XXXX for the treatment of metastatic @entity1149 .

@entity1 @entity137 @entity3136 @entity4562 @entity1910 @entity470 @entity12379 @entity20570 @entity1149 @entity294 @entity9512 @entity669 @entity58183 @entity3866
Targeting the @entity470 ( @entity470 ) in @entity1 with @entity1149 ( @entity1149 ) harboring sensitizing mutations in the @entity669 kinase (TKI) domain has led to a significant change in the management of this disease. The classic or sensitizing mutations are @entity58183 mutation in exon 18, in-frame deletions or insertion of exon 19, @entity9512 or @entity20570 mutation in exon 21. Approximately 90% of these mutations are exon 19 deletion or exon 21 @entity9512 point mutation. @entity4562 and @entity3866 are reversible first-generation inhibitors of mutant @entity470 , and treatment with these agents in the first-line setting has demonstrated a progression-free survival of 9.5-13.7 months. However, the majority of these @entity1 ultimately develop resistance to these drugs. @entity12379 is an irreversible pan- @entity470 inhibitor that was developed to circumvent the problem of resistance to first-generation TKIs. The LUX-Lung studies have evaluated the efficacy and @entity137 of @entity12379 in treatment-na  ve and refractory @entity1149 @entity1 . The promising results of some of these trials led to approval of @entity12379 by the US Food and Drug Administration for @entity1 with advanced @entity1149 and @entity470 exon 19 deletions or exon 21 ( @entity9512 ) substitution mutations. @entity12379 causes @entity137 similar to those of the first-generation @entity470 TKIs, such as @entity294 , @entity1910 , acne, and @entity3136 , and overall is well tolerated. This article focuses on the clinical studies of @entity12379 in @entity1 with @entity1149 .
