US Market News
3週前
Telomir Pharmaceuticals Reports Peer-Reviewed Publication of Telomir-Zn Data Demonstrating Improved Survival and Multiple Endpoint Benefits in Wilson's DiseaseMay 20, 2026 8:00 AM
ACCESS NewswireStudy Published in Advances in Redox Research Demonstrated Dose-Dependent Survival Improvement, Reduced Hepatic Copper Burden, Improved Liver Biomarkers, and Reduced Tissue Degeneration in a Preclinical Wilson's Disease Model.MIAMI, FL / ACCESS Newswire / May 20, 2026 / Telomir Pharmaceuticals, Inc. (NASDAQ:TELO) ("Telomir" or the "Company"), a clinical-stage biotechnology company developing small-molecule therapeutics targeting epigenetic and metabolic drivers of cancer and age-related disease, today announced the peer-reviewed publication of preclinical data showing that Telomir-Zn produced dose-dependent survival improvement across multiple endpoints in a Wilson's disease model, supporting the biological activity of Telomir-Zn in Wilson's disease. The study, titled "Intracellular copper redox modulation disrupts ROS-Ca²? amplification in an ATP7B-deficient zebrafish model of Wilson's disease," was published in Advances in Redox Research.The publication reports that Telomir-Zn produced dose-dependent improvements across multiple endpoints in the preclinical Wilson's Disease model, including reduced copper-associated oxidative stress, reduced hepatic copper burden, improved liver injury biomarkers, attenuated intracellular calcium dysregulation, improved locomotor function, reduced tissue degeneration, and enhanced survival.The publication is available online at:
Advances in Redox Research PublicationWilson's disease is a rare genetic disorder caused by mutation in the ATP7B gene, resulting in impaired copper excretion and toxic copper accumulation in the liver, brain, and other organs. The condition leads to progressive oxidative stress, mitochondrial dysfunction, inflammation, and multi-organ tissue injury. Current standard-of-care treatments, primarily copper chelation agents, address systemic copper levels but do not directly target the downstream oxidative and mitochondrial injury pathways associated with disease progression.According to the publication, Telomir-Zn demonstrated improvements across cellular and in vivo endpoints in the Wilson's disease model, including:Reduction of copper-induced reactive oxygen species (ROS) amplificationAttenuation of intracellular calcium dysregulation associated with oxidative stress signalingPreservation of metabolic viability under copper and peroxide challengeReduction of hepatic copper accumulationImprovement in locomotor and neuromotor performanceReduction of liver injury biomarkers, including ALT, AST, and bilirubinReduction of hepatorenal histopathological degenerationImproved survival in a dose-dependent manner in the Wilson's disease modelThe authors concluded that targeted modulation of labile intracellular copper pools disrupted ROS-Ca²? feedback amplification, mitigated mitochondrial-associated tissue injury associated with copper overload, and produced dose-dependent improvements in survival.This publication represents Telomir-Zn's first peer-reviewed publication in Wilson's disease and adds independently validated preclinical data across biochemical, functional, histological, and survival endpoints to the Company's scientific package. The findings further support the mechanistic relevance of Telomir-Zn's approach across pathways involving oxidative stress and dysregulated metal homeostasis, including its lead program in Triple-Negative Breast Cancer, for which the Company received FDA IND clearance in April 2026."This study demonstrated that modulation of intracellular copper-driven redox activity can disrupt ROS-Ca²? amplification cascades associated with copper toxicity and mitochondrial injury," said Dr. Itzchak Angel, Chief Scientific Advisor of Telomir Pharmaceuticals and corresponding author of the publication.Dr. Angel continued, "The findings support intracellular metal homeostasis and redox regulation as potentially important biological pathways across diseases involving oxidative stress, mitochondrial dysfunction, and epigenetic dysregulation, including oncology.""This peer-reviewed publication is an important scientific milestone for Telomir-Zn. The data demonstrated meaningful improvements across a comprehensive set of endpoints in the Wilson's disease model, and we believe the findings are consistent with the broader mechanistic profile of Telomir-Zn as we advance our lead program in Triple-Negative Breast Cancer toward Phase 1/2 clinical initiation," said Erez Aminov, CEO of Telomir Pharmaceuticals.Telomir Pharmaceuticals will continue evaluating the Wilson's disease program and potential regulatory considerations alongside advancement of its lead TNBC program toward Phase 1/2 clinical initiation.About Telomir PharmaceuticalsTelomir Pharmaceuticals, Inc. (NASDAQ:TELO) is a clinical-stage biotechnology company developing small-molecule therapeutics targeting epigenetic and metabolic pathways implicated in cancer, aging, and degenerative disease. The Company's lead program, Telomir-1 (Telomir-Zn), is designed to modulate intracellular metal homeostasis and epigenetic regulation and has received IND clearance from the U.S. Food and Drug Administration for a Phase 1/2 clinical trial in Triple-Negative Breast Cancer. For more information, please visit https://telomirpharma.com/.Forward-Looking StatementsThis press release contains "forward-looking statements" within the meaning of the Private Securities Litigation Reform Act of 1995. These forward-looking statements generally can be identified by the use of words such as "anticipate," "expect," "plan," "can," "could," "would," "may," "will," "believe," "estimate," "forecast," "goal," "project," "guidance," "potential," "intend," "seek," "target" and other words of similar meaning, although not all forward-looking statements include these words. Forward-looking statements may include, but are not limited to, statements regarding the therapeutic potential, mechanism of action, development plans, regulatory pathway, safety profile, clinical utility, market opportunity, and future development of Telomir-1 (Telomir-Zn) and the Company's other product candidates. These forward-looking statements are based on current expectations, estimates, forecasts, and projections, as well as management's beliefs and assumptions, and are subject to significant risks and uncertainties that could cause actual results to differ materially from those expressed or implied by such statements. These risks and uncertainties include, among others, risks related to preclinical and clinical development, the ability to obtain regulatory approvals, the outcome of future studies, reliance on third parties, intellectual property protection, financing needs, market conditions, and the other risks identified in the Company's under the heading "Risk Factors" contained in the Company's Annual Report on Form 10-K and the Company's other filings with the U.S. Securities and Exchange Commission ("SEC"). Forward-looking statements contained in this press release speak only as of the date hereof, and the Company undertakes no obligation to update or revise such statements, whether as a result of new information, future events, or otherwise, except as required by applicable law.We caution investors not to place undue reliance on the forward-looking statements contained in this press release. You are encouraged to read our filings with the SEC, available at the SEC website, and in the "Investors" section of our website, for a discussion of these and other risks and uncertainties.Contact InformationKrystina Quintana
Email:
US Market News
1月前
Telomir Pharmaceuticals Announces FDA Clearance of IND for Telomir-Zn in Triple-Negative Breast CancerApril 30, 2026 8:00 AM
ACCESS NewswireCompany Plans to Initiate First-in-Human Phase 1/2 Trial in 1H 2026, Anchored by a Leading U.S. Academic Medical Center.MIAMI, FL / ACCESS Newswire / April 30, 2026 / Telomir Pharmaceuticals, Inc. (NASDAQ:TELO) ("Telomir" or the "Company"), a clinical-stage biotechnology company developing small-molecule therapeutics targeting epigenetic and metabolic drivers of cancer and age-related disease, today announced that the U.S. Food and Drug Administration (FDA) has cleared the Company's Investigational New Drug (IND) application for its lead candidate, Telomir-Zn, for the treatment of patients with advanced or metastatic triple-negative breast cancer (TNBC).This IND clearance enables the Company to advance Telomir-Zn into clinical evaluation, representing an important step toward addressing a significant unmet need in patients with advanced or metastatic triple-negative breast cancer, where treatment options remain limited, and outcomes are poor.IND Clearance and Development PackageThe FDA's clearance reflects review of a comprehensive IND submission supporting advancement of Telomir-Zn into clinical evaluation. The submission included pharmacology, toxicology, manufacturing data, and the Company's first-in-human Phase 1/2 clinical study protocol (TELO-001).The IND package was supported by completed IND-enabling studies, including pharmacology and toxicology evaluations, pharmacokinetic data demonstrating systemic exposure, and preclinical data indicating activity in models of triple-negative breast cancer.Planned Phase 1/2 Clinical TrialThe planned clinical study (TELO-001) is designed to evaluate the safety, tolerability, pharmacokinetics, pharmacodynamics, and preliminary antitumor activity of Telomir-Zn as an oral monotherapy in patients with advanced or metastatic TNBC.Study OverviewFirst-in-human, multicenter, open-label Phase 1/2 trialAdult patients with advanced or metastatic TNBC who have received prior systemic therapyPlanned enrollment of approximately 76 patientsPhase 1: Dose EscalationModified 3+3 dose-escalation designEvaluation of safety, tolerability, and dose-limiting toxicitiesDetermination of maximum tolerated dose and recommended Phase 2 doseAssessment of pharmacokinetics, pharmacodynamics, and preliminary antitumor activityIntegrated biomarker analyses to evaluate epigenetic modulation, gene re-expression, and telomere-related biology associated with cellular aging and genomic stabilityPhase 2: Dose ExpansionSimon's two-stage design to assess preliminary efficacyPrimary endpoint is objective response rate (ORR)Secondary endpoints include duration of response (DoR), progression-free survival (PFS), overall survival (OS), and safetyThe study will incorporate pharmacokinetic, pharmacodynamic, and biomarker analyses to evaluate target engagement and explore potential correlations between epigenetic modulation and clinical outcomesTranslational and Biomarker StrategyThe study includes an integrated biomarker program designed to evaluate pharmacodynamic activity, target engagement, and potential predictors of response.Biomarker analyses will assess changes in epigenetic regulation, including global DNA methylation, gene re-expression of epigenetically silenced tumor suppressor pathways, and histone modification patterns associated with tumor biology.In addition, exploratory analyses will evaluate biomarkers related to cellular aging and genomic stability, including telomere dynamics and associated epigenetic signatures, with the objective of understanding the broader biological activity of Telomir-Zn across oncology and age-related pathways.The study will also assess correlations between biomarker modulation and clinical outcomes, including preliminary antitumor activity, objective response, and progression-free survival, and may inform identification of potential predictive biomarkers of response.Clinical Development StrategyThe Company plans to initiate the Phase 1/2 clinical trial in the first half of 2026, anchored by a leading U.S. academic medical center, with potential expansion to additional oncology sites.Mechanism of ActionTelomir-Zn is an investigational small-molecule designed to represent a novel therapeutic approach and a potentially first-in-class strategy focused on modulation of intracellular metal homeostasis and downstream epigenetic regulation.Unlike conventional cytotoxic chemotherapy, immune checkpoint inhibition, antibody-drug conjugates, or classic epigenetic drugs, Telomir-Zn is being developed to target metal-dependent epigenetic vulnerabilities that may contribute to tumor progression, treatment resistance, genomic instability, and cancer-associated aging biology.Preclinical studies indicate that Telomir-Zn alters intracellular iron and zinc balance, modulates iron-dependent chromatin-regulating enzymes, and influences gene expression and cellular pathways associated with tumor biology, genomic stability, and cellular aging.Clinical ContextBreast cancer is the most commonly diagnosed cancer worldwide, with approximately 2.3 million new cases diagnosed annually, according to the World Health Organization.Triple-negative breast cancer represents approximately 10 to 