Company: TELO
Filing Date: 2025-11-10
Form Type: 10-Q
Source: 0001493152-25-021496
Chunk: 19

Company: Telomir Pharmaceuticals, Inc.
Filing Date: 2025-11-10
Form: 10-Q
Item: Item 1
Chunk 19
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, and copper, Telomir-1 may help protect against age related conditions, including Progeria (a rare genetic disorder
that causes rapid aging in children), Wilson’s disease (a genetic disorder leading to toxic copper buildup in the body), and Age-related
Macular Degeneration (AMD), as well as Type 2 diabetes, cancer, and Alzheimer’s disease.

Telomir-1
Program Overview

Telomir-1
is an investigational, orally administered small-molecule candidate designed to target fundamental biological processes believed to contribute
to aging, cancer, metabolic, and other age-related diseases. The compound acts as a regulator of essential metal ions and an epigenetic
modulator, influencing cellular pathways that govern oxidative stress, mitochondrial function, DNA methylation, and telomere maintenance—core
mechanisms broadly implicated in degenerative, inflammatory, metabolic, and oncologic conditions.

Epigenetics
refers to the way cells control gene activity without altering the underlying DNA sequence. One important epigenetic process, DNA methylation,
functions as 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