Telomir Pharmaceuticals Reports New Data Showing Telomir-1 Resets Cancer's “Kill-and-Clean” Defense Systems in an Aggressive Prostate Cancer Model, Outperforming Rapamycin and Chemo
Telomir Pharmaceuticals (NASDAQ:TELO) reported preclinical in vivo data (mice with aggressive human prostate tumors) showing oral Telomir-1 reduced DNA methylation of CASP8 and GSTP1 versus vehicle and chemotherapy at Day 10 and Day 21.
Telomir-1 produced a progressive, sustained methylation decrease through Day 21, while Rapamycin's early Day 10 effect partially rebounded by Day 21. Chemotherapy alone did not lower methylation. Combination Telomir-1 + chemotherapy showed lower methylation than chemotherapy alone.
Telomir Pharmaceuticals (NASDAQ:TELO) ha riportato dati preclinici in vivo (mice con tumori prostatici umani aggressivi) che mostrano che l'assunzione orale di Telomir-1 ha ridotto la metilazione del DNA di CASP8 e GSTP1 rispetto al veicolo e alla chemioterapia al Day 10 e al Day 21.
Telomir-1 ha prodotto una diminuzione di metilazione progressiva e sostenuta fino al Day 21, mentre l'effetto precoce del Rapamicina al Day 10 è parzialmente riacutizzato entro il Day 21. La chemioterapia da sola non ha ridotto la metilazione. La combinazione Telomir-1 + chemioterapia ha mostrato una metilazione inferiore rispetto alla chemioterapia da sola.
Telomir Pharmaceuticals (NASDAQ:TELO) presentó datos preclínicos in vivo (ratones con tumores prostáticos humanos agresivos) que muestran que la administración oral de Telomir-1 redujo la metilación del ADN de CASP8 y GSTP1 frente a vehículo y a la quimioterapia en el Día 10 y el Día 21.
Telomir-1 produjo una disminución de la metilación progresiva y sostenida hasta el Día 21, mientras que el efecto temprano de la rapamicina en el Día 10 se recuperó parcialmente para el Día 21.La quimioterapia por sí sola no redujo la metilación. La combinación Telomir-1 + quimioterapia mostró una metilación menor que la quimioterapia por sí sola.
Telomir Pharmaceuticals (NASDAQ:TELO)는 공격적으로 성장한 인간 전립선 종양을 가진 마우스에서의 전임상 인바이오 데이터를 보고했으며, 경구 Telomir-1이 DNA 메틸화 CASP8과 GSTP1를 차량 및 화학요법 대비 Day 10 및 Day 21에서 감소시켰다고 밝혔습니다.
Telomir-1은 Day 21까지 점진적이고 지속적인 메틸화 감소를 나타낸 반면, Rapamycin의 Day 10 조기 효과는 Day 21까지 부분적으로 되돌아왔습니다. 단독 화학요법은 메틸화를 낮추지 못했습니다. Telomir-1 + 화학요법의 병용은 단독 화학요법보다 낮은 메틸화를 보였습니다.
Telomir Pharmaceuticals (NASDAQ:TELO) a rapporté des données précliniques in vivo (souris porteuses de tumeurs prostatiques humaines agressives) montrant que l’administration orale de Telomir-1 réduisait la méthylation de l’ADN de CASP8 et GSTP1 par rapport au véhicule et à la chimiothérapie au Jour 10 et au Jour 21.
Telomir-1 a produit une diminution progressive et soutenue de la méthylation jusqu’au Jour 21, tandis que l’effet précoce du Rapamycine au Jour 10 s’est partiellement rétabli d’ici le Jour 21. La chimiothérapie seule n’a pas réduit la méthylation. L’association Telomir-1 + chimiothérapie a montré une méthylation inférieure à celle de la chimiothérapie seule.
Telomir Pharmaceuticals (NASDAQ:TELO) berichtete präklinische In-vivo-Daten (Mäuse mit aggressiven menschlichen Prostatatumoren), die zeigen, dass die orale Verabreichung von Telomir-1 die DNA-Methylierung von CASP8 und GSTP1 im Vergleich zu Vehikel und Chemotherapie am Tag 10 und Tag 21 reduziert.
Telomir-1 verursacht eine fortschreitende, anhaltende Abnahme der Methylierung bis Tag 21, während der frühe Tag-10-Effekt von Rapamycin bis Tag 21 teilweise wieder anstieg. Chemotherapie allein senkte die Methylierung nicht. Die Kombination Telomir-1 + Chemotherapie zeigte eine niedrigere Methylierung als Chemotherapie allein.
