1,2 suggested that the drug works primarily in patients with mutations in the ErbB1 epidermal growth factor receptor. The inner workings of the ErbB receptor family, with its sprawling pathways and multiple phosphatases, had long been a headache for drug makers. That complexity showed itself in this instance, too - sometimes the drug was effective in patients lacking the mutation, or didn't work in people who carried the mutated receptor. The studies presented more questions than they answered. In December 2004, a trial showed that Iressa failed to increase survival in a 1,700-patient clinical trial that AstraZeneca sponsored.
To solve the mystery of why Iressa failed, AstraZeneca hired Bart Hendriks, a biological engineer. Hendriks was a graduate of Doug Lauffenburger's systems biology lab at Massachusetts Institute of Technology, and he had worked on a handful of EGF receptor types for his thesis. The company asked him to ...
