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
Telomir Pharmaceuticals (NASDAQ:TELO) reported preclinical results dated October 7, 2025 showing its candidate Telomir-1 reset DNA methylation and reactivated tumor suppressor genes MASPIN and RASSF1A in aggressive prostate cancer models.
Key findings: dose-dependent reduction in RASSF1A methylation, reversal of chemotherapy-induced MASPIN hypermethylation, ~50% tumor volume reduction in vivo, and elimination of chemotherapy-related mortality in the reported models. Telomir-1 also showed prior preclinical effects on STAT1, CDKN2A, histone demethylases, mitochondrial function, and telomere/epigenetic markers. Telomir is advancing Telomir-1 into IND-enabling preclinical studies.
Telomir Pharmaceuticals (NASDAQ:TELO) ha riportato risultati preclinici datati 7 ottobre 2025 che mostrano che il suo candidato Telomir-1 ripristina la metilazione del DNA e riattiva i geni soppressori tumorali MASPIN e RASSF1A in modelli di cancro alla prostata aggressivi.
Principali risultati: una riduzione dose-dipendente della metilazione di RASSF1A, l'inversione dell'ipermetilazione di MASPIN indotta dalla chemioterapia, una riduzione di circa il 50% del volume tumorale in vivo e l'eliminazione della mortalità legata alla chemioterapia nei modelli riportati. Telomir-1 ha mostrato anche effetti preclinici precedenti su STAT1, CDKN2A, demetilasi degli istoni, funzione mitocondriale e marker telomero/epigenetici. Telomir sta avanzando Telomir-1 in studi preclinici IND-enabling.
Telomir Pharmaceuticals (NASDAQ:TELO) informó resultados preclínicos fechados 7 de octubre de 2025 que muestran que su candidato Telomir-1 restablece la metilación del ADN y reactivó los genes supresores de tumores MASPIN y RASSF1A en modelos de cáncer de próstata agresivo.
Hallazgos clave: reducción dependiente de la dosis de la metilación de RASSF1A, inversión de la hipermetilación de MASPIN inducida por quimioterapia, ~reducción del 50% del volumen tumoral in vivo y eliminación de la mortalidad relacionada con la quimioterapia en los modelos reportados. Telomir-1 también mostró efectos preclínicos previos sobre STAT1, CDKN2A, desmetilasas de histonas, función mitocondrial y marcadores telómero/epigenéticos. Telomir está avanzando Telomir-1 en estudios preclínicos IND-enabling.
Telomir Pharmaceuticals (NASDAQ:TELO)은 2025년 10월 7일자로 기재된 전임상 결과를 발표했으며, 그 후보물질 Telomir-1이 DNA 메틸화를 재설정하고 공격적인 전립선암 모델에서 종양억제유전자 MASPIN과 RASSF1A를 재활성화했다고 밝혔다.
주요 발견: 용량 의존적으로 RASSF1A 메틸화 감소, 화학요법으로 유도된 MASPIN 하이메틸화의 역전, 생체 내 약 50% 종양 부피 감소, 보고된 모델에서 화학요법 관련 사망률의 제거. Telomir-1은 또한 STAT1, CDKN2A, 히스톤 디메틸레이스, 미토콘드리아 기능 및 텔로미어/에피제네틱 마커에 대한 선행 전임상 효과를 보였다고 한다. Telomir는 Telomir-1을 IND-enabling 전임상 연구로 진행 중이다.
Telomir Pharmaceuticals (NASDAQ:TELO) a publié des résultats précliniques datés du 7 octobre 2025 montrant que son candidat Telomir-1 réinitialise la méthylation de l'ADN et réactive les gènes suppresseurs de tumeurs MASPIN et RASSF1A dans des modèles de cancer de la prostate agressifs.
Principales constatations : réduction indépendante de la dose de la méthylation de RASSF1A, inversion de l'hyperméthylation de MASPIN induite par la chimiothérapie, une réduction d'environ 50% du volume tumoral in vivo et élimination de la mortalité liée à la chimiothérapie dans les modèles rapportés. Telomir-1 a également montré des effets précliniques antérieurs sur STAT1, CDKN2A, déméthylases des histones, fonction mitochondriale et marqueurs télomères/épigénétiques. Telomir fait avancer Telomir-1 dans des études précliniques IND-enabling.
