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QIAGEN and Amgen to develop tissue-based therascreen® test, paired with investigational treatment AMG 510, to identify patients whose cancers have KRAS G12C mutation
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QIAGEN to pursue global regulatory approvals, including Premarket Approval from FDA
QIAGEN N.V. (NYSE: QGEN; Frankfurt Prime Standard: QIA) today announced a strategic collaboration to develop tissue-based companion diagnostics for Amgen’s investigational cancer treatment AMG 510 to identify patients with cancers that have the KRAS G12C mutation. The agreement focuses initially on companion diagnostics for non-small cell lung cancer (NSCLC) but allows for further development of the tests for Amgen’s other oncology clinical development programs.
“We are pleased to support Amgen by building on the success of our therascreen platform to develop a tissue-based companion diagnostic to identify patients who would benefit from AMG510. QIAGEN’s Sample to Insight workflows and experience in developing diagnostic solutions for Precision Medicine are well-suited to help aid in evaluating patients with non-small cell lung cancer,” said Thierry Bernard, Interim CEO of QIAGEN and Senior Vice President, Head of the Molecular Diagnostics Business Area. “The success of our long-standing collaboration with Amgen is a demonstration of QIAGEN’s capabilities as a preferred partner of pharmaceutical and biotech companies for the creation of companion diagnostics.”
“Amgen is committed to driving broad accessibility to biomarker testing in order to select appropriate patients who will directly benefit from targeted treatments,” said David M. Reese, M.D., Executive Vice President of Research and Development at Amgen. “With one in eight patients with NSCLC having KRAS G12C, there’s a critical need to improve access to high quality diagnostics and more routine screening.”
The therascreen-based companion diagnostic will screen for KRAS G12C, a genetic mutation that is one of the most common causes of cancer. The RAS gene family, studied for almost 40 years, includes the most frequently mutated oncogenes in human cancers with KRAS being the most prevalent driver mutation in NSCLC.
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