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anti-EGFR Drugs

They are drugs that work by blocking the function of the epidermal growth factor receptor (EGFR or Epidermal Growth Factor Receptor and HER-1).

This receptor binding to specific growth factors (e.g. Epidermal Growth Factor Receptor, also known as EGF or Transforming Growth Factor-α o TGF-α) triggers an intracellular transduction mechanism “cascade” that influences the synthesis of DNA, growth and cell survival.

In recent years numerous studies have been conducted to highlight, in different tumors, EGFR alterations in order to identify, in the above cascade of molecular signal, potential therapeutic targets for new drugs.

EGFR is expressed in many solid tumors (e.g. colorectal, pancreatic, lung, breast, genitourinary tract, glioblastoma, head and neck).

The inhibition of the function of this receptor results in a therapeutic potential to inhibit the growth or progression of tumors that express it.

Based on the structure and function of EGFR have been recently developed two different therapeutic strategies:











1. the first uses monoclonal antibodies that affect the extracellular domain of the receptor, thereby blocking the binding site with EGF resulting in inhibition of the processes of growth and progression of cancer cells;












2. the latter determines the block EGFR activation through the use of small molecules that can bind to the tyrosine kinase receptor which is the enzyme responsible for post-receptor signal transduction within the cell.

In various types of cancer are currently being studied and used, among others, the following molecules “organic” that block in these two different ways the activity of EGFR: cetuximab (Erbitux), gefitinib (Iressa), erlotinib (Tarceva).

Importance of the EGFR target and mechanism of action of anti-EGFR (monoclonal antibodies and small molecules)

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