Telomir Pharmaceuticals (NASDAQ:TELO) veröffentlichte präkline Ergebnisse vom 7. Oktober 2025, die zeigen, dass sein Kandidat Telomir-1 die DNA-Methylierung zurücksetzt und die Tumorsuppressorgene MASPIN und RASSF1A in aggressiven Prostatakrebsmodellen reaktiviert.
Wesentliche Ergebnisse: dosenabhängige Reduktion der RASSF1A-Methylierung, Umkehrung der durch Chemotherapie induzierten MASPIN-Hypermetylierung, ca. 50% Reduktion des Tumorvolumens in vivo und Eliminierung der durch Chemotherapie bedingten Mortalität in den berichteten Modellen. Telomir-1 zeigte außerdem vorangegangene präklinische Effekte auf STAT1, CDKN2A, Histon-Demethylasen, mitochondriale Funktion und telomere/epigenetische Marker. Telomir bringt Telomir-1 in IND-enabling präklinische Studien voran.
Telomir Pharmaceuticals (NASDAQ:TELO) أصدرت نتائج ما قبل السريرية المؤرخة 7 أكتوبر 2025 تُظهر أن مرشحها Telomir-1 يعيد ضبط ميثلة DNA ويعيد تنشيط جينات مثبطة الورم MASPIN و RASSF1A في نماذج سرطان البروستاتا العدوانية.
النتائج الرئيسية: انخفاض يعتمد على الجرعة في ميثلة RASSF1A، عكس فرط ميثلة MASPIN الناتجة عن العلاج الكيميائي، نحو خفض بحوالي 50% في حجم الورم حيّاً، وإزالة الوفيات المرتبطة بالعلاج الكيميائي في النماذج المذكورة. كما أظهر Telomir-1 تأثيرات قبل السريرية على STAT1، CDKN2A، ديميتلازات الهستونات، وظيفة الميتوكوندريا وعلامات التيلومير/الإبيجينيتية. تتقدم Telomir في دراسات ما قبل السريرية IND-enabling.
Telomir Pharmaceuticals (NASDAQ:TELO) 报告了日期为 2025年10月7日 的前临床结果，显示其候选药物 Telomir-1 重置 DNA 甲基化，并在侵袭性前列腺癌模型中重新激活肿瘤抑制基因 MASPIN 和 RASSF1A。
关键发现：剂量相关的 RASSF1A 甲基化下降、化疗诱导的 MASPIN 过甲基化的逆转、体内约 50% 的肿瘤体积缩小，以及在所报道的模型中消除了与化疗相关的死亡率。Telomir-1 还显示在 STAT1、CDKN2A、组蛋白去甲基化酶、线粒体功能以及端粒/表观遗传标志物等方面的先前前临床效应。Telomir 正将 Telomir-1 推进到 IND-enabling 的前临床研究中。
- Dose-dependent reduction in RASSF1A methylation
- Reversal of chemotherapy-induced MASPIN hypermethylation
- ~50% tumor volume reduction in vivo
- Elimination of chemotherapy-related mortality in models
- Advancing to IND-enabling preclinical studies
- Preclinical-stage results; no human safety or efficacy data yet
- Clinical translatability from models to patients remains unproven
Insights
Preclinical evidence shows Telomir-1 resets methylation of MASPIN and RASSF1A and reduces tumor burden in prostate models.
Telomir-1 demonstrated reactivation of two silenced tumor suppressors, MASPIN and RASSF1A, by reducing DNA hypermethylation in aggressive prostate cancer models. The program reported a dose-dependent reduction in RASSF1A methylation, stronger effects with chemotherapy, a restoration of MASPIN after chemotherapy-induced methylation, ~
Key dependencies and risks include translation from animal models to humans and reproducibility of the methylation and functional results. The data are preclinical and limited to in vivo models; clinical relevance requires IND-enabling toxicology, pharmacokinetics, and human biomarker confirmation. Watch for completion of IND-enabling studies, formal toxicology readouts, and biomarker-driven proof-of-mechanism data such as changes in tumor MASPIN/RASSF1A methylation and expression in
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
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.
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.
