company developing therapies that target epigenetic drivers of cancer, aging, and age-related disease, today announced new preclinical results showing that its investigational therapy Telomir-1 reactivated two of the body's most important tumor suppressor genes, MASPIN ("tumor suppressor shield") and RASSF1A ("guardian gene"; also called SERPINB5), through DNA methylation reset in prostate cancer models. By restoring the activity of these genes, Telomir-1 may help prevent cancer spread and improve chemotherapy response
Key New Findings
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MASPIN ("tumor suppressor shield"): MASPIN is a natural defense protein that blocks tumor invasion, regulates cell migration and angiogenesis, promotes apoptosis, and enhances treatment sensitivity. In an aggressive prostate-cancer model in vivo, MASPIN was silenced by DNA hypermethylation. Telomir-1 reversed the chemotherapy-induced DNA methylation to restore MASPIN activity, consistent with reactivation of this key tumor-suppressor pathway.
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RASSF1A ("guardian gene", also called SERPINB5):
RASSF1A is a critical regulator of cell cycle brakes, apoptosis, and suppression of metastasis. It is commonly silenced in aggressive cancers by hypermethylation. Telomir-1 reduced RASSF1A methylation in a dose-dependent manner, with stronger effects when combined with chemotherapy. -
Implication: These results suggest Telomir-1 may reactivate natural tumor defenses, counteract chemotherapy-induced resistance mechanisms, and help limit metastasis - two of the most persistent challenges in oncology.
Why This Matters
Metastasis is responsible for the vast majority of cancer deaths, and chemotherapy resistance remains a major barrier to durable responses. Tumors often silence genes like MASPIN and RASSF1A by hypermethylation to disable the body's natural defenses.
Telomir-1's ability to reset DNA methylation, restore tumor suppressor activity, and synergize with chemotherapy provides a compelling preclinical rationale for its potential as a first-in-class epigenetic reset therapy in oncology.

