Telomir Pharmaceuticals Announces New Cancer Data in Aggressive Human Prostate Cancer Cells Showing Telomir-1 Resets DNA Methylation to Reactivate CDKN2A, a Master Tumor Suppressor, Outperforming Rapamycin and Chemotherapy
Telomir Pharmaceuticals (NASDAQ:TELO) has announced significant preclinical data showing that its drug candidate Telomir-1 effectively resets DNA methylation to reactivate CDKN2A, a crucial tumor suppressor gene, in aggressive prostate cancer cells. The study demonstrated that Telomir-1 outperformed both Rapamycin and chemotherapy in inhibiting CDKN2A DNA methylation.
The findings build upon previous research showing Telomir-1's ability to reset STAT1, suggesting the drug can broadly reverse cancer-induced silencing of key tumor suppressors through two mechanisms: controlling unchecked cell growth and preventing immune evasion. The company is advancing its pre-IND program with ongoing CMC activities and IND-enabling studies, positioning Telomir-1 as a potential first-in-class longevity drug candidate targeting both cancer and aging.
Telomir Pharmaceuticals (NASDAQ:TELO) ha reso noti dati preclinici importanti che mostrano come il suo candidato farmacologico Telomir-1 riesca a ripristinare la metilazione del DNA per riattivare CDKN2A, un gene oncosoppressore cruciale, in cellule di carcinoma prostatico aggressivo. Lo studio ha evidenziato che Telomir-1 è risultato più efficace di Rapamicina e della chemioterapia nell’inibire la metilazione di CDKN2A.
I risultati confermano ricerche precedenti che indicavano la capacità di Telomir-1 di ripristinare STAT1, suggerendo che il composto possa in generale invertire il silenziamento indotto dal cancro di importanti oncosoppressori attraverso due vie: controllando la crescita cellulare incontrollata e impedendo l’evasione immunitaria. L’azienda sta portando avanti il programma pre-IND con attività CMC e studi per l’abilitazione dell’IND, posizionando Telomir-1 come possibile candidato first-in-class per la longevità, mirato sia al cancro sia all’invecchiamento.
Telomir Pharmaceuticals (NASDAQ:TELO) ha anunciado datos preclínicos significativos que muestran que su candidato farmacológico Telomir-1 restablece eficazmente la metilación del ADN para reactivar CDKN2A, un gen supresor de tumores clave, en células de cáncer de próstata agresivo. El estudio demostró que Telomir-1 superó tanto a la Rapamicina como a la quimioterapia al inhibir la metilación de CDKN2A.
Los hallazgos se basan en investigaciones previas que mostraban la capacidad de Telomir-1 para restaurar STAT1, lo que sugiere que el fármaco puede revertir de forma amplia el silenciamiento inducido por el cáncer de supresores tumorales clave mediante dos mecanismos: controlando el crecimiento celular desmesurado y evitando la evasión inmune. La compañía avanza su programa pre-IND con actividades CMC en curso y estudios para habilitar el IND, posicionando a Telomir-1 como un posible candidato first-in-class para la longevidad dirigido tanto al cáncer como al envejecimiento.
Telomir Pharmaceuticals (NASDAQ:TELO)는 후보 약물 Telomir-1이 공격적 전립선암 세포에서 중요한 종양억제유전자인 CDKN2A를 재활성화하기 위해 DNA 메틸화를 효과적으로 재설정한다는 유의한 전임상 데이터를 발표했습니다. 연구 결과 Telomir-1은 CDKN2A DNA 메틸화 억제에서 라파마이신과 화학요법보다 우수한 성능을 보였습니다.
이 결과는 Telomir-1이 STAT1을 복원할 수 있다는 이전 연구를 확장한 것으로, 이 약물이 두 가지 경로를 통해 암이 유도한 주요 종양억제자의 침묵을 광범위하게 되돌릴 수 있음을 시사합니다: 통제되지 않은 세포 성장 억제와 면역 회피 방지. 회사는 CMC 활동 및 IND 허가 지원 연구를 진행하며 pre-IND 프로그램을 진척시키고 있으며, Telomir-1을 암과 노화 모두를 겨냥하는 잠재적 first-in-class 장수(롱제비티) 약물 후보로 자리매김하고 있습니다.
