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News
Cancer's ability to outsmart treatment may have met its match. Researchers at Baylor College of Medicine developed CS18, an experimental drug that targets a key "biological switchboard" in cancer cells, disabling multiple survival pathways at once. In lab studies, CS18 boosted the effectiveness of existing therapies, reversed drug resistance in lung cancer cells, and slowed tumor growth in animal models — with minimal toxicity to healthy cells.
Cancer's ability to outsmart treatment may have met its match. Researchers at Baylor College of Medicine have developed an experimental drug called CS18 that targets TopBP1-BRCT7/8 — a "biological switchboard" that regulates multiple cancer-promoting pathways simultaneously. By disrupting this central hub, CS18 dials down the activity of key cancer drivers like MYC and mutant p53, reduces DNA repair activity in tumor cells, and nudges cancer cells toward self-destruction.
What makes CS18 especially promising is its performance in combination with existing therapies. When paired with PARP inhibitors or osimertinib, it outperformed either drug alone — and crucially, it restored drug sensitivity in lung cancer cells that had already become resistant to osimertinib. Animal models showed significant tumor growth reduction with no major signs of toxicity.
By the Numbers:
Why it matters: Drug resistance is one of the biggest barriers to effective cancer treatment. A drug that can simultaneously target multiple resistance mechanisms — and potentially restore sensitivity to therapies that have stopped working — could be a game-changer for patients who have run out of options.