Telomir Pharmaceuticals (NASDAQ:TELO) أصدرت بيانات قبل السريرية حية في المختبر (فئران لديها أورام بروستاتية بشرية عدوانية) تُظهر أن الإعطاء الفموي لـTelomir-1 قلل من مثيلة DNA لـCASP8 وGSTP1 مقارنة بالحمل التجريبي والدواء الكيميائي في اليوم 10 و21.
قدّم Telomir-1 انخفاضاً تدريجياً ومستداماً في المثيلة حتى اليوم 21، بينما ارتد أثر الراباميسين المبكر في اليوم 10 جزئياً حتى اليوم 21. العلاج الكيميائي وحده لم يخفّض المثيلة. أظهر الجمع Telomir-1 + الكيميائي انخفاضاً في المثيلة أكثر من الكيميائي وحده.
Telomir Pharmaceuticals (NASDAQ:TELO) 报告了体内前临床数据（携带侵袭性人前列腺肿瘤的小鼠），显示口服 Telomir-1 相对于载体和化疗在第10天和第21天降低了 CASP8 和 GSTP1 的DNA甲基化水平。
Telomir-1 在第21天之前呈现出逐步、持续的甲基化降低，而雷帕霉素在第10天的早期效应在第21天部分回弹。单独化疗并未降低甲基化。Telomir-1 + 化疗的联合显示的甲基化水平低于单纯化疗。
- CASP8 promoter methylation reduced at Day 10 and Day 21 versus vehicle and chemotherapy
- GSTP1 methylation decreased versus vehicle and chemotherapy by Day 21
- Progressive, sustained Telomir-1 methylation decrease through Day 21
- Telomir-1 + chemotherapy lowered CASP8 and GSTP1 methylation versus chemotherapy alone
- Rapamycin methylation reduction at Day 10 partially rebounded by Day 21
- Chemotherapy alone did not reduce CASP8 or GSTP1 methylation
Insights
Preclinical data show Telomir-1 reduced promoter methylation of CASP8 and GSTP1 more durably than rapamycin in a mouse prostate tumor model.
Telomir-1 associated with decreased DNA methylation at the CASP8 and GSTP1 promoters at
Caveats include that results derive from a single in vivo model and measure DNA methylation only; the release does not report gene expression, protein activity, tumor shrinkage, survival, or statistical details. Watch for follow-up reports with expression/protein data, functional apoptosis assays, tumor growth or survival endpoints, and replication across models in the next preclinical study reports or conference presentations.
Findings suggest Telomir-1 modulates epigenetic marks on apoptosis and detox genes more persistently than rapamycin, but efficacy and clinical relevance remain unproven.
The reported pattern shows progressive methylation decreases with Telomir-1 through
Key dependencies are missing: quantitative effect sizes, statistical significance, downstream mRNA/protein changes, pharmacokinetics, dosing, and any tumor-level efficacy metrics. Monitor upcoming preclinical disclosures for expression/protein correlation, dose–response, tumor growth or survival data, and any move toward a formal IND or first-in-human study within typical translational timelines.
New findings highlight Telomir-1's impact on CASP8 and GSTP1, two critical genes that regulate cell death and glutathione-based detoxification pathways often disrupted in cancer.
MIAMI, FLORIDA / ACCESS Newswire / October 23, 2025 / Telomir Pharmaceuticals, Inc. (NASDAQ:TELO) ("Telomir" or the "Company"), a pre-clinical biotechnology company developing therapies that target the epigenetic roots of cancer, aging, and age-related disease, today reported new preclinical data from an in vivo study in mice bearing human aggressive prostate cancer tumors evaluating DNA-methylation changes in two key defense genes - CASP8 and GSTP1 - following treatment with oral Telomir-1, Rapamycin, chemotherapy, and combination regimens.
Apoptosis ("kill") and detoxification ("clean") pathways are two of the body's fundamental defense systems against cancer initiation and progression, and Telomir-1's observed modulation of these pathways through DNA-methylation control may represent an important area of ongoing scientific evaluation in oncology research.
Overview of Findings
The study examined DNA methylation, a central epigenetic process that helps determine whether genes are active or silenced. In this model, baseline tumor samples exhibited DNA hypermethylation of CASP8 and GSTP1, a pattern often associated with reduced activity in genes involved in apoptosis and detoxification.