Telomir Pharmaceuticals (NASDAQ:TELO) a annoncé des données précliniques importantes montrant que son candidat-médicament Telomir-1 réinitialise efficacement la méthylation de l’ADN pour réactiver CDKN2A, un gène suppresseur de tumeur crucial, dans des cellules de cancer de la prostate agressif. L’étude a démontré que Telomir-1 surpassait à la fois la rapamycine et la chimiothérapie dans l’inhibition de la méthylation de CDKN2A.
Ces résultats s’appuient sur des recherches antérieures montrant la capacité de Telomir-1 à rétablir STAT1, suggérant que le médicament peut, par deux mécanismes, inverser de manière générale le silence induit par le cancer de suppresseurs tumoraux clés : contrôler la croissance cellulaire non régulée et prévenir l’évasion immunitaire. La société fait progresser son programme pré-IND avec des activités CMC en cours et des études d’autorisation IND, positionnant Telomir-1 comme un candidat potentiel first-in-class de longévité ciblant à la fois le cancer et le vieillissement.
Telomir Pharmaceuticals (NASDAQ:TELO) hat bedeutende präklinische Daten veröffentlicht, die zeigen, dass sein Wirkstoffkandidat Telomir-1 die DNA-Methylierung effektiv zurücksetzt, um CDKN2A, ein entscheidendes Tumorsuppressorgen, in aggressiven Prostatakrebszellen wieder zu reaktivieren. Die Studie zeigte, dass Telomir-1 bei der Hemmung der CDKN2A-DNA-Methylierung sowohl Rapamycin als auch Chemotherapie übertraf.
Die Befunde bauen auf früheren Untersuchungen auf, die die Fähigkeit von Telomir-1 zur Wiederherstellung von STAT1 belegten, und deuten darauf hin, dass das Medikament das krebsbedingte Stilllegen wichtiger Tumorsuppressoren über zwei Mechanismen breit umkehren kann: Steuerung unkontrollierten Zellwachstums und Verhinderung von Immunflucht. Das Unternehmen treibt sein Pre-IND-Programm mit laufenden CMC-Aktivitäten und IND-ermöglichenden Studien voran und positioniert Telomir-1 als potenziellen First-in-Class-Kandidaten für Langlebigkeit, der sowohl Krebs als auch Alterung adressiert.
- Drug candidate shows superior performance compared to Rapamycin and chemotherapy in preclinical trials
- Demonstrates dual mechanism of action targeting both cell growth control and immune surveillance
- Pre-IND program progressing with ongoing CMC activities and IND-enabling studies
- Potential first-in-class broad-spectrum DNA methylation reset therapy
- Still in preclinical stage with no human trial data
- Results limited to prostate cancer cell models only
- Significant regulatory hurdles ahead before potential commercialization
Insights
Telomir-1 shows promise by reactivating critical tumor suppressor genes through DNA methylation reset, potentially targeting both cancer and aging mechanisms.
This preclinical data represents a significant mechanistic advance in the field of cancer epigenetics. Telomir-1's ability to reverse DNA methylation of CDKN2A addresses a fundamental cancer evasion strategy. When CDKN2A is silenced through methylation, cancer cells can proliferate unchecked; by reactivating this "cell cycle brake," Telomir-1 may restore a critical tumor suppression mechanism.
The data showing Telomir-1 outperforming both rapamycin (an established mTOR inhibitor with known anti-aging properties) and conventional chemotherapy in prostate cancer models is particularly noteworthy. This suggests superior efficacy in the specific mechanism of epigenetic reprogramming.
What makes this approach distinctive is the dual-pathway restoration. By targeting both CDKN2A (cell cycle control) and previously reported STAT1 reactivation (immune surveillance), Telomir-1 addresses two critical hallmarks of cancer simultaneously: uncontrolled growth and immune evasion. Few therapeutic candidates demonstrate this mechanistic breadth.