15 percent of cases and is associated with aggressive disease biology and limited treatment options, particularly in the advanced or metastatic setting.Despite available therapies, outcomes remain poor, and TNBC continues to represent a multi-billion-dollar global market with significant unmet medical need.Management Commentary"The clearance of our IND, including the Phase 1/2 clinical protocol, marks an important step as we advance Telomir-Zn into clinical evaluation," said Erez Aminov, CEO of Telomir."Triple-negative breast cancer remains one of the most difficult cancers to treat in the advanced or metastatic setting, with limited options and consistently poor outcomes. There is a clear need for new therapeutic approaches, and we look forward to evaluating Telomir-Zn in this patient population."Dr. Itzchak Angel, Chief Scientific Advisor, added:"Telomir-Zn is designed to target fundamental aspects of tumor biology through modulation of intracellular metal balance and epigenetic regulation. This metal-epigenetic approach represents a differentiated therapeutic strategy that may have relevance not only in triple-negative breast cancer but also across broader cancer and age-related disease biology."About Telomir PharmaceuticalsTelomir Pharmaceuticals, Inc. (NASDAQ:TELO) is a clinical-stage biotechnology company developing small-molecule therapeutics targeting epigenetic and metabolic pathways implicated in cancer, aging, and degenerative disease. The Company's lead program, Telomir-1 (Telomir-Zn), is designed to modulate intracellular metal homeostasis and epigenetic regulation.Cautionary Note Regarding Forward-Looking StatementsThis press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995, including statements regarding the Company's plans to initiate clinical trials, clinical development strategy, and the potential therapeutic effects of Telomir-Zn. These statements are based on current expectations and involve risks and uncertainties that could cause actual results to differ materially.Such risks include, but are not limited to, regulatory developments, the timing and outcome of clinical trials, and the Company's ability to execute its development plans. Additional risks are described in the Company's filings with the U.S. Securities and Exchange Commission, including its Annual Report on Form 10-K. The Company undertakes no obligation to update forward-looking statements except as required by law.Contact InformationKrystina Quintana
Email:
US Market News
2月前
Telomir Pharmaceuticals Completes Acquisition of TELI Pharmaceuticals, Securing Global Rights to Telomir-1 (Telomir-Zn)April 24, 2026 9:00 AM
ACCESS NewswireTransaction establishes global ownership rights of lead program and includes initial capital funding with additional optional milestone-based capital support aligned with key clinical milestones.MIAMI, FL / ACCESS Newswire / April 24, 2026 / Telomir Pharmaceuticals, Inc. (NASDAQ:TELO) ("Telomir" or the "Company"), a biotechnology company developing small-molecule therapeutics targeting epigenetic and metabolic drivers of cancer and age-related diseases, today announced the successful closing of its previously announced acquisition of TELI Pharmaceuticals, Inc. ("TELI").The transaction, which was approved by Telomir's shareholders at the Company's Annual Meeting held on March 23, 2026, establishes Telomir as the sole holder of the global rights of Telomir-1 (Telomir-Zn), consolidating worldwide rights under a single corporate structure.Management CommentaryErez Aminov, Chief Executive Officer of Telomir, stated:"The closing of this transaction represents a defining milestone for Telomir. By securing worldwide rights to Telomir-1 (Telomir-Zn), we have established a globally unified platform as we advance toward clinical development.Combined with our recent IND submission for Telomir-Zn, this positions the Company to progress into the clinic while maintaining the flexibility to evaluate global partnership opportunities."The acquisition eliminates prior geographic fragmentation of the Telomir-1 (Telomir-Zn) platform and provides Telomir with full control over development and potential commercialization across major international markets. Prior to the transaction, North American and international rights were held separately.In connection with the transaction, the Company received $1.0 million in funding at closing and may receive up to an additional $4.0 million in milestone-based contributions from certain former TELI shareholders. These potential contributions are tied to key development milestones, including acceptance of an Investigational New Drug (IND) application and initiation of a Phase 1/2 clinical trial, and are subject to participation by such shareholders, aligning potential capital support with clinical advancement.Clinical DevelopmentThe closing follows Telomir's recent submission of an Investigational New Drug (IND) application to the U.S. Food and Drug Administration (FDA) for Telomir-Zn for the treatment of advanced and metastatic triple-negative breast cancer.If the IND is cleared, the Company plans to initiate a Phase 1/2 clinical trial evaluating Telomir-Zn as an oral monotherapy in patients with advanced or metastatic triple-negative breast cancer.Transaction SummaryTELI is now a wholly owned subsidiary of TelomirTransaction completed as a stock-for-stock acquisitionFormer TELI shareholders received shares of Telomir common stock based on an independently determined exchange ratioShares issued are subject to a six-month lock-up, subject to customary exceptionsTransaction includes $1.0 million funded at closing and up to an additional $4.0 million in optional milestone-based contributions, subject to participation by such shareholdersAbout Telomir PharmaceuticalsTelomir Pharmaceuticals, Inc. (NASDAQ:TELO) is a biotechnology company developing small-molecule therapeutics designed to target epigenetic and metabolic mechanisms implicated in cancer, aging, and degenerative disease. Its lead candidate, Telomir-1 (Telomir-Zn), is an investigational therapy that has demonstrated activity in preclinical studies involving modulation of intracellular metal homeostasis, epigenetic regulation, mitochondrial function, and genomic stability.Cautionary Note Regarding Forward-Looking StatementsThis press release contains forward-looking statements within the meaning of the Private Securities Litigation Reform Act of 1995, including statements regarding the expected benefits of the acquisition, the Company's plans for clinical development, the potential for additional capital contributions, and the Company's ability to pursue strategic partnerships.Forward-looking statements are based on current expectations and assumptions and are subject to risks and uncertainties that could cause actual results to differ materially. These risks include, but are not limited to, the Company's ability to obtain regulatory clearance for its IND, the timing and success of clinical trials, the availability of additional funding, and other risks described in the Company's filings with the U.S. Securities and Exchange Commission, including its most recent Annual Report on Form 10-K.The Company undertakes no obligation to update forward-looking statements except as required by law.Contact InformationKrystina Quintana
