EGFR-mutant Non-Small Cell Lung Cancer (NSCLC)
Typically, targeted therapies act on specific proteins that have become altered (mutated) and are not functioning properly within the cancer. The epidermal growth factor receptor (EGFR) is found to be mutated in 10-15% of Caucasian and as many as 50% of Asian patients with lung cancer.
Tyrosine kinase inhibitors (TKIs) can inhibit the mutated EGFR, stopping cells from dividing, and blocking or reducing tumor growth.
Mutations in the EGFR protein cause cells to divide uncontrollably. Drugs known as tyrosine kinase inhibitors (TKIs) can inhibit mutated EGFR, stopping cells from dividing, and thereby blocking or reducing cancer growth. While several TKIs are available to treat EGFR-mutant NSCLC, these drugs are not effective in all patients. Furthermore, overtime NSCLC cells often develop mechanisms to bypass the anti-cancer effects of some TKIs so patients no longer benefit from them. Consequently, new drugs are needed to ensure every patient with NSCLC has access to an effective treatment.
While several therapies have been approved for the treatment of EGFR-mutant NSCLC, significant unmet needs remain.
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For detailed information about completed and ongoing clinical studies for Abivertinib (AC0010), ACEA’s EGFR-inhibitor, please visit www.clinicaltrials.gov.