CASP8 (Apoptosis Pathway)
CASP8 helps initiate programmed cell death. Telomir-1 treatment was associated with reduced methylation of the CASP8 promoter at Day 10 and 21 relative to vehicle and chemotherapy group, suggesting potential reactivation of apoptotic pathway control.GSTP1 (Detoxification and Glutathione Pathway)
GSTP1 encodes glutathione S-transferase Pi 1, an enzyme that uses glutathione (GSH) - one of the body's most important natural antioxidants - to neutralize reactive oxygen species and chemical stress. Telomir-1 was associated with decreased DNA-methylation of GSTP1 compared with vehicle and chemotherapy, consistent with partial restoration of this critical detoxification and antioxidant defense system.Chemotherapy Alone
Chemotherapy did not appear to reduce methylation of either gene, consistent with prior observations that certain cytotoxic agents can reinforce methylation stress - a process that may contribute to taxane resistance (reduced tumor response to chemo drugs like paclitaxel) driven by transcriptional and epigenetic rewiring.Combination of Chemotherapy + Telomir-1
When Telomir-1 was administered with chemotherapy, both CASP8 and GSTP1 showed lower methylation than with chemotherapy alone, suggesting that Telomir-1 may help counteract chemotherapy related epigenetic silencing in this setting.
Why These Pathways Matter in Cancer Biology
Apoptosis and detoxification represent two of the body's most fundamental defense systems against cancer initiation and progression.
Apoptosis - the "Kill System"
This pathway allows damaged or abnormal cells to self-destruct before they proliferate. In many cancers, genes such as CASP8 become silenced through abnormal DNA methylation, preventing programmed cell death and enabling tumor survival and resistance to therapy.Detoxification - the "Clean System"
The GSTP1 glutathione axis helps remove oxidative and chemical stress that accumulates during inflammation, environmental exposure, or treatment. When DNA sequence for GSTP1 is hypermethylated and silenced, cells lose part of this antioxidant capacity, leading to higher oxidative stress and DNA instability. Supporting glutathione related detoxification may reduce the cellular conditions that favor tumor persistence and therapy resistance.
By addressing both apoptotic and detoxification imbalances through DNA methylation modulation, Telomir-1 may engage two complementary mechanisms commonly disrupted in cancer biology.
Rapamycin Comparison
At earlier observation points (Day 10), Rapamycin - an mTOR-pathway inhibitor - was associated with an initial reduction in DNA methylation for both genes. This observation aligns with Rapamycin's indirect influence on cellular metabolism and oxidative stress, which can temporarily affect DNA methylating enzyme activity.
By Day 21, methylation levels partially rebounded, suggesting that the effect may have been transient and metabolically driven rather than a direct epigenetic reset.
Telomir-1, by contrast, was associated with a progressive and more sustained decrease in methylation through Day 21. Unlike Rapamycin, Telomir-1 is believed to interact with epigenetic regulatory enzymes that add or remove methyl groups from DNA and histones, which may contribute to the durability of its observed effects in this preclinical model.
Interpretation
Collectively, these preclinical observations indicate that Telomir-1 influenced two complementary cellular pathways - apoptosis and detoxification - through DNA methylation modulation not observed with chemotherapy and more sustained than that seen with Rapamycin.
The data suggest Telomir-1 may act at the level of epigenetic enzyme regulation, whereas Rapamycin's effects appear secondary to metabolic signaling.
Further studies are planned to clarify these mechanisms and their potential relevance for oncology research.
Scientific Perspective
"This preclinical work, which supports earlier studies with Telomir-1 on DNA methylation in cancer, helps differentiate the epigenetic modulation observed with Telomir-1 from the indirect metabolic effects of Rapamycin," said Dr. Itzchak Angel, CSA at Telomir. "By evaluating DNA methylation dynamics in apoptosis and detoxification pathways, we are building a scientific framework for understanding how Telomir-1 may help restore epigenetic balance in cancer models."
CEO Perspective
"Our goal is to develop medicines that don't just treat what cancer becomes but help reset the biology that lets it begin. Telomir-1 may represent that next frontier."
- Erez Aminov, CEO, Telomir
About Telomir Pharmaceuticals
Telomir Pharmaceuticals (NASDAQ:TELO) is a pre-clinical stage biotechnology company developing therapies designed to target the root epigenetic mechanisms underlying cancer, aging, and degenerative disease. The Company's lead candidate, Telomir-1, has demonstrated activity in preclinical studies involving modulation of DNA and histone methylation patterns, which may contribute to balanced gene expression, cellular function, and genomic stability.
For more information, please 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
What did Telomir Pharmaceuticals (TELO) report on October 23, 2025 about Telomir-1?
How did Telomir-1 compare with Rapamycin in the TELO preclinical study?
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Which cancer pathways did Telomir-1 affect in the TELO announcement?
Did chemotherapy alone change methylation of CASP8 or GSTP1 in the TELO data?
What are Telomir's next steps after the October 23, 2025 preclinical results?