Email:
US Market News
2月前
Telomir Pharmaceuticals Submits IND to FDA for Telomir-1 (Telomir-Zn) in Advanced and Metastatic Triple-Negative Breast CancerMarch 31, 2026 8:00 AM
ACCESS NewswireFirst-in-class metal-modulating epigenetic therapy targeting iron-dependent pathways with preclinical efficacy and a favorable GLP safety profile.MIAMI, FL / ACCESS Newswire / March 31, 2026 / Telomir Pharmaceuticals, Inc. (NASDAQ:TELO) ("Telomir" or the "Company"), a biotechnology company developing small-molecule therapeutics targeting epigenetic and metabolic drivers of cancer and age-related disease, today announced the submission of an Investigational New Drug (IND) application to the U.S. Food and Drug Administration for its lead candidate, Telomir-1 (Telomir-Zn), for the treatment of advanced and metastatic Triple-Negative Breast Cancer (TNBC).The IND submission includes data from completed IND-enabling pharmacology, toxicology, and manufacturing studies. Subject to IND clearance, the Company plans to initiate a Phase 1/2 clinical trial evaluating Telomir-1 as an oral monotherapy in patients with advanced or metastatic TNBC.Mechanism and Scientific RationaleTelomir-Zn is a first-in-class metal-modulating epigenetic agent designed to restore transcriptional control in tumor cells by targeting intracellular iron-zinc homeostasis, an upstream regulatory node governing several histone demethylases (KDMs) activity, mitochondrial function, and oxidative stress response.Preclinical studies indicate that Telomir-1 reduces intracellular redox-active iron while increasing zinc availability. This shift suppresses iron-dependent KDMs activities, driving accumulation of repressive histone methylation marks, downregulating oncogenic transcriptional programs, and disrupting cancer cell metabolism. The approach does not rely on nonspecific cytotoxic mechanisms, potentially offering a more targeted profile.Preclinical Efficacy and SafetyAcross multiple preclinical TNBC models, Telomir-Zn demonstrated:Reduction in tumor growth in aggressive TNBC modelsReduction in metastatic dissemination in a chemotherapy-resistant settingIron-dependent tumor cell mortality across human TNBC cell linesEnhanced activity in combination with chemotherapy in select modelsTelomir-Zn has completed IND-enabling GLP safety studies demonstrating:No treatment-related adverse or dose-limiting toxicitiesFavorable cardiovascular, respiratory, and phototoxicity profilesConsistent systemic exposure and predictable pharmacokineticsThe program is supported by multi-level preclinical studies spanning cellular, in vivo, and safety studies, providing a supportive translational framework for clinical evaluation.Phase 1/2 Clinical Development PlanFollowing IND clearance, the Company plans to initiate a Phase 1/2 clinical study evaluating Telomir-Zn as an oral monotherapy in patients with advanced or metastatic Triple-Negative Breast Cancer.The Phase 1 portion will utilize a standard 3+3 dose-escalation design to evaluate safety, tolerability, dose-limiting toxicities, and determination of the recommended Phase 2 dose.The Phase 2 portion will evaluate preliminary antitumor activity using a Simon two-stage design, with objective response rate (ORR) as the primary endpoint, along with duration of response (DoR), progression-free survival (PFS), and continued safety.The study is designed to identify a clinically meaningful signal of activity.The Company is also evaluating biomarker strategies aligned with Telomir-Zn's mechanism of action to support patient selection and clinical response assessment.The Company is currently in discussions with multiple leading U.S.-based cancer centers regarding participation in the planned clinical program.Clinical Context and Unmet NeedAccording to Breastcancer.org, breast cancer remains one of the leading causes of cancer-related death globally, with hundreds of thousands of deaths reported each year.Triple-Negative Breast Cancer accounts for approximately 10-15% of all breast cancer cases and represents one of the most aggressive subtypes, with limited treatment options and poor clinical outcomes.In advanced disease, median overall survival remains approximately 11-13 months, with five-year survival rates of approximately 12-15%. Despite available therapies-including chemotherapy, immune checkpoint inhibitors such as Keytruda, and antibody-drug conjugates such as Trodelvy-response rates typically range from 20% to 40%, and most patients either do not respond or experience rapid disease progression.Therapies that can meaningfully improve response rates or durability of response in TNBC have the potential to significantly impact both patient outcomes and the treatment landscape.The global market for TNBC therapeutics is estimated to be in the multi-billion-dollar range, based on published market research reports, reflecting the significant unmet need for more effective and durable treatment options.Management Commentary"This IND submission marks a critical transition from preclinical proof-of-concept to clinical development for Telomir-Zn," said Erez Aminov, Chief Executive Officer of Telomir Pharmaceuticals."TNBC patients with advanced disease have few durable treatment options, and we believe that targeting the biological mechanisms driving treatment resistance, specifically iron-dependent epigenetic dysregulation, represents a differentiated and scientifically grounded approach. We look forward to advancing this program into the clinic."Dr. Itzchak Angel, Chief Scientific Advisor at Telomir Pharmaceuticals, added:"Epigenetic dysregulation, including aberrant histone modification mediated by iron-dependent KDMs, is a central driver of oncogenic transcriptional programs in aggressive