In silico Molecular Docking Analysis of Afatinib Targeting the Marker Proteins of Lung Cancer

<p>Cancer encompasses a group of diseases marked by the uncontrolled proliferation of cells and their tendency to infiltrate or metastasize to various organs. This progression stems from genetic mutations that interfere with normal cellular regulations. Among the types, Lung cancer ranks as a leading global cause of cancer mortality, claiming more lives than breast, prostate and colorectal cancers combined. Tobacco use remains the most significant risk factor. Common treatments include chemotherapy (cisplatin, carboplatin, and etoposide), targeted therapies (afatinib, erlotinib, and osimertinib) and immunotherapies (pembrolizumab and nivolumab). This investigation focuses on the binding specificity of Afatinib against critical molecular drivers of lungs cancer namely Anaplastic Lymphoma Kinase (ALK), Epidermal growth factor receptor (EGFR), Kirsten rat sarcoma viral oncogene (KRAS), Protein Phosphatase 2A (PP2A), ROS proto-oncogene 1 (ROS1) and Vascular Endothelial Growth Factor (VEGF). Using Schrodinger’s molecular docking tools and computational simulations, the study assessed Afatinib’s interaction potential and pharmacokinetic characteristics. Findings indicate Afatinib exhibits stronger affinity for EGFR and ALK, suggesting its therapeutic promise could be optimized based on target expression within the tumor microenvironment.</p>