Fig. 3

Typical examples in (epidermal growth factor receptor) EGFR-mutant non-small cell lung cancer (NSCLC) patients successfully treated with furmonertinib 160 mg as salvage treatment who had intracranial progression to prior tyrosine kinase inhibior (TKI). A A female patient had extracranial progression along with newly-diagnosed brain metastases (BM) and leptomeningeal metastases (LM) after first-line chemotherapy and afatinib. A secondary genetic test has shown EGFR exon 19del mutation (73.8%), EGFR exon20 T790M mutation (28.7%), and EGFR amplification (CN = 11.9). The patients then received furmonertinib 160 mg combining with bevacizumab as second-line treatment, and had a significant improvement in dizziness which was related to her central nervous system (CNS) disease. The targeted lesion in her brain had a complete response (CR), and the metastatic cervical lymph nodes also had a partial response (PR). 1) Multiple lesions in brain after first-line treatment; 2) Complete response to furmonertinib; 3) Cervical lymphnodes after first-line treatment; 4) Partial response to furmonertinib. B A male patient diagnosed as advanced EGFR-mutant NSCLC with BM received afatinib as first-line treatment for 14 months, and had an intracranial progression and edema with severe CNS-related symptoms such as fatigue and vomiting. A gene detection at progression showed EGFR exon19 deletion mutation (1.36%) and TP53 mutation (0.85%), whereas no T790M mutation in circulating tumor DNA (ctDNA). The patient then received furmonertinib 160 mg and bevacizumab along with radiotherapy in CNS. The targeted lesion in her brain and the primary lesion in lungs had a PR, and her symptoms were significantly relieved. 1) Multiple lesions in brain after first-line treatment; 2) Partial response to furmonertinib; 3) Primary lesion in lung after first-line treatment; 4) Partial response to furmonertinib