cancers such as TNBC. Our data support a mechanistic framework in which modulating intracellular metal homeostasis resets this dysregulation, enabling transcriptional repression of tumor-supporting gene networks without cytotoxic stress. We are excited to evaluate this biology in patients."Next StepsSubject to IND clearance, Telomir plans to initiate its Phase 1/2 clinical trial in advanced TNBC and continue advancing biomarker-driven development strategies.In parallel, the Company is continuing to expand its preclinical program, including evaluation of Telomir-Zn in additional TNBC animal models and further characterization of its mechanism of action.The Company has submitted scientific manuscripts to peer-reviewed journals and plans to present data at scientific conferences, including the AACR Annual Meeting 2026.About Telomir PharmaceuticalsTelomir Pharmaceuticals, Inc. (NASDAQ:TELO) is a preclinical-stage biotechnology company developing small-molecule therapeutics designed to target fundamental epigenetic and metabolic mechanisms implicated in cancer, aging, and degenerative disease. The Company's lead program, Telomir-1 (Telomir-Zn), has demonstrated activity in preclinical studies involving modulation of intracellular metal homeostasis, redox balance, epigenetically regulated gene expression, mitochondrial function, and genomic stability.Cautionary Note Regarding Forward-Looking StatementsThis 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 InformationKrystina Quintana
Email:
US Market News
4月前
Telomir Pharmaceuticals Reports New Data Supporting an Epigenetic Modulation Mechanism Implicated in Cancer and AgingFebruary 5, 2026 8:00 AM
ACCESS NewswireCellular findings show Telomir-Zn modulates intracellular metal balance linked to oxidative stress, mitochondrial dysfunction, DNA methylation instability, and genomic integrity-without relying on cytotoxic mechanisms.MIAMI, FLORIDA / ACCESS Newswire / February 5, 2026 / Telomir Pharmaceuticals, Inc. (NASDAQ:TELO) ("Telomir" or the "Company"), a preclinical-stage biotechnology company developing small-molecule therapeutics targeting fundamental biological mechanisms implicated in cancer, aging, and degenerative disease, today announced new cellular study results demonstrating that Telomir-1, in the form of Telomir-Zn, induces a rapid and coordinated intracellular redistribution of zinc and iron.These findings extend Telomir's previously reported intracellular iron-reduction data by directly demonstrating, for the first time, that Telomir-Zn simultaneously increases intracellular zinc while reducing redox-active ferrous iron inside living cells. The coupled nature of these effects supports a differentiated intracellular metal-modulating mechanism rather than simple extracellular metal chelation.Why This Biology Matters in Cancer and AgingCancer and accelerated aging are increasingly understood to share common upstream biological drivers, including dysregulated metal homeostasis, excess oxidative stress, mitochondrial dysfunction, epigenetic instability, and cumulative genomic damage.Redox-active metals such as iron and copper can catalyze the formation of reactive oxygen species (ROS), which, over time, contribute to mitochondrial damage, oxidative DNA lesions, disruption of DNA methylation patterns, and telomere attrition. These processes are closely associated with epigenetic drift, impaired DNA repair, and genomic instability-hallmarks observed across both tumor biology and age-associated cellular decline.Zinc plays a distinct biological role. Unlike iron and copper, zinc is redox-inert under physiological conditions and supports chromatin structure, DNA repair, antioxidant defense systems, and telomere-associated genomic stability. Maintaining appropriate intracellular zinc availability while limiting excess redox-active metals is therefore central to preserving cellular function over time.Study Overview and Key FindingsTo assess whether Telomir-Zn alters intracellular metal pools, Telomir Pharmaceuticals, in collaboration with Smart Assays Biotechnologies, has quantified labile intracellular zinc and iron levels in cultured human HaCaT cells using complementary live-cell fluorescent probes.Key observations include:Rapid, dose-dependent zinc accumulation: Telomir-Zn exposure resulted in a measurable increase in intracellular zinc within 30 minutes, sustained over a two-hour period at low-micromolar concentrations, without loss of cell confluence or viability.Reciprocal reduction of redox-active iron: Increasing Telomir-Zn concentrations were associated with progressive depletion of the intracellular ferrous iron pool, most closely linked to oxidative stress.Coordinated intracellular modulation: Zinc accumulation and iron reduction occurred over similar concentration ranges and timeframes, supporting a coordinated intracellular process rather than independent or nonspecific metal effects.Mechanistic Interpretation: Linking Metals, Mitochondria, Epigenetics, and TelomeresExcess intracellular iron and copper are known to impair mitochondrial respiration, amplify ROS generation, and disrupt metal-dependent enzymes that regulate chromatin structure and DNA methylation. Several histone demethylases and DNA repair enzymes require tightly regulated Fe²? availability, and metal imbalance can destabilize epigenetic control systems and accelerate genomic stress.The observed Telomir-Zn-associated increase in intracellular zinc, coupled with a reduction of labile iron, is consistent with a proposed intracellular mechanism by which modulation of metal availability may attenuate oxidative stress while supporting zinc-dependent regulatory functions. These pathways are closely linked to mitochondrial health, epigenetic regulation, telomere maintenance, and long-term genomic stability, supporting the potential relevance of this mechanism across both oncology and age-associated disease biology.Importantly, the epigenetically associated effects observed in these studies do not rely on inducing cellular damage or cytotoxic stress, distinguishing this approach from many existing epigenetic strategies that act through DNA damage or broad transcriptional disruption.Management Commentary"These findings link our earlier epigenetic and mitochondrial observations to a clear upstream mechanism-intracellular metal imbalance," said Erez Aminov, CEO of Telomir Pharmaceuticals. "By simultaneously reducing redox-active iron while introducing protective zinc, Telomir-Zn appears to influence oxidative