Telomir says data shows Telomir-1 resets cancer ‘kill-and-clean’ defense system

Telomir Pharmaceuticals (TELO) reported new preclinical data from an in vivo study in mice bearing human aggressive prostate cancer tumors evaluating DNA-methylation changes in two key defense genes – CASP8 and GSTP1 – following treatment with oral Telomir-1, Rapamycin, chemotherapy, and combination regimens. Apoptosis and detoxification pathways are two of the body’s fundamental defense systems against cancer initiation and progression, and Telomir-1’s observed modulation of these pathways through DNA-methylation control may represent an important area of ongoing scientific evaluation in oncology research. The study examined DNA methylation, a central epigenetic process that helps determine whether genes are active or silenced. In this model, baseline tumor samples exhibited DNA hypermethylation of CASP8 and GSTP1, a pattern often associated with reduced activity in genes involved in apoptosis and detoxification. CASP8 helps initiate programmed cell death. Telomir-1 treatment was associated with reduced methylation of the CASP8 promoter at Day 10 and 21 relative to vehicle and chemotherapy group, suggesting potential reactivation of apoptotic pathway control. GSTP1 encodes glutathione S-transferase Pi 1, an enzyme that uses glutathione- one of the body’s most important natural antioxidants – to neutralize reactive oxygen species and chemical stress. Telomir-1 was associated with decreased DNA-methylation of GSTP1 compared with vehicle and chemotherapy, consistent with partial restoration of this critical detoxification and antioxidant defense system. Chemotherapy did not appear to reduce methylation of either gene, consistent with prior observations that certain cytotoxic agents can reinforce methylation stress – a process that may contribute to taxane resistance driven by transcriptional and epigenetic rewiring. When Telomir-1 was administered with chemotherapy, both CASP8 and GSTP1 showed lower methylation than with chemotherapy alone, suggesting that Telomir-1 may help counteract chemotherapy related epigenetic silencing in this setting. Collectively, these preclinical observations indicate that Telomir-1 influenced two complementary cellular pathways – apoptosis and detoxification – through DNA methylation modulation not observed with chemotherapy and more sustained than that seen with Rapamycin. The data suggest Telomir-1 may act at the level of epigenetic enzyme regulation, whereas Rapamycin’s effects appear secondary to metabolic signaling. Further studies are planned to clarify these mechanisms and their potential relevance for oncology research.