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Telomir Pharmaceuticals Announces Telomir-1 Kills Aggressive Human Leukemia Cells
The findings expand Telomir-1's oncology profile into cancers of the blood, adding to previously reported activity in triple-negative breast, pancreatic, and aggressive prostate cancer models.
Telomir Pharmaceuticals, Inc. (NASDAQ:TELO) ("Telomir" or the "Company"), a preclinical-stage biotechnology company developing small-molecule therapies targeting the epigenetic and metabolic roots of cancer, aging, and age-related disease, today announced new in vitro findings showing that its investigational compound Telomir-1 kills aggressive human leukemia (HL60) cells.
Study Summary
Human HL60 leukemia cells were exposed to Telomir-1 across a range of concentrations. Telomir-1 produced a clear, dose-dependent reduction in leukemia cell viability. HL60 is an established model used to study aggressive forms of acute myeloid leukemia (AML).
Iron Dependence and Epigenetic Silencing in Leukemia
Leukemia is a cancer of the blood and bone marrow marked by uncontrolled growth of abnormal white blood cells. Scientific literature describes how leukemia cells depend heavily on intracellular iron to support DNA synthesis, mitochondrial energy production, and rapid proliferation. Multiple leukemia subtypes accumulate excess iron through increased uptake or reduced efflux.
Iron also serves as a required cofactor for several epigenetic enzymes, including iron-dependent histone demethylases. When dysregulated, these enzymes can contribute to silencing tumor-suppressor genes through abnormal DNA methylation. These processes have been described in the scientific literature as supporting leukemia cell survival, impaired apoptosis, and treatment resistance.
Relevance to Prior Telomir-1 Research
Although the leukemia study measured cell viability only, earlier Telomir-1 research provides important biological context:
Intracellular Iron Modulation
In prior live-cell imaging studies using human cell systems, Telomir-1 produced a marked, concentration-dependent reduction of intracellular Fe²⁺, demonstrating strong cell penetration and significantly greater intracellular iron-lowering activity than Deferoxamine (DFO) at the same concentrations.
DFO is known to act primarily in the bloodstream and extracellular space and has limited ability to penetrate living cells, whereas Telomir-1 was directly observed lowering intracellular iron levels.
Because leukemia cells rely heavily on elevated intracellular iron to fuel DNA replication, mitochondrial activity, and iron-dependent epigenetic enzymes, the ability of a compound to modulate iron inside the cell represents an important biological distinction.
Epigenetic Regulation
In earlier cancer research, Telomir-1 reduced abnormal DNA methylation of several tumor-suppressor genes—including STAT1, CDKN2A, MASPIN, RASSF1A, CASP8, and GSTP1—genes associated with immune surveillance, apoptosis, detoxification, and cell cycle control.
Several of these regulatory mechanisms are described in the scientific literature as highly implicated in leukemia biology. In addition, the recent findings that Telomir-1 inhibits three major families of lysin histone-demethylase (KDMs) enzymes, belonging to the KDM2, KDM5 and KDM6, reinforce its potential in cancer treatment. KDMs are major epigenetic regulators that control histone methylation and thereby influence transcription, differentiation, and stemness. In leukemia, several KDMs become overexpressed, mutated, or integrated into oncogenic complexes, driving leukemogenesis.
Interpretation
Taken together, Telomir-1's observed activity in HL60 leukemia cells, along with previously reported effects involving intracellular iron handling and epigenetic regulation, contribute to a scientific basis for Telomir's ongoing oncology research.
Posted In: TELO