stress, DNA methylation, and genomic stability in a way that does not rely on cellular damage. We believe this approach has important implications for how cancer and age-related disease may be addressed at their biological roots.""For decades, cancer and age-related diseases have largely been approached by targeting downstream consequences-uncontrolled growth, accumulated damage, or end-stage dysfunction," said Dr. Itzchak Angel, Chief Scientific Advisor at Telomir Pharmaceuticals. "What is emerging here is a different biological strategy: addressing upstream drivers such as oxidative stress, mitochondrial instability, and epigenetic drift that are shared across these conditions. By demonstrating for the first time that Telomir-Zn can simultaneously modulate intracellular zinc and iron-key regulators of DNA methylation, redox balance, and telomere-associated genomic stability-these findings support a framework that could fundamentally change how we think about intervening in cancer and aging biology, without relying on toxicity or cellular injury."Ongoing Activities and Upcoming Scientific PresentationsTelomir Pharmaceuticals plans to present data related to Telomir-Zn and its mechanism of action at several upcoming scientific and industry meetings, including:16th World Congress on Breast Cancer Research & Therapies, March 23-24, 2026 (Paris, France)AACR Annual Meeting 2026, April 17-22, 2026 (San Diego, CA)BIO International Convention, June 22-25, 2026 (San Diego, CA)3rd International Conference on Women's Health and Breast Cancer, October 5-6, 2026 (Tokyo, Japan)IND Preparation and Ongoing Research ActivitiesTelomir Pharmaceuticals is finalizing IND-enabling activities for Telomir-Zn, including assembly of the required data package to support regulatory submission. The Company currently plans to submit an Investigational New Drug (IND) application in the first quarter of 2026.In parallel, Telomir continues to advance a portfolio of ongoing and completed preclinical research programs, including studies in triple-negative breast cancer (TNBC) models and longevity-focused models, evaluating the biological relevance of Telomir-Zn's intracellular metal-modulating and epigenetically associated mechanisms.Based on data generated from completed studies, manuscript submissions to peer-reviewed journals have been initiated, while additional data continue to be generated from ongoing preclinical studies. These efforts also support planned and upcoming scientific conference presentations.About Telomir PharmaceuticalsTelomir Pharmaceuticals, Inc. (NASDAQ:TELO) is a preclinical-stage biotechnology company developing small-molecule therapeutics designed to target fundamental epigenetic and metabolic mechanisms implicated in cancer, aging, and degenerative disease. The Company's lead program, Telomir-1 (Telomir-Zn), has demonstrated activity in preclinical studies involving modulation of intracellular metal homeostasis, redox balance, epigenetically regulated gene expression, mitochondrial function, and genomic stability.Cautionary Note Regarding Forward-Looking StatementsThis 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 InformationKrystina Quintana
Email:
INV4
7月前
Form 8-K - Current report
Nov 12, 2025
Item 8.01 Other Events
Telomir Pharmaceuticals Reports That Telomir-1 Outperforms FDA-Approved Gold-Standard Iron Chelator Deferoxamine (DFO) in Reducing Intracellular Iron in a Human Cell Line
New live-cell imaging data show that Telomir-1 markedly lowers intracellular iron levels at submicromolar concentrations in human keratinocytes, demonstrating potent cell penetration and iron-modulating activity—key to its broader epigenetic mechanism of action.
Telomir Pharmaceuticals, Inc. (NASDAQ: TELO) (“Telomir” or the “Company”) reports new preclinical data demonstrating that its lead investigational compound Telomir-1 produced a strong, dose-dependent reduction of intracellular iron in human keratinocyte (HaCaT) cells, significantly exceeding the effect observed with the FDA-approved iron chelator Deferoxamine (DFO).
These results extend the Company’s research into the relationship between metal-ion imbalance, oxidative stress, and epigenetic enzyme regulation.
Study Overview
The evaluation utilized FerroOrange, a fluorescent probe that selectively detects ferrous iron (Fe²?) in living cells. HaCaT cells were incubated with Telomir-1 or DFO at several time points. After three, six and sixteen hours, fluorescence microscopy showed substantially lower intracellular iron signal intensity in Telomir-1–treated cells at various concentrations, indicating greater cellular penetration and iron-modulating activity relative to DFO at the same concentrations.
Scientific Context and Importance of the Findings
Iron plays a vital role in human biology. It enables oxygen transport, mitochondrial energy generation, and DNA synthesis—processes essential for growth and cellular development. In early life, iron is beneficial and tightly regulated by proteins such as ferritin, transferrin, and ceruloplasmin that maintain balance between storage, transport, and utilization.
With aging, however, these control systems become less efficient. Reactive forms of iron can accumulate within cells, participating in chemical reactions that generate reactive oxygen species (ROS) capable of damaging DNA, proteins, and membranes. This imbalance contributes to oxidative stress, mitochondrial dysfunction, and genomic instability—factors increasingly associated with accelerated aging, neurodegenerative, metabolic, cardiovascular, and oncologic diseases.
Cancer biology further highlights the dual nature of iron. Many tumors depend on iron for rapid proliferation, using it to drive DNA replication, sustained proliferation and energy production. Yet excessive intracellular iron also amplifies oxidative and methylation stress, disrupting normal gene regulation and potentially promoting disease progression.
Understanding how to safely modulate intracellular iron levels is therefore an important area of pre-clinical research. The ability of Telomir-1 to enter cells and influence iron balance at low concentrations provides a basis for continued investigation into metal-ion homeostasis and its link to cellular health and epigenetic control.
Key Observations
• Telomir-1 reduced intracellular Fe²? levels in a time- and dose-dependent manner at low-micromolar concentrations.
• Deferoxamine (DFO), while FDA-approved, exhibited limited intracellular activity under equivalent conditions.
