TELO News & Events

Telomir Pharmaceuticals announced new in vitro data demonstrating that Telomir-1 induces broad tumor cell mortality across biologically distinct subtypes of triple-negative breast cancer. Iron-rescue experiments confirmed that the observed tumor cell mortality is iron-dependent, directly supporting Telomir-Zn's proposed intracellular metal-modulating mechanism and distinguishing the effect from nonspecific cytotoxicity. Triple-negative breast cancer is an aggressive and molecularly heterogeneous disease lacking estrogen receptor, progesterone receptor and HER2 expression. Although chemotherapy, immunotherapy, PARP inhibitors, and antibody-drug conjugates have expanded available treatment options, outcomes in metastatic and treatment-resistant TNBC remain limited, and relapse rates remain high. Many TNBC tumors exhibit elevated intracellular iron levels and heightened oxidative stress, creating a biological reliance on redox-active metals to sustain proliferation and epigenetic modifications. Telomir-Zn is designed to modulate intracellular metal balance by reducing labile redox-active iron while increasing zinc availability. In the newly reported studies, tumor cell mortality observed across TNBC models was significantly attenuated when supplemental iron was introduced, confirming that the effect is mechanistically linked to disruption of tumor iron dependency. The study, conducted in collaboration with Pharmaseed, is evaluating five human TNBC cell lines representing distinct molecular subtypes. Three models have been completed to date: MDA-MB-468 - Near-complete tumor cell mortality at 72 hours HCC70 - Significant partial mortality MDA-MB-231 - Significant partial mortality Two additional models, BT-549 and HCC1806, are currently under evaluation. Across all completed models, supplemental iron significantly reduced Telomir-Zn-induced tumor cell death. The variability in magnitude of response across subtypes is consistent with the established biological heterogeneity of TNBC.

Telomir Pharmaceuticals 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. To 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.

Telomir Pharmaceuticals announced results from a completed efficacy study evaluating Telomir-1 in zebrafish tumor xenograft animal models of triple-negative breast cancer. The study was conducted in collaboration with BioReperia using its ZTX ONCOLEADS platform. In one of these animal models, Telomir-1 demonstrated statistically significant reductions in primary tumor growth and in the spread of cancer cells beyond the primary tumor in an aggressive TNBC model with limited responsiveness to the chemotherapy agent paclitaxel. In a separate aggressive TNBC model where paclitaxel demonstrated antitumor activity, Telomir-1 produced a comparable reduction in primary tumor growth as a monotherapy, and the combination treatment with Telomir-1 and paclitaxel resulted in greater tumor growth inhibition than either agent alone. Representative zebrafish tumor xenograft images from the BT549 xenografts and HCC1806 triple-negative breast cancer models illustrating primary BT549 xenografts tumor size and cancer cell spread of HCC1806 cells. Images compare untreated control tumors with tumors treated with Telomir-1, demonstrating reduced primary tumor burden and reduced dissemination of cancer cells beyond the primary tumor site. Images are representative of quantified and statistically analyzed results reported in this study. Telomir-1 demonstrated statistically significant tumor growth inhibition in aggressive TNBC models representing an estimated 40-60% of TNBC cases. Telomir-1 demonstrated statistically significant reduction in cancer cell spread in an aggressive TNBC model with limited chemotherapy responsiveness. In a broadly treatment-resistant TNBC subtype representing an estimated 15-25% of cases, neither Telomir-1 nor chemotherapy produced measurable effects, underscoring the biological specificity of response and providing important guidance for patient selection and clinical trial design. Combination treatment with paclitaxel enhanced tumor growth inhibition in models responsive to Telomir-1. Importantly, the observed biology-driven activity and lack of effect in broadly treatment-resistant models provide valuable guidance for patient selection and trial design, which may improve the likelihood of observing clear clinical benefit in future studies.