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Boehringer Ingelheim will present new data on the company’s two lead oncology compounds, BIBW 2992 and BIBF 1120, at the 2009 Annual Meeting of the American Society of Clinical Oncology (ASCO), the company announced today.
Two studies in the LUX-Lung clinical development programme for BIBW 2992 and a phase II study of BIBF 1120 in ovarian cancer patients will be presented.
LUX Lung 2 interim results
Interim phase II data from the LUX-Lung 2 study suggest BIBW 2992 has anti-tumour activity in advanced second-line non-small cell lung cancer (NSCLC) patients who have epidermal growth factor receptor (EGFR) mutations.
Interim phase II data from the LUX-Lung 2 study suggest BIBW 2992 has anti-tumour activity in advanced second-line non-small cell lung cancer (NSCLC) patients who have epidermal growth factor receptor (EGFR) mutations.
“Lung cancer kills more people than any other cancer. The LUX-Lung 1 and 2 studies represent an opportunity to investigate BIBW 2992 across a range of different patient populations,” said Dr Manfred Haehl, Corporate Senior Vice President Medicine at Boehringer Ingelheim.
“The preliminary data from the LUX-Lung 2 study suggests that BIBW 2992 may have activity in the second-line setting among NSCLC patients with EGFR mutations, which is encouraging news.”
BIBW 2992 is an orally administered irreversible dual inhibitor of the epidermal growth factor receptor (EGFR) and human epithelial receptor 2 (HER2) tyrosine kinases. It is the first irreversible EGFR-TKI (tyrosine kinase inhibitor) to reach phase III for third/fourth-line NSCLC.
In the emerging era of personalised cancer medicine, Boehringer Ingelheim is one of the first companies to prospectively identify appropriate patients for clinical trials based on biomarkers. As part of the LUX-Lung clinical development programme, Boehringer Ingelheim is evaluating BIBW 2992 in NSCLC patients who test positive for EGFR activating mutations.
“It is well documented that ‘activating’ mutations that arise in the tyrosine kinase (TK) domain of the EGFR gene are associated with an increased sensitivity to first-generation EGFR TKIs. The majority of patients who initially respond to EGFR TKIs such as gefitinib or erlotinib will eventually develop resistance, often through gaining another mutation, such as the so-called T790M resistance mutation,” said Dr Haehl.