• Telomir-1 has also been formulated with zinc (Telomir-Zn) to enable a controlled intracellular exchange of metal ions—binding excess reactive metals such as iron and copper while contributing zinc, a cofactor for enzymes involved in antioxidant defense and DNA stability.
These data support the Company’s ongoing pre-clinical research focused on metal-ion balance, oxidative stress, and epigenetic enzyme dynamics in aging and degenerative disease.
Link 8-K
$TELO
INV4
8月前
Telomir Pharmaceuticals Announces New Data Showing That Telomir-1 Kills Aggressive Pancreatic Cancer Cells, One of the Deadliest Forms of Cancer
Oct 14, 2025
Findings complement previously announced results in triple-negative breast cancer (TNBC) and prostate cancer models, highlighting Telomir-1's consistent impact on cancer cell survival pathways.
MIAMI, FLORIDA / ACCESS Newswire / October 14, 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 laboratory findings demonstrating that Telomir-1 kills aggressive pancreatic cancer cells.
Study Summary
In laboratory studies using human pancreatic cancer (PANC-1) cells, Telomir-1 produced a concentration-dependent reduction in cancer cell survival and mitochondrial activity. These data suggest Telomir-1 influences cellular pathways related to energy metabolism and oxidative balance. The findings align with previously reported results in triple-negative breast and prostate cancer models, indicating that Telomir-1 may engage fundamental biological processes involved in cancer cell regulation.
Similar to the observation in TNBC, Telomir-1's effects in pancreatic-cancer cells were partially reversed by iron re-addition, suggesting that Telomir-1's activity in both TNBC and pancreatic cancer involves iron-dependent processes. The incomplete reversal supports the interpretation that additional metabolic or epigenetic mechanisms are also engaged.
Pancreatic-cancer cells are known for metabolic flexibility - the ability to use glucose, lipids, and amino acids to survive in low-oxygen, nutrient-poor environments. TNBC cells, by comparison, rely more heavily on iron-driven oxidative metabolism. The lower sensitivity of pancreatic cells to Telomir-1 in the presence of iron restoration may therefore reflect modulation of broader mitochondrial or energy-control systems, consistent with Telomir-1's function as an epigenetic modulator.
Mechanistic Context: Key Genes and Enzymes
Telomir-1 has previously been shown to influence several tumor suppressor genes and iron-dependent histone demethylases that are also relevant to pancreatic-cancer biology:
• MASPIN (SERPINB5) - A "tumor suppressor shield" that regulates cell migration, invasion, and therapy response. Its loss through hypermethylation correlates with poor prognosis in pancreatic and prostate cancers. Telomir-1 has been observed to reduce MASPIN hypermethylation in preclinical models.
• RASSF1A ("guardian gene") - A regulator of cell-cycle braking and apoptosis, frequently silenced by promoter methylation in pancreatic, breast, and lung cancers. Telomir-1 has previously decreased RASSF1A methylation in a dose-dependent manner.
• STAT1 - A master coordinator of immune surveillance. When hypermethylated, tumors can evade immune detection. Telomir-1 has shown modulation of STAT1 methylation status in laboratory models, informing its potential relevance to immune-related control mechanisms.
• KDM2B (FBXL10) and KDM6B (JMJD3) - Iron-dependent histone demethylases overexpressed in pancreatic and other aggressive cancers, driving transcriptional reprogramming, inflammation, and stem-like tumor behavior. Telomir-1 has demonstrated inhibitory activity against these enzymes.
Together, these previously reported effects provide biological context for Telomir-1's observed activity in pancreatic cancer models. By modulating genes and enzymes that coordinate DNA-methylation, oxidative stress, and cellular energy regulation, Telomir-1 may offer a unifying framework for understanding shared epigenetic and metabolic vulnerabilities across multiple tumor types.
Executive Commentary
Erez Aminov, Chief Executive Officer of Telomir Pharmaceuticals, stated:
"Our mission has always been to understand and address the root biological drivers of disease, not just their downstream symptoms. Pancreatic cancer is one of the hardest and deadliest malignancies known, and these data advance our understanding of how Telomir-1 interacts with the underlying mechanisms that sustain aggressive tumor biology. Each new finding brings us closer to our goal of translating deep science into meaningful innovation."
Dr. Angel, Chief Scientific Advisor of Telomir Pharmaceuticals, added:
"From a scientific standpoint, these results continue to refine our mechanistic understanding of Telomir-1. The differential behavior seen in pancreatic versus breast-cancer models helps us map how Telomir-1 influences iron-dependent and mitochondrial pathways in the context of epigenetic regulation. This type of multi-dimensional insight is precisely what's needed to design smarter, targeted approaches in preclinical oncology research."
Telomir intends to expand its preclinical research into additional cancer models, including leukemia, and to initiate in vivo validation studies as part of its ongoing Investigational New Drug (IND) preparation.
The Unmet Need in Pancreatic Cancer
Pancreatic cancer remains one of the most lethal malignancies, with an estimated 66,440 new U.S. cases and 51,750 deaths projected in 2024 (American Cancer Society). The five-year survival rate is approximately 12%, the lowest among major cancers (National Cancer Institute SEER).
Current standards of care - FOLFIRINOX, gemcitabine plus nab-paclitaxel and selected targeted or immunotherapy combinations - extend survival modestly but are limited by toxicity and the rapid emergence of resistance. The disease's dense stromal barrier, late detection, and ability to rewire its metabolism make it one of the most difficult cancers to treat. This has driven growing interest in therapies that address the epigenetic and metabolic mechanisms enabling tumor persistence.
