Afatinib

Afatinib tablets are a kinase inhibitor indicated for: ; First-line treatment of patients with metastatic non-small cell lung cancer (NSCLC) whose tumors have non-resistant epidermal growth factor receptor (EGFR) mutations as detected by an FDA-approved test ( 1.1 ) Limitations of Use : Safety and efficacy of afatinib tablets were not established in patients whose tumors have resistant EGFR mutations ( 1.1 ) ; Treatment of patients with metastatic, squamous NSCLC progressing after platinum-based chemotherapy ( 1.2 ) 1.1 EGFR Mutation-Positive, Metastatic Non-Small Cell Lung Cancer Afatinib tablets are indicated.

12.1 Mechanism of Action Afatinib covalently binds to the kinase domains of EGFR (ErbB1), HER2 (ErbB2), and HER4 (ErbB4) and irreversibly inhibits tyrosine kinase autophosphorylation, resulting in downregulation of ErbB signaling. Certain mutations in EGFR, including non-resistant mutations in its kinase domain, can result in increased autophosphorylation of the receptor, leading to receptor activation, sometimes in the absence of ligand binding, and can support cell proliferation in NSCLC.

With Biphasic clearance with 5–11 hr terminal t½ under Afatinib maintenance residence kinetics and ~92% systemic bioavailability (Afatinib) bioavailability, Afatinib undergoes primary p-gp cytochrome processing paired with glucuronide elimination for afatinib and establishes therapeutic activity over initial pharmacodynamic onset within 1–4 hrs (peak cmax) for afatinib.

Standard adult regimens span 40 mg/1 Tablet, Film Coated, 20 mg/1 Tablet, Film Coated, 30 mg/1 Tablet, Film Coated. Prescribers screen specifically against documented intolerance or hypersensitivity reaction involving afatinib (kinase inhibitor); concurrent restricted medications flagged in section 4/7 of the afatinib dailymed monograph (1430446), while community micro-logs most frequently note nausea (12.8% of reports), diarrhea (10.1% of reports), vomiting (6.4% of reports).