Telomir says Telomir-1 selectively kills agressive TNBC cells

Telomir Pharmaceuticals (TELO) announced new findings demonstrating that Telomir-1 significantly decreases the viability of aggressive triple-negative breast cancer 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 caused a clear, dose-dependent reduction in cancer cell survival. As concentrations increased, more cancer cells lost their ability to grow and survive. When researchers added iron back to the system, the cells recovered, confirming that Telomir-1’s activity depends on 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, 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.