{"success":true,"data":{"pressRelease":{"id":"113902","rtpr_id":"nGNX68SKnP","ticker":"TELO","exchange":"NASDAQ","all_tickers":["TELO"],"title":"Telomir Announces Peer-Reviewed Publication Demonstrating Telomir-Zn Suppresses Tumor Growth in TNBC and Prostate Cancer Models","author":"Globe Newswire","published_at":"2026-08-10T12:00:00.692Z","article_body":"MIAMI, Aug. 10, 2026 (GLOBE NEWSWIRE) -- Telomir Pharmaceuticals, Inc.\n(NASDAQ:TELO), a clinical-stage biotechnology company developing\nsmall-molecule therapeutics targeting epigenetic and metabolic drivers of\ncancer, today announced the peer-reviewed publication of preclinical data of\nTelomir-Zn suppressing tumor growth in prostate and triple-negative breast\ncancer (TNBC) models through selective modulation of intracellular iron and\ncopper.\n\nThe manuscript, titled \"Telomir-Zn Modulates Intracellular Iron and Copper to\nInhibit JmjC Histone Demethylases and Suppress Tumor Growth in Prostate and\nTriple-Negative Breast Cancer,\" has been published in the Journal of Oncology\nResearch and Therapy, Volume 11, Issue 3. These preclinical findings provide\nthe scientific foundation supporting advancement of Telomir-Zn toward the\nCompany's planned Phase 1/2 clinical trial in TNBC.\n\nPublication Highlights\n\nKDM Inhibition: The Target at the Core\n\nHistone demethylases, or KDMs, specifically the KDM2, KDM5, and KDM6 families,\nare often overexpressed in aggressive cancers, where they can promote\ntumorigenesis by either silencing tumor-suppressor genes or activating\noncogenic programs, depending on their substrate specificity and cellular\ncontext. Telomir-Zn targets these KDM enzymes by depleting the intracellular\niron they require for catalytic activity. This study demonstrates that this\nKDM-targeting approach translates to meaningful anti-cancer activity.\n\nIron-Dependent Mechanism Proved\n\nThe study's most critical finding was direct proof that Telomir-Zn's\nanti-cancer activity depends on iron depletion. When researchers added iron\nback to treated TNBC cells, the compound's killing effect was significantly\nreversed. This iron-rescue result eliminates alternative explanations and\ndemonstrates the mechanism is real and specific, not a general toxin or\noff-target effect.\n\nSelective Targeting of Cancer Over Normal Cells\n\nTelomir-Zn killed iron-dependent TNBC cancer cells at low concentrations while\nleaving normal cells unharmed at concentrations more than 50-fold higher. This\nselectivity window demonstrates the compound preferentially targets cancer\ncells with elevated iron dependence, a hallmark of aggressive malignancies\nlike TNBC.\n\nTumor Suppressor Gene Reactivation\n\nIn a prostate cancer model, oral Telomir-Zn suppressed tumor growth and\nreactivated silenced tumor-suppressor genes (STAT1, GSTP1, RASSF1A, CDKN2A,\nand MASPIN). In TNBC and prostate cancer, both elevated KDM activity and\nabnormal DNA methylation can silence tumor-suppressor genes through distinct\nbut complementary epigenetic mechanisms. The compound works through an\nupstream mechanism distinct from approved drugs that target downstream\nepigenetic machinery.\n\nAnti-Tumor and Anti-Metastatic Activity\n\nIn TNBC human xenograft models, Telomir-Zn reduced primary tumor size across\nseveral cell lines. In HCC1806 xenografts, the compound also significantly\nreduced metastatic dissemination, a critical finding, as most TNBC patients\ndie from spread disease, not the primary tumor. In BT-549 xenografts,\nTelomir-Zn combined with paclitaxel produced significantly greater tumor\nreduction than either drug alone, a finding that suggests potential for\ncombination therapy approaches in the clinic and positions Telomir-Zn as both\na monotherapy and a chemotherapy partner. Notably, MDA-MB-231 xenografts did\nnot respond, indicating heterogeneous sensitivity based on tumor-specific\niron-metabolism features. It tells us that in the future we could be able to\nstratify patients based on personalized iron-handling signatures and\npotentially enrich for responders in future clinical development.