Telomir Pharmaceuticals announces in vitro data on Telomir-1

Telomir Pharmaceuticals (TELO) announced new in vitro pharmacology results demonstrating that Telomir-1 potently inhibits three members of the KDM5 histone demethylase family. Histone demethylases are upstream gene regulators that cancers exploit to silence tumor suppressors and activate inflammatory programs. Blocking these enzymes has long been viewed as scientifically important but clinically challenging, with KDM5 often described as challenging for development. Cancer and aging are driven in part by the silencing of protective genes that regulate cell growth, repair, and survival. When these genes are inactive, cells lose critical defenses, enabling tumors to expand and age-related decline to progress. This silencing occurs through two major mechanisms: Histone demethylases: Members of the KDM5 family are frequently overactive in cancers. Their role is to erase the “on” marks from tumor suppressor genes. When members of the KDM5 family do this, critical genes that normally stop uncontrolled cell growth, repair damage, or trigger cell death are effectively turned off – leaving cancer cells free to divide and accumulate mutations. KDM5 family members are mainly involved in cell cycle progression, stemness, and cancer drug resistance. Members of the KDM2 and KDM6 families work differently. They remove “off” marks from genes that drive inflammation and cell proliferation. While KDM2 family members are mainly involved in gene repression or silencing, often linked with chromatin remodeling and some anti-cancer effects, the KDM6 family members are known for promoting gene activation which is tightly associated with developmental processes, inflammatory responses, and cancer subtype determination Together, these enzymes push the balance in the wrong direction: shutting down the genes that protect cells while activating the ones that promote disease. DNA methylation: After histone changes switch genes off, a second layer of control reinforces the silence through DNA methylation. This process involves adding small chemical tags directly onto the DNA near gene promoters. When these tags accumulate, the gene is no longer accessible to the cell’s transcription machinery – in effect, the gene is shut down. Importantly, these methylation patterns are copied every time a cell divides, which means the silence is passed on from one generation of cells to the next. In cancer, this permanently disables tumor suppressor genes like CDKN2A and STAT1, removing critical brakes on cell growth and immune defense. In aging, widespread changes in DNA methylation contribute to epigenetic drift – the gradual loss of normal gene regulation that underlies tissue decline and age-related disease. Telomir-1 has now demonstrated the potential to reset both layers of control: In the new in vitro studies, Telomir-1 potently inhibited three members of the KDM5 family, blocking the silencing of protective genes and preventing the activation of harmful inflammatory pathways. Telomir-1 previously demonstrated activity across other families of histone demethylases, including UTX, JMJD3, FBXL10, and FBXL11. These enzymes are associated with cancer progression, stemness, immune evasion, and age-related decline. Telomir-1 was also shown to spare broad acetyltransferases such as GCN5L2, which are associated with systemic toxicity when inhibited. In other previously reported in vivo prostate cancer studies, Telomir-1 reduced abnormal DNA methylation and reactivated tumor suppressors such as CDKN2A and STAT1, with greater activity than chemotherapy and rapamycin.