Material Event (Form 8-K)

Item 8.01 Other Events

Telomir Pharmaceuticals Reports New Data Showing Telomir-1 Resets Cancer's "Kill-and-Clean" Defense Systems in an Aggressive Prostate Cancer Model, Outperforming Rapamycin and Chemo

New findings highlight Telomir-1's impact on CASP8 and GSTP1, two critical genes that regulate cell-death and glutathione-based detoxification pathways often disrupted in cancer.

On October 22, 2025, Telomir Pharmaceuticals, Inc. (the "Company") reported new preclinical data from an aggressive prostate-cancer model evaluating its investigational compound Telomir-1.

The study focused on DNA methylation, an epigenetic process that influences whether genes are active or silenced, and assessed two additional defense genes central to cancer biology:

CASP8, which regulates apoptosis (programmed cell death), and GSTP1, which encodes glutathione S-transferase Pi 1 - a key enzyme in the body's detoxification system that uses glutathione to neutralize oxidative and chemical stress and help maintain cellular balance.

Apoptosis ("kill") and detoxification ("clean") pathways are two of the body's fundamental defense systems against cancer initiation and progression. The Company believes that modulation of these pathways through DNA-methylation control may represent an important area of ongoing scientific evaluation for Telomir-1 and related oncology research programs.

The study was conducted in mice bearing human aggressive prostate cancer tumor and were treated daily with oral Telomir-1 or reference compounds. On Day 21 of the study, Telomir-1 treatment was associated with reduced DNA methylation of both CASP8 and GSTP1 relative to vehicle and chemotherapy groups, suggesting potential re-activation of apoptosis and detoxification-related gene functions. Chemotherapy alone did not appear to reduce methylation of both genes, while the combination of Telomir-1 and chemotherapy showed lower DNA methylation levels than chemotherapy alone, indicating that combined therapy with Telomir-1 may potentiate chemotherapy related epigenetic effects in this model.

At earlier time points (Day 10), the mTOR pathway inhibitor Rapamycin was associated with an initial reduction in methylation for both genes, consistent with indirect effects on cellular metabolism and oxidative stress. By Day 21, the Rapamycin related effect had partially rebounded, whereas Telomir-1 continued to show a progressive and more sustained decrease in DNA methylation. The Company believes these data help differentiate Telomir-1's epigenetic activity from the effects of Rapamycin and underscore Telomir-1's potential relevance to oncology research.