Non-small cell lung cancer (NSCLC) is a challenge to treat. Due in part to the heterogeneous nature of the disease in terms of etiology, histology, pathophysiology, and molecular biology. Nevertheless, recent advances in the understanding of its pathogenesis enable the development of numerous molecular-targeted therapies. Actionable somatic mutations and genomic rearrangements occur frequently in lung adenocarcinoma, the most common histologic type of NSCLC. These alterations can affect critical components of receptor tyrosine kinase (RTK) signaling networks. They include the epidermal growth factor receptor (EGFR), KRAS, and BRAF and their downstream effectors, and lead to dysregulated cellular proliferation and cell-cycle progression. In this study, Mobocertinib is an EGFR inhibitor and an antineoplastic agent.
EGFR is a member of the ErbB family of structurally related RTKs, consisting of the EGFR (ErbB1), as well as human epidermal growth factor receptor 2 (ErbB2; HER2), ErbB3 (HER3) and ErbB4 (HER4). Meanwhile, these proteins form an array of homo- or heterodimers at the cell surface and play a key role in the normal physiological regulation of cellular proliferation. The development and progression of many human cancers involve aberrant ErbB family signaling, including NSCLC. In addition, tumors harboring EGFR mutations are dependent on the activity of the EGFR for their growth and survival.
In summary, the EGFR is a therapeutic target in NSCLC. Approximately 10%-15% and 50% of tumors in Caucasian and Asian patient populations, respectively, harbor mutations in the EGFR. Thus, EGFR tyrosine kinase inhibitors are the first-line standard of care for patients with advanced NSCLC harboring EGFR mutations. Thus, Mobocertinib has great potential for NSCLC.