EGFR Inhibitor — Targeted Cancer Therapy

Epidermal growth factor receptor (EGFR) inhibitors are specialised medicines developed to interfere with a cell-surface receptor protein that regulates cell survival and proliferation. In healthy tissue, EGFR acts as an on-off switch that tells cells when to grow and divide. However, genetic alterations can cause this receptor to remain permanently active, triggering rapid tumour progression.

EGFR inhibitors generally fall into two broad classes: small-molecule tyrosine kinase inhibitors (TKIs) and monoclonal antibodies. TKIs, such as osimertinib and erlotinib, work inside the cell to stop intracellular signalling pathways. Monoclonal antibodies, such as cetuximab and panitumumab, attach to the outer part of the receptor on the cell surface, preventing growth factors from binding and activating it. Together, these therapies provide a focused mechanism to disrupt tumour biology without the widespread cellular damage often associated with traditional chemotherapy.

EGFR inhibitors represent an important shift towards personalised oncology. For patients whose tumours carry specific EGFR mutations or overexpress the protein, these drugs can offer effective disease control while often sparing them some of the conventional side effects of cytotoxic chemotherapy. Knowing whether a tumour responds to an EGFR inhibitor allows clinical teams to select the most appropriate first-line treatment. It also guides long-term management, because tumours can develop resistance over time, prompting oncologists to switch to newer-generation inhibitors or alternate treatment combinations to sustain tumour control and maintain quality of life.

Before prescribing an EGFR inhibitor, doctors test tumour tissue or blood for specific genetic changes. Next-generation sequencing (NGS) and polymerase chain reaction (PCR) tests look for activating EGFR mutations in non-small cell lung cancer. In colorectal cancer, testing focuses on KRAS, NRAS, and BRAF genes, because mutations in these downstream pathways render EGFR inhibitors ineffective. When tissue biopsies are difficult to obtain safely, a liquid biopsy using circulating tumour DNA (ctDNA) from a standard blood draw can detect relevant EGFR alterations and identify resistance mutations such as T790M or C797S.

EGFR inhibitors are most widely used in non-small cell lung cancer (NSCLC), particularly in tumours harbouring sensitising EGFR mutations such as exon 19 deletions or L858R. They are also central to the management of metastatic colorectal cancer, where monoclonal antibodies targeting EGFR are given to patients whose tumours have wild-type (non-mutated) KRAS and NRAS genes. Additionally, these targeted drugs play an established therapeutic role in squamous cell carcinoma of the head and neck, as well as selected cases of advanced pancreatic cancer.

The presence of sensitising EGFR mutations often establishes EGFR TKIs as the preferred first-line systemic therapy in advanced lung cancer, frequently delaying the need for intravenous chemotherapy. In colorectal cancer, anti-EGFR monoclonal antibodies are combined with chemotherapy regimens like FOLFOX or FOLFIRI, or used as monotherapy in later lines. Common side effects of these agents include acne-like skin rashes, diarrhoea, paronychia, and fatigue. Clinical teams monitor these symptoms closely, adjusting doses or providing supportive dermatology treatments to keep patients comfortable throughout their therapy course.