\n\nWhy This Matters for Clinical Development\n\nTriple-negative breast cancer remains a significant clinical challenge. Most\npatients receive chemotherapy as a backbone, with limited options for targeted\nor precision-based approaches. Current approved therapies and those in\ndevelopment address symptoms of epigenetic dysregulation but do not target the\nunderlying metabolic drivers, specifically, the dysregulated iron homeostasis\nthat fuels overactive KDM enzymes in iron-addicted cancers.\n\nThis publication establishes dysregulated KDM-driven epigenetic silencing as a\nfundamental cancer vulnerability that can be targeted through selective iron\nmodulation. Unlike conventional epigenetic drugs that broadly inhibit\nmethylation-modifying enzymes (DNMT or HDAC inhibitors), Telomir-Zn targets\nthe upstream metabolic dependency, excess intracellular iron, that fuels KDM\noveractivity. By depleting labile iron and disabling KDM enzymes, the compound\ndisrupts epigenetic silencing at its root, enabling tumor-suppressor\nreactivation. This mechanistically distinct approach addresses a therapeutic\ngap in the current TNBC treatment landscape.\n\nThe iron-rescue experiments provide the strongest possible proof that this\nmechanism is real and specific, enabling clinical strategies for patient\nselection based on iron-metabolism biomarkers. The preclinical anti-metastatic\nactivity in HCC1806 xenografts is particularly noteworthy, as it suggests\npotential to address both primary tumor control and disseminated disease, a\nkey unmet need in TNBC.\n\nManagement Commentary\n\n\"In several cancer types, cancer cells silence critical tumor-suppressor genes\nthrough abnormal DNA methylation, essentially turning off the cell's brakes,\"\nsaid Dr. Itzchak Angel, Chief Scientific Advisor of Telomir. \"Overactive KDM\nenzymes also play a role as important drivers of this epigenetic silencing.\nCurrent TNBC treatments address downstream consequences of this dysregulation\nbut do not target the KDM-driven mechanism itself. Our data implicates that by\nreversing the abnormal methylation and by KDM inhibition, Telomir-Zn can\nreactivate these silenced tumor-suppressor genes, promoting cell killing.\nWe're seeing tumor suppression and, in some models, reduced metastatic spread.\nThis is a mechanistically different approach to TNBC, and we believe it\naddresses a fundamental vulnerability that existing therapies don't. We're\nencouraged by the preclinical evidence and eager to test it in patients.\"\n\n\"Triple-negative breast cancer represents one of oncology's most significant\nunmet needs,\" said Erez Aminov, CEO of Telomir. \"Most patients with advanced\ndisease have limited treatment options and poor survival outcomes. We're\nexcited to advance Telomir-Zn into our Phase 1/2 program under our active IND\nto test whether this approach can meaningfully improve outcomes for TNBC\npatients.\"\n\nAbout Telomir Pharmaceuticals\n\nTelomir Pharmaceuticals, Inc. (NASDAQ:TELO) is a clinical-stage biotechnology\ncompany developing small-molecule therapeutics targeting epigenetic and\nmetabolic pathways implicated in cancer. The Company's lead program,\nTelomir-Zn, is designed to modulate intracellular metal homeostasis and\nepigenetic regulation and has received Investigational New Drug (IND)\nclearance from the U.S. Food and Drug Administration for a Phase 1/2 clinical\ntrial in patients with advanced or metastatic triple-negative breast cancer.\nFor more information, please visit https://telomirpharma.com/.\n\nForward-Looking Statements\n\nThis press release contains \"forward-looking statements\" within the meaning of\nthe Private Securities Litigation Reform Act of 1995. These forward-looking\nstatements generally can be identified by the use of words such as\n\"anticipate,\" \"expect,\" \"plan,\" \"can,\" \"could,\" \"would,\" \"may,\" \"will,\"\n\"believe,\" \"estimate,\" \"forecast,\" \"goal,\" \"project,\" \"guidance,\" \"potential,\"\n\"intend,\" \"seek,\" \"target\" and other words of similar meaning, although not\nall forward-looking statements include these words.