Telomir Pharmaceuticals announces new laboratory findings on Telomir-1

Telomir Pharmaceuticals (TELO) announced new laboratory findings demonstrating that Telomir-1 kills aggressive pancreatic cancer cells. In laboratory studies using human pancreatic cancer cells, Telomir-1 produced a concentration-dependent reduction in cancer cell survival and mitochondrial activity. These data suggest Telomir-1 influences cellular pathways related to energy metabolism and oxidative balance. The findings align with previously reported results in triple-negative breast and prostate cancer models, indicating that Telomir-1 may engage fundamental biological processes involved in cancer cell regulation. Similar to the observation in TNBC, Telomir-1’s effects in pancreatic-cancer cells were partially reversed by iron re-addition, suggesting that Telomir-1’s activity in both TNBC and pancreatic cancer involves iron-dependent processes. The incomplete reversal supports the interpretation that additional metabolic or epigenetic mechanisms are also engaged. Pancreatic-cancer cells are known for metabolic flexibility – the ability to use glucose, lipids, and amino acids to survive in low-oxygen, nutrient-poor environments. TNBC cells, by comparison, rely more heavily on iron-driven oxidative metabolism. The lower sensitivity of pancreatic cells to Telomir-1 in the presence of iron restoration may therefore reflect modulation of broader mitochondrial or energy-control systems, consistent with Telomir-1’s function as an epigenetic modulator. Telomir-1 has previously been shown to influence several tumor suppressor genes and iron-dependent histone demethylases that are also relevant to pancreatic-cancer biology: MASPIN – A “tumor suppressor shield” that regulates cell migration, invasion, and therapy response. Its loss through hypermethylation correlates with poor prognosis in pancreatic and prostate cancers. Telomir-1 has been observed to reduce MASPIN hypermethylation in preclinical models. RASSF1A – A regulator of cell-cycle braking and apoptosis, frequently silenced by promoter methylation in pancreatic, breast, and lung cancers. Telomir-1 has previously decreased RASSF1A methylation in a dose-dependent manner. STAT1 – A master coordinator of immune surveillance. When hypermethylated, tumors can evade immune detection. Telomir-1 has shown modulation of STAT1 methylation status in laboratory models, informing its potential relevance to immune-related control mechanisms. KDM2B and KDM6B – Iron-dependent histone demethylases overexpressed in pancreatic and other aggressive cancers, driving transcriptional reprogramming, inflammation, and stem-like tumor behavior. Telomir-1 has demonstrated inhibitory activity against these enzymes. Together, these previously reported effects provide biological context for Telomir-1’s observed activity in pancreatic cancer models. By modulating genes and enzymes that coordinate DNA-methylation, oxidative stress, and cellular energy regulation, Telomir-1 may offer a unifying framework for understanding shared epigenetic and metabolic vulnerabilities across multiple tumor types.