Why Pancreatic Cancer Remains So Difficult to Treat-and How Telomir-1 Differs
Pancreatic cancer is one of the most complex and treatment-resistant malignancies, driven by a unique combination of biological and environmental challenges. The tumors develop a dense fibrotic stroma that limits drug penetration and oxygen flow, creating a microenvironment that supports survival rather than destruction. These cells also exhibit remarkable metabolic flexibility, switching among glucose, lipid, and amino acid utilization to sustain growth even when nutrients are scarce. This adaptability, together with profound epigenetic dysregulation, enables pancreatic tumors to resist chemotherapy and immune-based therapies alike.
Current front-line regimens-FOLFIRINOX or gemcitabine combined with nab-paclitaxel-attack rapidly dividing cells throughout the body. While these treatments can temporarily slow disease progression, they are often associated with severe fatigue, gastrointestinal distress, immune suppression, and peripheral neuropathy, and the benefit typically lasts only months before resistance emerges.
Telomir-1 represents a fundamentally different approach. Rather than relying on cytotoxic mechanisms that indiscriminately damage dividing cells, Telomir-1 is being studied for its ability to modulate epigenetic and metabolic regulators that underlie cancer cell survival. By influencing pathways that control DNA methylation, histone demethylation, mitochondrial activity, and iron balance, Telomir-1 may help reset the abnormal cellular programs that fuel aggressive cancers. This approach aims to reveal tumor vulnerabilities at their regulatory source - potentially offering a more targeted and mechanistically precise strategy for future development.
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.
$TELO
INV4
8月前
Nice news 🗞️ $2.15+ 😃
===============
Form 8-K - Current report
Oct 8, 2025
Telomir Pharmaceuticals Reports Discovery That Telomir-1 Selectively Kills Aggressive Triple-Negative Breast Cancer Cells
New findings show Telomir-1 shuts down cellular energy pathways and mitochondrial function in aggressive breast cancer cells, leading to cell death through iron-dependent regulation.
Telomir Pharmaceuticals, Inc. (NASDAQ: TELO), a preclinical-stage biotechnology company developing therapies that target epigenetic drivers of cancer, aging, and age-related disease, announced new findings demonstrating that Telomir-1 significantly reduces the survival of aggressive triple-negative breast cancer (TNBC) cells — a highly invasive form of breast cancer that lacks hormone and HER2 receptors, offers limited treatment options, and carries one of the poorest survival rates among breast cancer subtypes.
In laboratory studies using human triple-negative breast cancer cells, Telomir-1 produced a clear, concentration-dependent reduction in cancer cell survival. As Telomir-1 concentrations increased, more cancer cells lost their ability to grow and survive. When iron was added back to the system, the cells recovered, confirming that the compound’s activity is linked to the regulation of cellular iron and energy balance.
The iron dependency observed in this study is significant because aggressive cancer cells, such as those found in TNBC, are among the most metabolically active of all breast cancer types. These cells depend on iron to support their rapid growth and survival, and iron metabolism contributes directly to this aggressive behavior. By disrupting that iron-driven process, Telomir-1 appears to exploit a core metabolic weakness unique to these tumors. This selectivity is important because normal cells manage iron differently and are less dependent on it, suggesting that Telomir-1 may preferentially affect cancer cells while sparing healthy tissue.
Telomir-1 has previously been shown to reset abnormal DNA methylation patterns and restore balanced gene expression in models of cancer and age-related disease. In TNBC, certain iron-dependent enzymes—known as Jumonji domain histone demethylases (KDMs), including KDM5A/B and KDM6B—are thought to drive gene expression changes that make cancer cells more aggressive and resistant to therapy. The new findings suggest that Telomir-1’s observed effects on energy regulation and iron balance may stem from its ability to influence these same epigenetic mechanisms. Many aggressive cancers show methylation changes that activate pathways controlling iron use, oxidative stress, and energy metabolism. By helping to restore normal epigenetic control, Telomir-1 may indirectly rebalance these pathways, offering new insight into its broader mechanism of action.
The Company plans to expand these studies to include additional cancer types, such as pancreatic and leukemia models, and to conduct further animal studies in preparation for its Investigational New Drug (IND) submission.
https://investorshub.advfn.com/stock-market/NASDAQ/telomir-pharmaceuticals-TELO/stock-news/96973366/form-8-k-current-report
$TELO 💹
INV4
8月前
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
Oct 7, 2025
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, October 7, 2025 (Newswire.com) - 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.
https://www.newswire.com/news/telomir-pharmaceuticals-announces-new-findings-in-a-prostate-cancer-model
$TELO 💹
INV4
8月前
Form 8-K - Current report
Oct 6, 2025
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 prostate cancer models.
On October 6, 2025, Telomir Pharmaceuticals, Inc. (the “Company”) announced new cancer results from preclinical studies of its lead investigational compound, Telomir-1, in aggressive prostate cancer models.
The studies demonstrated that Telomir-1 resets abnormal DNA methylation to restore the function of two additional critical tumor suppressor genes — MASPIN and RASSF1A. Both genes are frequently silenced in cancer, a change that is closely linked to metastasis and treatment resistance, two of the most significant challenges in oncology.
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.
By reactivating MASPIN and RASSF1A through DNA methylation reset, Telomir-1 expands the potential to restore natural tumor defenses, counteract chemotherapy-induced resistance, and help limit cancer metastasis.
The Company is continuing its preclinical development of Telomir-1 and is currently advancing the program with IND-enabling studies.
Link article:
https://investorshub.advfn.com/stock-market/NASDAQ/telomir-pharmaceuticals-TELO/stock-news/96956101/form-8-k-current-report
$TELO 💹
Hot Features
プレミアム
登録してリアルタイムのチャート、分析ツール、価格を入手してください。
81vette
2週前
JJ8
3週前
glenn1919
7月前
tw0122
7月前
Monroe1
8月前
Hercules1
8月前
メールアドレスで登録
