Approximately 50% of Taiwanese non-small cell lung cancer patients have EGFR mutations, but relapse after EGFR TKI treatment is common. Our breakthrough research shows that reducing EGFR protein expression via shRNA inhibits growth in over 20 TKI-resistant cell lines. We identified a novel small molecule, 35d, with superior anticancer efficacy by reducing EGFR protein. Combining 35d with TKIs delayed tumor regrowth and extended treatment efficacy in EGFR-mutant TKI-resistant lung cancer.

EGFR-mutated lung cancer relapses and develops drug resistance to traditional EGFR kinase inhibitors, which recurrent disease did not have effective treatments. Our team discovered a new approach targeting total EGFR protein expression to suppress cancer cell growth and overcome resistance. Using small molecule 35d, we reduce EGFR protein levels in drug-resistant lung tumors and show promise for further clinical used. Our discovery offers a potential solution for treating resistant lung cancer.

About 50% of Asia non-small cell lung cancer patients have EGFR mutations, compared to 15% in the West. Most EGFR-mutated patients relapse due to drug resistance after EGFR inhibitor treatment. This product may benefit over 370,000 relapsed patients worldwide annually with EGFR-mutated, inhibitor-resistant lung cancer, either alone or in combination with EGFR inhibitors to delay resistance development. Collaboration with EGFR inhibitor manufacturers is anticipated for joint market development.