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news.A recent study comparing two cancer treatments has shown that although ImClone Systems' Erbitux and AstraZeneca's Iressa both target the same molecule, only Iressa is effective against mutated versions of the particle.
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The two designer cancer drugs appear to perform dramatically differently in a laboratory test comparing their ability to shut down a mutant, overactive growth signal in lung cancer cells.
Although both drugs killed cells containing a normal but overactive EGFR (epidermal growth factor receptor) molecule, only gefitinib (Iressa) killed lung cancer cells containing a mutated EGFR molecule. The monoclonal antibody drug cetuximab (Erbitux) had little affect on the mutant signal, evidently because it strikes at a different part of the EGFR molecule.
The researchers say that the divergent results add to growing evidence that mutations in the targets of designer drugs critically influence their effectiveness.
Iressa and Erbitux both are designed to suppress an overexpressed, or overactive, EGFR signal that spurs growth in several types of cancer. In most forms of the disease, including lung cancer of the non-small-cell type, and colorectal cancer, the abnormal signals are generated by a normal EGFR molecule.
In a small percentage of patients with non-small-cell lung cancer (NSCLC), the overactivity stems from a mutant EGFR protein: those patients tend to have a better outlook, and Iressa and Tarceva (produced by OSI Pharmaceuticals), are particularly effective for them.
The research suggests that to inhibit the growth of mutated EGFR the drug needs to inhibit the area of the EGFR molecule that sits within the cell. As Erbitux is a monoclonal antibody drug that binds to a portion of the EGFR receptor that extends outside the cell, it is ineffective against such mutations.