Scientific Perspective
"The potential reactivation of MASPIN and RASSF1A by inhibition of hypermethylation is highly significant because these genes play a central role in blocking tumor invasion, uncontrolled growth, and metastasis," said Dr. Itzchak Angel, CSA at Telomir. "By demonstrating that in addition to an effect on DNA methylation of other key proteins, such as STAT1 and CDKN2A, Telomir-1 can also reset DNA methylation and restore the function of these silenced tumor suppressors, we are providing strong mechanistic evidence that this drug candidate could address cancer at its epigenetic roots in a broader manner."
CEO Perspective
"These results highlight Telomir-1's potential to change the way we think about treating cancer and aging," said Erez Aminov, CEO of Telomir. "Instead of only managing disease progression; Telomir-1 may reset the underlying epigenetic programs that drive tumor growth, resistance, and cellular decline. By reawakening the body's natural defenses, this approach could mark a new era in medicine - one where we target the root biology of cancer and age-related disease."
Building on Prior Work
Telomir-1 has previously demonstrated in preclinical studies:
Reactivating tumor suppressors such as STAT1 (immune surveillance), CDKN2A (cell cycle brake), and TMS1 (apoptosis mediator).
Histone demethylase inhibition: activity across JMJD3 (KDM6B), UTX (KDM6A), FBXL10 (KDM2B), FBXL11 (KDM2A), and the KDM5 family - enzymes long considered undruggable despite their central role in cancer, inflammation, and resistance.
Mitochondrial health restoration: improved energy production while reducing oxidative stress (ROS) and avoiding unwanted cell proliferation, suggesting relevance to cancer metabolism as well as Alzheimer's, Parkinson's, ALS, and Progeria.
Wnt "fuel line" modulation: modest Tankyrase inhibition that may cut off cancer's growth signaling without telomere-shortening toxicity.
Selectivity advantage: sparing broad acetyltransferases such as GCN5L2, reducing systemic toxicity risk.
Telomere & aging benefits: elongated telomeres and reversal of epigenetic drift in accelerated-aging models.
Functional in vivo outcomes: ~
50% tumor volume reduction and elimination of chemotherapy-related mortality in aggressive prostate cancer models.
Together, these findings support Telomir-1's emerging profile as a broad-spectrum epigenetic and metabolic reset therapy with potential applications across oncology, neurodegeneration, autoimmune disease, metabolic dysfunction, and aging.
Next Steps
Telomir is advancing Telomir-1 through preclinical development and IND-enabling studies. Additional evaluations are underway in prostate cancer and other aggressive tumor models where epigenetic silencing and metabolic dysfunction drive metastasis and treatment resistance.
About Telomir Pharmaceuticals
Telomir Pharmaceuticals, Inc. (NASDAQ: TELO) is a preclinical-stage biotechnology company developing small-molecule therapies that target the root causes of cancer, aging, and age-related diseases by resetting dysregulated epigenetic programs. The Company's lead candidate, Telomir-1, is being advanced across oncology and longevity indications based on its differentiated ability to restore tumor suppressors, block undruggable enzymes, and reprogram gene control. For more information, visit www.telomirpharma.com.
Cautionary Note Regarding Forward-Looking Statements
This press release, statements of Telomir's management or advisors related thereto, and the statements contained in the news story linked in this release contain "forward-looking statements," which are statements other than historical facts made pursuant to the safe harbor provisions of Section 27A of the Securities Act of 1933, as amended, and Section 21E of the Securities Exchange Act of 1934, as amended. These risks and uncertainties include, but are not limited to, the potential use of the data from our studies, our ability to develop and commercialize Telomir-1 for specific indications, and the safety of Telomir-1.
Any forward-looking statements in this press release are based on Telomir's current expectations, estimates and projections only as of the date of this release. These and other risks concerning Telomir's programs and operations are described in additional detail in its Annual Report on Form 10-K for the fiscal year ended December 31, 2024, which are on file with the SEC and available at www.sec.gov. Telomir explicitly disclaims any obligation to update any forward-looking statements except to the extent required by law.
Contact Information
Helga Moya
info@telomirpharma.com
(786) 396-6723
SOURCE: Telomir Pharmaceuticals, Inc
View the original press release on ACCESS Newswire
FAQ
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