Material Event (Form 8-K)

Item 8.01 Other Events

Telomir Pharmaceuticals Announces In Vitro Data Showing Telomir-1 Targets Additional Histone Demethylase Families, a Unique Profile in Cancer and Aging Not Seen in Other Therapies

New in vitro results show Telomir-1 adds KDM5 family inhibition to its previously reported KDM2/KDM6 and DNA methylation activity, potentially representing a novel frontier in epigenetic therapy where no existing candidates have shown comparable breadth.

Telomir Pharmaceuticals, Inc. (NASDAQ: TELO) today 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.

In cancer and aging, the silencing of protective genes occurs through two major mechanisms. First, histone demethylases act as switches: proteins of the KDM5 family erase activation marks from tumor suppressor genes and remove repressive marks from genes that drive proliferation and inflammation. Together, these enzymes disable cell-protective pathways and enhance harmful ones. Second, DNA methylation then reinforces the silencing by adding chemical tags to gene promoters, locking tumor suppressors in an inactive state making the silence durable and heritable as cells divide.

In the new in vitro studies carried out by Eurofins Discovery, Telomir-1 inhibited three members of the KDM5 family, thereby blocking the silencing of protective genes and preventing the activation of harmful inflammatory pathways.

In addition to these findings, Telomir-1 has previously demonstrated activity across other families of histone demethylases, including UTX (KDM6A), JMJD3 (KDM6B), FBXL10 (KDM2B), and FBXL11 (KDM2A). 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.

Taken together, these results indicate that Telomir-1 has demonstrated broad-spectrum activity across both DNA methylation and several histone demethylation pathways, the two fundamental axes of epigenetic control. The company continues to advance IND-enabling studies and GMP scale-up of Telomir-1, with additional preclinical evaluations ongoing across aggressive cancers and models of aging.