This new drug could break cancer’s resistance to treatment — SkimNews
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- CS18, an experimental drug developed at Baylor College of Medicine and published in Science Advances, targets TopBP1 — described as a "biological switchboard" that regulates multiple cancer-promoting pathways at once
- CS18 binds specifically to the BRCT7/8 switch on TopBP1, which interacts with cancer regulators including MIZ1, mutant p53, PLK1, and CIP2A; binding decreased MYC and mutant p53 activity, dampened DNA repair proteins, and increased cancer cell death
- Researchers observed these effects across triple-negative breast cancer, ovarian cancer, lung adenocarcinoma, lung squamous cell carcinoma, and acute myeloid leukemia, with CS18 showing less toxicity to non-cancerous cells
- CS18 combined with existing PARP inhibitors or osimertinib killed cancer cells more effectively than either treatment alone, and in osimertinib-resistant lung cancer cells, adding CS18 restored sensitivity to the drug
- Animal models showed significant tumor growth reduction with no major weight loss or other signs of toxicity, supporting further development as a component of combination cancer therapies
- The study was supported by NIH grants (R01CA203824, R01CA269971, T32CA174647, T32GM136560), multiple Department of Defense grants, a Rivkin Center for Ovarian Cancer Pilot Award, and a Taiwan Ministry of Science and Technology grant
Why it matters: For patients whose tumors have stopped responding to osimertinib or PARP inhibitors, CS18's ability to restore drug sensitivity could meaningfully extend the useful life of existing therapies across at least five cancer types. The results remain preclinical — tested only in cells and animal models — so human trials and years of development still separate this from any clinical use.
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