From a translational perspective, epigenetic therapies like DNA methyltransferase inhibitors have shown clinical utility in certain cancers, but often with significant toxicity. If Telomir-1 can achieve targeted methylation reset with improved safety, it could represent a meaningful advancement. However, as with all preclinical findings, there remains a significant gap between these promising results in cell models and demonstrating similar efficacy and safety in humans.
While these results strengthen Telomir-1's scientific rationale, investors should note that the company remains in the preclinical stage, with IND-enabling studies still ongoing and no human data yet available to confirm these mechanisms translate to clinical benefit.
New preclinical findings highlight Telomir-1's ability to reverse CDKN2A gene silencing by DNA methylation, reactivating this gene - often called the body's natural "cell cycle brake." These results build on prior STAT1 data, supporting Telomir-1's profile as a potential first-in-class broad-spectrum DNA methylation reset therapy.
MIAMI, FLORIDA / ACCESS Newswire / September 9, 2025 / Telomir Pharmaceuticals, Inc. (NASDAQ:TELO), a preclinical-stage biotechnology company developing therapies that target the root causes of biological aging, cancer, and age-related diseases, today announced new preclinical cancer data showing that Telomir-1 reverses DNA methylation of CDKN2A, a master tumor suppressor gene silenced in many aggressive cancers.
Reactivating Cancer's Brakes
CDKN2A is one of the body's most important natural defenses against cancer. Often called the "cell cycle brake," this gene tells cells when to stop dividing and helps damaged cells self-destruct. In many cancers, CDKN2A is switched off by abnormal DNA methylation, leaving tumors free to grow unchecked. By resetting this methylation, Telomir-1 appears to turn the brake back on - restoring a critical safeguard that cancer cells had disabled.
Why DNA Methylation Matters
DNA methylation is a key epigenetic process that controls whether genes are switched on or off. In healthy cells, methylation helps regulate normal development and repair. In cancer, however, abnormal DNA methylation can silence critical tumor suppressor genes like CDKN2A and STAT1, allowing tumors to grow unchecked and evade the immune system. Similarly, widespread changes in DNA methylation patterns are recognized as one of the hallmarks of aging, contributing to the loss of cellular function and the onset of age-related diseases.
By demonstrating the ability to reduce DNA methylation of these important targets, Telomir-1 is showing potential to directly address these fundamental biological processes. This positions Telomir-1 not only as a novel oncology candidate, but also as a potential first-in-class longevity drug candidate targeting the root causes of aging and disease.
In aggressive human prostate cancer cell models (PC3 xenografts), Telomir-1 inhibited CDKN2A DNA methylation more effectively than both Rapamycin and chemotherapy. These results complement Telomir's previously reported data showing that Telomir-1 also resets STAT1, a master regulator of immune surveillance. Together, these findings suggest that Telomir-1 may broadly reverse cancer-induced silencing of key tumor suppressors - tackling two of cancer's most fundamental escape mechanisms: unchecked growth and immune evasion.
CEO Perspective
"This new evidence reinforces Telomir-1's potential as a first-in-class longevity drug candidate that addresses the root causes of aging and age-related diseases through its ability to reset abnormal DNA methylation patterns," said Erez Aminov, Chief Executive Officer of Telomir. "By demonstrating that Telomir-1 can reverse cancer-induced gene silencing in tumor suppressors such as CDKN2A and STAT1, we are beginning to show how epigenetic reprogramming may restore fundamental cellular functions that are disrupted in both cancer and aging."
Scientific Perspective
"These findings are highly significant," said Dr. Itzchak Angel, Chief Scientific Advisor at Telomir. "By simultaneously reactivating STAT1 and CDKN2A, Telomir-1 demonstrates the ability to reset epigenetic silencing across multiple tumor suppressor pathways. This dual restoration of both immune surveillance and cell cycle control represents a powerful mechanistic advance in cancer epigenetics and provides a compelling rationale for further translational development."
Advancing Toward the Clinic
Telomir is actively assessing Telomir-1 across multiple aggressive cancers beyond prostate, with additional studies underway. The company's pre-IND program is running in full gear, with CMC activities scaling up toward GMP production and IND-enabling studies ongoing as Telomir moves toward its first IND submission.
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
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