\n\nForward-looking statements may include, but are not limited to, statements\nregarding the therapeutic potential, mechanism of action, development plans,\nregulatory pathway, safety profile, clinical utility, market opportunity, and\nfuture development of Telomir-1 (Telomir-Zn) and the Company's other product\ncandidates. Forward-looking statements may also include statements regarding\nthe significance of the published preclinical findings, the relevance of such\nfindings to the Company's oncology development programs, the advancement of\nthe Company's Phase 1/2 TNBC clinical trial, and the potential applicability\nof Telomir-Zn across multiple disease areas.\n\nThese forward-looking statements are based on current expectations, estimates,\nforecasts, and projections, as well as management's beliefs and assumptions,\nand are subject to significant risks and uncertainties that could cause actual\nresults to differ materially from those expressed or implied by such\nstatements. These risks and uncertainties include, among others, risks related\nto preclinical and clinical development, the ability to obtain regulatory\napprovals, the outcome of future studies, reliance on third parties,\nintellectual property protection, financing needs, market conditions, and the\nother risks identified under the heading \"Risk Factors\" contained in the\nCompany's Annual Report on Form 10-K and the Company's other filings with the\nU.S. Securities and Exchange Commission (\"SEC\").\n\nForward-looking statements contained in this press release speak only as of\nthe date hereof, and the Company undertakes no obligation to update or revise\nsuch statements, whether as a result of new information, future events, or\notherwise, except as required by applicable law.\n\nWe caution investors not to place undue reliance on the forward-looking\nstatements contained in this press release. You are encouraged to read our\nfilings with the SEC, available at the SEC website and in the \"Investors\"\nsection of our website, for a discussion of these and other risks and\nuncertainties.\n\nContact Information\n\nKrystina Quintana\nEmail: info@telomirpharma.com\nPhone: (786) 396-6723\n\n(https://www.globenewswire.com/NewsRoom/AttachmentNg/cc74273a-ee3e-4dae-8ce1-11b23816056b)\n\n\n\nGlobeNewswire, Inc. 2026","article_body_html":"","raw_payload":{"data":{"id":"nGNX68SKnP","title":"Telomir Announces Peer-Reviewed Publication Demonstrating Telomir-Zn Suppresses Tumor Growth in TNBC and Prostate Cancer Models","author":"Globe Newswire","ticker":"TELO","created":"2026-08-10T12:00:00.692Z","tickers":["TELO"],"exchange":"NASDAQ","article_body":"MIAMI, Aug. 10, 2026 (GLOBE NEWSWIRE) -- Telomir Pharmaceuticals, Inc.\n(NASDAQ:TELO), a clinical-stage biotechnology company developing\nsmall-molecule therapeutics targeting epigenetic and metabolic drivers of\ncancer, today announced the peer-reviewed publication of preclinical data of\nTelomir-Zn suppressing tumor growth in prostate and triple-negative breast\ncancer (TNBC) models through selective modulation of intracellular iron and\ncopper.\n\nThe manuscript, titled \"Telomir-Zn Modulates Intracellular Iron and Copper to\nInhibit JmjC Histone Demethylases and Suppress Tumor Growth in Prostate and\nTriple-Negative Breast Cancer,\" has been published in the Journal of Oncology\nResearch and Therapy, Volume 11, Issue 3. These preclinical findings provide\nthe scientific foundation supporting advancement of Telomir-Zn toward the\nCompany's planned Phase 1/2 clinical trial in TNBC.\n\nPublication Highlights\n\nKDM Inhibition: The Target at the Core\n\nHistone demethylases, or KDMs, specifically the KDM2, KDM5, and KDM6 families,\nare often overexpressed in aggressive cancers, where they can promote\ntumorigenesis by either silencing tumor-suppressor genes or activating\noncogenic programs, depending on their substrate specificity and cellular\ncontext. Telomir-Zn targets these KDM enzymes by depleting the intracellular\niron they require for catalytic activity. This study demonstrates that this\nKDM-targeting approach translates to meaningful anti-cancer activity.