Telomir Pharmaceuticals announces in vitro data on Telomir-1

Telomir Pharmaceuticals (TELO) announced new in vitro findings showing that its investigational compound Telomir-1 kills aggressive human leukemia cells. In this study, HL60 leukemia cells were treated with Telomir-1, which produced a clear, dose-dependent reduction in viable leukemia cells, indicating strong activity in this aggressive human model. Leukemia cells rely heavily on iron as a fuel source to support rapid DNA synthesis, mitochondrial energy production, and uncontrolled proliferation. Many leukemia subtypes increase iron uptake and accumulate excess intracellular iron, creating a metabolic environment that supports tumor growth. Elevated iron also powers iron-dependent epigenetic enzymes that leukemia cells use to silence tumor-suppressor genes-genes that normally regulate growth, promote apoptosis, or assist immune detection. Together, iron overload and epigenetic silencing form two of leukemia’s central biological survival strategies. In previously reported research, Telomir-1 demonstrated the ability to reduce intracellular iron levels in a live-cell human model, where fluorescence imaging with FerroOrange showed a robust, concentration-dependent reduction in ferrous iron relative to the FDA-approved iron chelator Deferoxamine. These findings confirmed Telomir-1’s intracellular penetration and iron-modulating activity at low micromolar concentrations. Because leukemia cells depend so heavily on iron, this type of intracellular iron modulation may be relevant to understanding how cancer cells respond to Telomir-1. Leukemia cells also frequently silence key tumor-suppressor pathways through abnormal DNA methylation and iron-dependent histone demethylases. Although the current leukemia study measured cytotoxicity only, Telomir-1 has previously been shown in a cancer model to reverse hypermethylation of several tumor-suppressor genes-including STAT1, CDKN2A, MASPIN, RASSF1A, CASP8, and GSTP1-genes involved in immune surveillance, apoptosis, detoxification, and cell-cycle braking. These findings demonstrate Telomir-1’s ability to influence epigenetic programs that many cancers, including leukemia, rely on for survival and treatment resistance. In addition, the recent findings that Telomir-1 inhibits three major families of lysin histone demethylase enzymes, belonging to the KDM2, KDM5 and KDM6, reinforce its potential in cancer treatment. KDMs are major epigenetic regulators that control histone methylation and thereby influence transcription, differentiation, and stemness. In leukemia, several KDMs become overexpressed, mutated, or integrated into oncogenic complexes, driving leukemogenesis. Through Telomir’s preclinical research, Telomir-1 has demonstrated activity across pathways involving iron handling, oxidative balance, and epigenetic regulation. The leukemia results add to this growing body of scientific evidence and extend it into cancers of the blood.