"Securing this NIH lung cancer grant continues our multiple indication momentum, coming less than six months after receiving FDA Fast Track designation for prostate cancer. Such dual external validations are rare and substantiate the strength of our scientific rationale and clinical observations," said Dr. Ken Schultz, Chairman and CEO of Trethera. "Combining TRE-515 with targeted KRAS therapies, is intended to exploit a metabolic vulnerability in NSCLC and address the significant unmet need for the 60% of patients who do not respond to KRASi monotherapy and those who experience relapse."
TRE-515 inhibits deoxycytidine kinase (dCK), the key enzyme for the nucleoside salvage pathway that becomes activated and essential for abnormal cell growth in autoimmune diseases and cancer. Consistent with observations that dCK activity is relatively minimal in the regulated cell division of healthy cells, inhibiting dCK with TRE-515 has demonstrated favorable safety in addition to clinical benefit in ongoing first-in-human trials.
Estimates by the World Health Organization indicate that more than 2.5 million new cases and 1.8 million deaths from lung cancer occurred globally in 2024. While FDA approved KRAS inhibitors have transformed the NSCLC market, KRASi have a 40% response rate. Thus, 6 of 10 patients experience no clinical benefit from the treatment. Furthermore, those patients who do benefit from KRASi therapy find their results transient, with an average duration of 8-10 months before tumor growth resumes.
When treated with KRAS inhibitors alone, cancer cells can escape destruction by using the salvage pathway to gather additional nucleosides to repair the DNA damage. Combining TRE-515 with KRAS targeting drugs synergistically cripples the ability of cancer cells to grow or recover from DNA damage and enhances the therapeutic response.
"We are excited to receive this grant award, which underscores the ...