\n\nIron-Dependent Mechanism Proved\n\nThe study's most critical finding was direct proof that Telomir-Zn's\nanti-cancer activity depends on iron depletion. When researchers added iron\nback to treated TNBC cells, the compound's killing effect was significantly\nreversed. This iron-rescue result eliminates alternative explanations and\ndemonstrates the mechanism is real and specific, not a general toxin or\noff-target effect.\n\nSelective Targeting of Cancer Over Normal Cells\n\nTelomir-Zn killed iron-dependent TNBC cancer cells at low concentrations while\nleaving normal cells unharmed at concentrations more than 50-fold higher. This\nselectivity window demonstrates the compound preferentially targets cancer\ncells with elevated iron dependence, a hallmark of aggressive malignancies\nlike TNBC.\n\nTumor Suppressor Gene Reactivation\n\nIn a prostate cancer model, oral Telomir-Zn suppressed tumor growth and\nreactivated silenced tumor-suppressor genes (STAT1, GSTP1, RASSF1A, CDKN2A,\nand MASPIN). In TNBC and prostate cancer, both elevated KDM activity and\nabnormal DNA methylation can silence tumor-suppressor genes through distinct\nbut complementary epigenetic mechanisms. The compound works through an\nupstream mechanism distinct from approved drugs that target downstream\nepigenetic machinery.\n\nAnti-Tumor and Anti-Metastatic Activity\n\nIn TNBC human xenograft models, Telomir-Zn reduced primary tumor size across\nseveral cell lines. In HCC1806 xenografts, the compound also significantly\nreduced metastatic dissemination, a critical finding, as most TNBC patients\ndie from spread disease, not the primary tumor. In BT-549 xenografts,\nTelomir-Zn combined with paclitaxel produced significantly greater tumor\nreduction than either drug alone, a finding that suggests potential for\ncombination therapy approaches in the clinic and positions Telomir-Zn as both\na monotherapy and a chemotherapy partner. Notably, MDA-MB-231 xenografts did\nnot respond, indicating heterogeneous sensitivity based on tumor-specific\niron-metabolism features. It tells us that in the future we could be able to\nstratify patients based on personalized iron-handling signatures and\npotentially enrich for responders in future clinical development.\n\nWhy This Matters for Clinical Development\n\nTriple-negative breast cancer remains a significant clinical challenge. Most\npatients receive chemotherapy as a backbone, with limited options for targeted\nor precision-based approaches. Current approved therapies and those in\ndevelopment address symptoms of epigenetic dysregulation but do not target the\nunderlying metabolic drivers, specifically, the dysregulated iron homeostasis\nthat fuels overactive KDM enzymes in iron-addicted cancers.\n\nThis publication establishes dysregulated KDM-driven epigenetic silencing as a\nfundamental cancer vulnerability that can be targeted through selective iron\nmodulation. Unlike conventional epigenetic drugs that broadly inhibit\nmethylation-modifying enzymes (DNMT or HDAC inhibitors), Telomir-Zn targets\nthe upstream metabolic dependency, excess intracellular iron, that fuels KDM\noveractivity. By depleting labile iron and disabling KDM enzymes, the compound\ndisrupts epigenetic silencing at its root, enabling tumor-suppressor\nreactivation. This mechanistically distinct approach addresses a therapeutic\ngap in the current TNBC treatment landscape.\n\nThe iron-rescue experiments provide the strongest possible proof that this\nmechanism is real and specific, enabling clinical strategies for patient\nselection based on iron-metabolism biomarkers. The preclinical anti-metastatic\nactivity in HCC1806 xenografts is particularly noteworthy, as it suggests\npotential to address both primary tumor control and disseminated disease, a\nkey unmet need in TNBC.\n\nManagement Commentary\n\n\"In several cancer types, cancer cells silence critical tumor-suppressor genes\nthrough abnormal DNA methylation, essentially turning off the cell's brakes,\"\nsaid Dr. Itzchak Angel, Chief Scientific Advisor of Telomir. \"Overactive KDM\nenzymes also play a role as important drivers of this epigenetic silencing.