Telomir Pharmaceuticals (TELO) announced new preclinical results showing that its lead compound, Telomir-1, restored mitochondrial function without triggering oxidative stress or cell proliferation in human cells derived from a patient with Hutchinson-Gilford Progeria Syndrome. The study was conducted in collaboration with Smart Assays Biotechnologies. Researchers used a Progeria human fibroblast cell line that models the mitochondrial dysfunction, oxidative stress, and premature aging associated with this rare genetic disorder. In this Progeria model, Telomir-1: Significantly increased mitochondrial energy production: Indicating improved energy generation in metabolically compromised cells-a fundamental requirement for cellular repair and function. Did not increase the number of live cells: Suggesting Telomir-1 restored energy without triggering cell division, which may offer important safety advantages in fragile or genetically damaged cells. Reduced reactive oxygen species under both basal and metal-induced stress conditions: ROS are damaging molecules linked to mitochondrial dysfunction and cellular decline. In this model, reducing ROS is especially important, as oxidative stress contributes to degeneration in genetically unstable cells such as those seen in Progeria and other mitochondrial-driven diseases. Showed a stronger effect in Progeria cells than in healthy fibroblast controls: Indicating a potentially selective effect in diseased tissue, with reduced risk of unwanted stimulation in healthy cells.
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