Telomir Pharmaceuticals announces new preclinical data on Telomir-1

Telomir Pharmaceuticals (TELO) reported new preclinical findings demonstrating that its lead therapeutic candidate, Telomir-1, reduced PSA levels in androgen-responsive human prostate cancer cells. PSA is one of the most widely used and FDA-accepted clinical biomarkers in evaluating prostate cancer treatment activity. PSA is a protein secreted by prostate cancer cells, and elevated PSA levels generally correlate with increased tumor burden and tumor activity. Demonstrating a reduction in PSA in vitro provides additional biological context relevant to Telomir-1’s ongoing preclinical characterization. In an in vitro study conducted by SmartAssays, LNCaP prostate cancer cells were stimulated with dihydrotestosterone, a potent androgen that increases PSA production. Under these conditions, Telomir-1 produced a concentration-related reduction in PSA release, paralleling its inhibitory effects on cellular energy metabolism and cell viability. These in vitro PSA findings are consistent with previously reported Telomir-1 activity in a mouse model implanted with aggressive, non-androgen responsive human prostate cancer cells. In that model, Telomir-1 demonstrated a measurable anti-tumor effect, including approximately 50% reduction in tumor volume when administered as a single agent. In the combination arm of paclitaxel plus Telomir-1, tumor volume was fully reduced, and no mortality occurred. By comparison, paclitaxel alone also resulted in full tumor-volume reduction but was associated with mortality in the study cohort. The PC3 model represents an androgen-independent tumor type, meaning the cancer cells no longer rely on hormones like testosterone to grow and are generally more aggressive and treatment-resistant. The PSA reductions observed in this new study were generated in androgen-responsive LNCaP cells, which depend on androgen signaling and reflect clinically relevant prostate cancer biology. Together, these datasets indicate that Telomir-1 has shown preclinical activity in both hormone-responsive and hormone-resistant prostate cancer models, based on epigenetic, metabolic, and viability-related measures.