Company: TELO
Filing Date: 2025-11-10
Form Type: 10-Q
Source: 0001493152-25-021496
Chunk: 51

Company: Telomir Pharmaceuticals, Inc.
Filing Date: 2025-11-10
Form: 10-Q
Item: Item 8
Chunk 51
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 a molecular “dimmer switch,” turning specific genes on or off. Over time, abnormal methylation patterns can
silence genes that help regulate cell repair, detoxification, or immune balance. Mitochondria are the cell’s energy-producing
structures and are sensitive to oxidative stress, while telomeres are protective DNA caps at the ends of chromosomes that naturally
shorten with each cell division. These systems collectively influence how quickly cells age and maintain healthy function.

Preclinical
studies indicate that Telomir-1 and its zinc-bound form (Telomir-Zn) exhibit selective metal-ion–binding properties. The molecule
demonstrates a high affinity for iron (Fe) and copper (Cu) ions and a lower affinity for zinc (Zn), allowing it to exchange or chelate
excess Fe and Cu while maintaining beneficial zinc balance. This selective exchange mechanism has been associated in laboratory models
with decreased redox stress, improved mitochondrial stability, and modulation of metal-dependent epigenetic enzymes such as histone demethylases
(KDM5, KDM6A/UTX, and JMJD3). These findings suggest that Telomir-1’s biological activity may derive in part from the restoration
of normal metal-ion homeostasis—a process believed to play a key role in oxidative stress, inflammation, and cellular aging.

In
preclinical models, Telomir-1 demonstrated metal-ion–dependent effects on oxidative balance and mitochondrial protection, including
normalization of intracellular calcium release and redox stress and restoration of mitochondrial activity in Progeria fibroblast
models. In an in-vivo Caenorhabditis elegans (C. elegans) longevity assay, Telomir-1 extended lifespan and improved mobility,
suggesting a possible impact on biological-aging rate.

Telomir-1
inhibited several iron- and copper-dependent histone demethylase enzymes (KDM5, KDM6A/UTX, and JMJD3) and in prostate-cancer xenograft
model derived from PC3 cells, reversed promoter hypermethylation of tumor-suppressor and immune-regulatory genes including STAT1, CDKN2A,
GSTP1, MASPIN, RASSF1A, CASP8, and TMS1, restoring pathways associated with apoptosis, detoxification, and immune signaling.

In
oncology research, Telomir-1 reduced tumor growth in a murine xenograft model of aggressive human prostate cancer (