Genmab's HuMax-EGFr shows broad potential in cancer treatment
In a novel cancer cell laboratory model, HuMax-EGFr effectively inhibited the growth of tumor cells that express both mutated or normal EGF receptors. This inhibition occurred through different mechanisms of action including direct inhibition of cancer cell growth and an immune cell-mediated killing activity known as antibody dependent cell-mediated cytotoxicity (ADCC).
Genmab scientists also used the model to test the effects of tyrosine kinase inhibitors (TKI) such as the marketed products Iressa and Tarceva on EGFr-expressing tumor cells. Tumor cells expressing various mutated EGFr varied strongly in their sensitivity to TKI therapy, whereas no differences in efficacy where observed for HuMax-EGFr.
"This pre-clinical data indicates that HuMax-EGFr may have more potential in the treatment of some types of cancer, such as lung cancer, than tyrosine kinase inhibitors," said Lisa N. Drakeman, Ph.D., Chief Executive Officer of Genmab.
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