\nCurrent TNBC treatments address downstream consequences of this dysregulation\nbut do not target the KDM-driven mechanism itself. Our data implicates that by\nreversing the abnormal methylation and by KDM inhibition, Telomir-Zn can\nreactivate these silenced tumor-suppressor genes, promoting cell killing.\nWe're seeing tumor suppression and, in some models, reduced metastatic spread.\nThis is a mechanistically different approach to TNBC, and we believe it\naddresses a fundamental vulnerability that existing therapies don't. We're\nencouraged by the preclinical evidence and eager to test it in patients.\"\n\n\"Triple-negative breast cancer represents one of oncology's most significant\nunmet needs,\" said Erez Aminov, CEO of Telomir. \"Most patients with advanced\ndisease have limited treatment options and poor survival outcomes. We're\nexcited to advance Telomir-Zn into our Phase 1/2 program under our active IND\nto test whether this approach can meaningfully improve outcomes for TNBC\npatients.\"\n\nAbout Telomir Pharmaceuticals\n\nTelomir Pharmaceuticals, Inc. (NASDAQ:TELO) is a clinical-stage biotechnology\ncompany developing small-molecule therapeutics targeting epigenetic and\nmetabolic pathways implicated in cancer. The Company's lead program,\nTelomir-Zn, is designed to modulate intracellular metal homeostasis and\nepigenetic regulation and has received Investigational New Drug (IND)\nclearance from the U.S. Food and Drug Administration for a Phase 1/2 clinical\ntrial in patients with advanced or metastatic triple-negative breast cancer.\nFor more information, please visit https://telomirpharma.com/.\n\nForward-Looking Statements\n\nThis press release contains \"forward-looking statements\" within the meaning of\nthe Private Securities Litigation Reform Act of 1995. These forward-looking\nstatements generally can be identified by the use of words such as\n\"anticipate,\" \"expect,\" \"plan,\" \"can,\" \"could,\" \"would,\" \"may,\" \"will,\"\n\"believe,\" \"estimate,\" \"forecast,\" \"goal,\" \"project,\" \"guidance,\" \"potential,\"\n\"intend,\" \"seek,\" \"target\" and other words of similar meaning, although not\nall forward-looking statements include these words.\n\nForward-looking statements may include, but are not limited to, statements\nregarding the therapeutic potential, mechanism of action, development plans,\nregulatory pathway, safety profile, clinical utility, market opportunity, and\nfuture development of Telomir-1 (Telomir-Zn) and the Company's other product\ncandidates. Forward-looking statements may also include statements regarding\nthe significance of the published preclinical findings, the relevance of such\nfindings to the Company's oncology development programs, the advancement of\nthe Company's Phase 1/2 TNBC clinical trial, and the potential applicability\nof Telomir-Zn across multiple disease areas.\n\nThese forward-looking statements are based on current expectations, estimates,\nforecasts, and projections, as well as management's beliefs and assumptions,\nand are subject to significant risks and uncertainties that could cause actual\nresults to differ materially from those expressed or implied by such\nstatements. These risks and uncertainties include, among others, risks related\nto preclinical and clinical development, the ability to obtain regulatory\napprovals, the outcome of future studies, reliance on third parties,\nintellectual property protection, financing needs, market conditions, and the\nother risks identified under the heading \"Risk Factors\" contained in the\nCompany's Annual Report on Form 10-K and the Company's other filings with the\nU.S. Securities and Exchange Commission (\"SEC\").\n\nForward-looking statements contained in this press release speak only as of\nthe date hereof, and the Company undertakes no obligation to update or revise\nsuch statements, whether as a result of new information, future events, or\notherwise, except as required by applicable law.