Material Event (Form 8-K)

Item 8.01 Other Events

Telomir Pharmaceuticals Announces New Cancer Data in Aggressive Human Prostate Cancer Cells Showing Telomir-1 Resets DNA Methylation to Reactivate CDKN2A, a Master Tumor Suppressor, Outperforming Rapamycin and Chemotherapy

New preclinical findings highlight Telomir-1's ability to reverse CDKN2A gene silencing by DNA methylation, reactivating this gene - often called the body's natural "cell cycle brake." These results build on prior STAT1 data, supporting Telomir-1's profile as a potential first-in-class broad-spectrum DNA methylation reset therapy.

Telomir Pharmaceuticals, Inc. (NASDAQ:TELO) today reported new preclinical cancer data in aggressive human prostate cancer cell models (PC3 xenografts) showing that Telomir-1 inhibited DNA hypermethylation of CDKN2A, a master tumor suppressor gene often referred to as the body's natural "cell cycle brake."

CDKN2A plays a central role in controlling uninhibited cell growth and initiating programmed cell death, and its silencing is a well-established hallmark of cancer progression.

Telomir-1 outperformed both Rapamycin and chemotherapy in inhibiting DNA hypermethylation of CDKN2A in the in vivo human prostate cancer model. These findings build upon previously reported data showing that Telomir-1 also resets DNA methylation of STAT1, a master immune regulator silenced in aggressive cancers.

Together, the STAT1 and CDKN2A results demonstrate Telomir-1's ability to reset epigenetic silencing across multiple tumor suppressor pathways. This dual effect addresses two of cancer's most fundamental escape mechanisms: unchecked cell proliferation and immune evasion.

Telomir is actively assessing Telomir-1 across multiple aggressive cancers beyond prostate, with additional studies underway. The company's pre-IND program is running in full gear, with CMC activities scaling up toward GMP production and IND-enabling studies ongoing as Telomir moves toward its first IND submission.