LOS ANGELES, July 16, 2026 (GLOBE NEWSWIRE) — Trethera Corporation (“Trethera”), a clinical stage biopharmaceutical company developing first-in-class therapies for cancer and autoimmune diseases, today announced a comprehensive peer-reviewed manuscript describing deoxycytidine kinase (dCK) as a promising novel metabolic target that may enable a new class of precision cancer therapies. The article, published in Nucleosides, Nucleotides & Nucleic Acids, reviews decades of scientific study of the deoxyribonucleoside salvage pathway and highlights TRE-515 as the first dCK inhibitor to advance into human clinical testing.
The review describes how many tumors become increasingly dependent on the salvage pathway to maintain DNA precursor pools during rapid proliferation, DNA damage, and therapeutic stress. By selectively inhibiting the salvage pathway’s rate-limiting enzyme dCK, TRE-515 is designed to exploit a metabolic vulnerability that may exist across multiple tumor types while sparing normal tissues that primarily rely on de novo nucleotide synthesis.
The publication summarizes evidence demonstrating that specific genetic alterations—including BRCA2 deficiency and mutant p53—increase tumor reliance on dCK-mediated deoxyribonucleoside salvage. The authors further review emerging preclinical data supporting dCK inhibition in combination with DNA-damaging agents and radiation therapy that cause replication stress, suggesting that nucleotide salvage inhibition may enhance the activity of standard-of-care therapies across multiple tumor types.
“The data linking deoxyribonucleoside salvage to tumor growth and survival are very compelling but underappreciated relative to the historical focus on the de novo synthesis pathway,” said Dr. Peter M. Clark, Professor of Molecular and Medical Pharmacology at the David Geffen School of Medicine at UCLA and publication first author. “This review highlights growing evidence that many tumors also depend on the deoxyribonucleoside salvage pathway under conditions of replication stress and DNA damage.”
“True innovation doesn’t come from improving yesterday’s medicines—it comes from opening entirely new biological pathways for therapy,” said Dr. Ken Schultz, Trethera Chief Executive Officer and publication co-author. “This publication reinforces the growing recognition that targeting dCK represents a new frontier in precision cancer medicine and positions TRE-515 at the forefront of that opportunity.”
The publication also highlights the translational tools supporting TRE-515 development, including pharmacodynamic biomarkers designed to measure dCK activity and pathway inhibition to help guide future clinical studies.
Figure 1: Biochemical pathways for the supply of deoxyribonucleoside triphosphate pools. TRE-515 blocks the salvage pathway, which becomes upregulated during cancer growth and autoimmune disease.
Reference: Clark PM, Thompson CB, Schultz KA. Deoxycytidine kinase inhibition: Rewiring tumor nucleotide metabolism for therapeutic gain. Nucleosides, Nucleotides & Nucleic Acids.
DOI: 10.1080/15257770.2026.2647890. https://pubmed.ncbi.nlm.nih.gov/41889017/
About Trethera and TRE-515
Trethera is a clinical stage, privately held, biopharmaceutical company dedicated to pioneering the development of novel treatments for autoimmune diseases and cancers. Trethera’s innovative approach to targeting nucleotide metabolism led to the development of TRE-515, an orally administered capsule. TRE-515 is a first-in-class clinical-stage drug that inhibits deoxycytidine kinase (dCK), the rate-limiting enzyme in the nucleoside salvage pathway, one of two biosynthetic pathways that generate DNA precursors. It is believed that some forms of cancer may be preferentially dependent on the salvage pathway to support tumor growth, and certain autoimmune diseases might also respond to TRE-515 treatment. The FDA has designated TRE-515 a Fast Track drug for prostate cancer and an Orphan Drug for two autoimmune neurologic diseases. Trethera is developing TRE-515 for use as a monotherapy or in combination to precisely target a metabolic vulnerability of cancer or autoimmune diseases that will transform outcomes for patients.
For more information, please visit us at trethera.com or e-mail Investor Relations at [email protected]. You can also follow Trethera on Facebook and LinkedIn.
Note on Forward-Looking Statements
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