\n\nWe caution investors not to place undue reliance on the forward-looking\nstatements contained in this press release. You are encouraged to read our\nfilings with the SEC, available at the SEC website and in the \"Investors\"\nsection of our website, for a discussion of these and other risks and\nuncertainties.\n\nContact Information\n\nKrystina Quintana\nEmail: info@telomirpharma.com\nPhone: (786) 396-6723\n\n(https://www.globenewswire.com/NewsRoom/AttachmentNg/cc74273a-ee3e-4dae-8ce1-11b23816056b)\n\n\n\nGlobeNewswire, Inc. 2026"},"type":"article","timestamp":"2026-08-10T12:00:00.789314631Z","server_sent_at_ms":1786363200789},"received_at":"2026-08-10T12:00:00.841Z","source_url":null},"analysis":{"id":"102902","press_release_id":"113902","analysis_json":{"industry":{"label":"Biotechnology","sector":"Health Care"},"redFlags":[],"eventType":"clinical_trial","narrative":"Telomir Pharmaceuticals announced the peer-reviewed publication of preclinical data for its lead asset Telomir-Zn, demonstrating tumor suppression in prostate and triple-negative breast cancer (TNBC) models.\n\nThe study, published in the Journal of Oncology Research and Therapy, shows Telomir-Zn selectively targets cancer cells by depleting intracellular iron to inhibit KDM enzymes, achieving a 50-fold selectivity window over normal cells.\n\nThese findings establish the scientific foundation for the company's planned Phase 1/2 clinical trial in TNBC, for which the company holds an active IND.","sentiment":"bullish","agentHooks":{"shouldPost":true,"suggestedAngle":"Peer-reviewed data validates Telomir-Zn mechanism for TNBC ahead of Phase 1/2 trial."},"keyFigures":{"phaseOfTrial":"Phase 1/2","customDimensions":{"selectivity_window":"50-fold"}},"quotedText":"We're encouraged by the preclinical evidence and eager to test it in patients.","namedEntities":{"people":[{"name":"Dr. Itzchak Angel","role":"Chief Scientific Advisor"},{"name":"Erez Aminov","role":"CEO"}],"products":["Telomir-Zn","Telomir-1"],"companies":[{"name":"Telomir Pharmaceuticals, Inc.","ticker":"TELO"},{"name":"Journal of Oncology Research and Therapy","relationship":"publisher"}],"dollarAmounts":[]},"materialImpact":{"score":3,"reasoning":"Peer-reviewed publication validates the mechanism of action for lead asset Telomir-Zn, showing selective anti-tumor and anti-metastatic activity in preclinical models. This provides the scientific foundation for the upcoming Phase 1/2 trial, representing a significant development milestone for a clinical-stage biotech."},"tickerRelevance":{"others":[],"primary":"TELO"},"globalImportance":25,"audienceRelevance":20,"eventTypeSecondary":[],"importanceComponents":{"tickerTier":"micro-cap","eventGravity":"preclinical_publication","sectorWeight":"biotech"}},"event_type":"clinical_trial","event_type_secondary":null,"sentiment":"bullish","material_impact_score":3,"narrative":"Telomir Pharmaceuticals announced the peer-reviewed publication of preclinical data for its lead asset Telomir-Zn, demonstrating tumor suppression in prostate and triple-negative breast cancer (TNBC) models.\n\nThe study, published in the Journal of Oncology Research and Therapy, shows Telomir-Zn selectively targets cancer cells by depleting intracellular iron to inhibit KDM enzymes, achieving a 50-fold selectivity window over normal cells.\n\nThese findings establish the scientific foundation for the company's planned Phase 1/2 clinical trial in TNBC, for which the company holds an active IND.","key_figures":{"phaseOfTrial":"Phase 1/2","customDimensions":{"selectivity_window":"50-fold"}},"named_entities":{"people":[{"name":"Dr. Itzchak Angel","role":"Chief Scientific Advisor"},{"name":"Erez Aminov","role":"CEO"}],"products":["Telomir-Zn","Telomir-1"],"companies":[{"name":"Telomir Pharmaceuticals, Inc.","ticker":"TELO"},{"name":"Journal of Oncology Research and Therapy","relationship":"publisher"}],"dollarAmounts":[]},"model_name":"glm-4.7","prompt_hash":"sha256:727b4b9429a443af","schema_hash":"sha256:05005c02d9cffac9","created_at":"2026-08-10T15:05:16.283Z","global_importance":25,"audience_relevance":20,"importance_components":{"tickerTier":"micro-cap","eventGravity":"preclinical_publication","sectorWeight":"biotech"}},"durationMs":312997,"modelName":"glm-4.7"}}