Telomir Pharmaceuticals announces in vitro data on Telomir-1

Telomir Pharmaceuticals (TELO) announced new preclinical data revealing that Telomir-1 potently inhibits three key histone demethylase enzymes-JMJD3, FBXL10, and FBXL11-that regulate gene expression through epigenetic mechanisms. These enzymes are known to influence tumor progression, immune response, metabolic function, and neuroinflammation. The study, conducted in collaboration with Eurofins Discovery, provides further clarity on Telomir-1’s mechanism of action and supports its continued development as a disease-modifying candidate across multiple therapeutic areas. Histone demethylases are upstream regulators of epigenetic silencing and activation. Overactivation of these enzymes can result from genetic amplification, chronic inflammation, or stress signals from the tumor microenvironment. These factors can lead to persistent gene silencing or inappropriate activation of disease-driving genes-contributing directly to tumor growth, immune dysfunction, metabolic imbalance, and neuroinflammation. Key Epigenetic Targets Inhibited by Telomir-1: FBXL11: A key regulator of gene expression, FBXL11 is overactive in several major cancers-including lung, gastric, and ovarian-where it helps tumors grow and avoid immune detection. It has also been linked to conditions like autism and impaired glucose control, highlighting its broader role in disease. FBXL10: A well-known driver of aggressive cancers like leukemia, breast, and pancreatic, FBXL10 enables tumors to resist treatment and maintain stem-like characteristics that fuel growth and recurrence. It also plays a role in metabolic and inflammatory pathways, making it a high-value target for therapies aiming to disrupt the root mechanisms of disease. JMJD3: A central regulator of inflammation and tumor progression, JMJD3 is overexpressed in several aggressive cancers-including prostate, glioma, and ovarian-where it promotes metastasis and immune dysfunction. It also plays a key role in chronic inflammatory, auto-immune and neurodegenerative diseases like lupus and Alzheimer’s, through activation of cytokines such as IL-6 and IL-4, making it a high-priority epigenetic target. These three targets are among the most validated histone demethylases in disease biology but have remained largely undruggable until now. Telomir-1’s ability to inhibit all three reinforces its potential as a broadly applicable therapeutic candidate. These new data build upon previously reported findings demonstrating that Telomir-1 reverses epigenetic gene silencing in aggressive prostate cancer models, specifically reactivating key tumor suppressors like STAT1 and TMS1 in PC3 xenograft studies. In head-to-head preclinical comparisons, Telomir-1 outperformed both Paclitaxel and Rapamycin in reactivating STAT1-delivering more complete demethylation and stronger expression of this critical tumor suppressor gene.