Abstract
The echinoderm microtubule-associated protein-like 4-anaplastic lymphoma kinase (EML4-ALK) fusion gene is observed in 4–5% of non-small cell lung cancer (NSCLC) (1). The first-generation ALK-targeted tyrosine kinase inhibitor (TKI), crizotinib, showed significantly better objective responses rates (ORR) and longer progression free survival (PFS) than the standard platinum doublet chemotherapy in those patients (median PFS: 10.9 vs . 7.0 months, respectively; hazard ratio for progression or death with crizotinib: 0.45; ORR: 74% vs . 45%, respectively) (PROFILE 1014) (2). Now, ALK-TKI is considered as the first line standard treatment for patients with newly diagnosed advanced ALK-fusion gene positive NSCLC. Ceritinib is a next-generation, selective ALK inhibitor, approximately 28 to 39 times more potent than crizotinib against ALK-positive NSCLC cells. Moreover, ceritinib overcame several acquired crizotinib-resistant ALK mutations in vitro and in vivo (3).
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