Company: TELO
Filing Date: 2025-11-10
Form Type: 10-Q
Source: 0001493152-25-021496
Chunk: 20

Company: Telomir Pharmaceuticals, Inc.
Filing Date: 2025-11-10
Form: 10-Q
Item: Item 1
Chunk 20
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 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 (PC3 cells) and decreased
cancer-cell viability in vitro in prostate, pancreatic, and triple-negative breast-cancer cell lines. In aging-related models, Telomir-1
reversed telomere shortening and restored telomere length beyond wild-type levels in an accelerated-aging zebrafish model mimicking Progeria
and Werner syndromes.

14

Additional
preclinical studies demonstrated disease-specific activity in degenerative and metabolic models. In an age-related macular-degeneration
(AMD) model, Telomir-1 restored visual function and retinal structure, reduced oxidative stress, and reconstituted multiple retinal layers,
supporting a potential regenerative mechanism in oxidative retinal injury. In a Wilson’s-disease model, Telomir-1 improved neuromotor
performance, reduced liver-copper accumulation, and normalized hepatic and renal histopathology scores, indicating multi-organ protective
effects distinct from traditional metal-chelating agents. In metabolic models of Type 2 diabetes, Telomir-1 improved glucose metabolism
and insulin sensitivity, consistent with its observed effects on mitochondrial and redox regulation.

Collectively,
these preclinical findings suggest that Telomir-1 may function as a multi-target small-molecule regulator that integrates metal-ion balance,
mitochondrial protection, epigenetic remodeling, and telomere preservation—biological processes thought to underlie aging, cancer,
met