TELO 8-K
Telomir Pharmaceuticals, Inc. (TELO)
UNITED STATES
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WASHINGTON, D.C. 20549
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Item 8.01 Other Events
Telomir Pharmaceuticals Reports That Telomir-1 Outperforms FDA-Approved Gold-Standard Iron Chelator Deferoxamine (DFO) in Reducing Intracellular Iron in a Human Cell Line
New live-cell imaging data show that Telomir-1 markedly lowers intracellular iron levels at submicromolar concentrations in human keratinocytes, demonstrating potent cell penetration and iron-modulating activity—key to its broader epigenetic mechanism of action.
Telomir Pharmaceuticals, Inc. (NASDAQ: TELO) (“Telomir” or the “Company”) reports new preclinical data demonstrating that its lead investigational compound Telomir-1 produced a strong, dose-dependent reduction of intracellular iron in human keratinocyte (HaCaT) cells, significantly exceeding the effect observed with the FDA-approved iron chelator Deferoxamine (DFO).
These results extend the Company’s research into the relationship between metal-ion imbalance, oxidative stress, and epigenetic enzyme regulation.
Study Overview
The evaluation utilized FerroOrange, a fluorescent probe that selectively detects ferrous iron (Fe²⁺) in living cells. HaCaT cells were incubated with Telomir-1 or DFO at several time points. After three, six and sixteen hours, fluorescence microscopy showed substantially lower intracellular iron signal intensity in Telomir-1–treated cells at various concentrations, indicating greater cellular penetration and iron-modulating activity relative to DFO at the same concentrations.
Scientific Context and Importance of the Findings
Iron plays a vital role in human biology. It enables oxygen transport, mitochondrial energy generation, and DNA synthesis—processes essential for growth and cellular development. In early life, iron is beneficial and tightly regulated by proteins such as ferritin, transferrin, and ceruloplasmin that maintain balance between storage, transport, and utilization.
With aging, however, these control systems become less efficient. Reactive forms of iron can accumulate within cells, participating in chemical reactions that generate reactive oxygen species (ROS) capable of damaging DNA, proteins, and membranes. This imbalance contributes to oxidative stress, mitochondrial dysfunction, and genomic instability—factors increasingly associated with accelerated aging, neurodegenerative, metabolic, cardiovascular, and oncologic diseases.
Cancer biology further highlights the dual nature of iron. Many tumors depend on iron for rapid proliferation, using it to drive DNA replication, sustained proliferation and energy production. Yet excessive intracellular iron also amplifies oxidative and methylation stress, disrupting normal gene regulation and potentially promoting disease progression.
Understanding how to safely modulate intracellular iron levels is therefore an important area of pre-clinical research. The ability of Telomir-1 to enter cells and influence iron balance at low concentrations provides a basis for continued investigation into metal-ion homeostasis and its link to cellular health and epigenetic control.
Key Observations
| ● | Telomir-1 reduced intracellular Fe²⁺ levels in a time- and dose-dependent manner at low-micromolar concentrations. | |
| ● | Deferoxamine (DFO), while FDA-approved, exhibited limited intracellular activity under equivalent conditions. | |
| ● | Telomir-1 has also been formulated with zinc (Telomir-Zn) to enable a controlled intracellular exchange of metal ions—binding excess reactive metals such as iron and copper while contributing zinc, a cofactor for enzymes involved in antioxidant defense and DNA stability. |
These data support the Company’s ongoing pre-clinical research focused on metal-ion balance, oxidative stress, and epigenetic enzyme dynamics in aging and degenerative disease.
SIGNATURES
Pursuant to the requirements of the Securities Exchange Act of 1934, the registrant has duly caused this report to be signed on its behalf by the undersigned hereunto duly authorized.
| TELOMIR PHARMACEUTICALS, INC. | ||
| Dated: November 12, 2025 | By: | /s/ Erez Aminov |
| Name: | Erez Aminov | |
| Title: | Chief Executive Officer | |