Topic: New Patent for Detecting Drug Resistance for EGFR Mutant
Dec. 9, 2011, 7:00 a.m. EST
MolecularMD Announces Issuance of Patent Covering Methods for Therapeutic Resistance Monitoring in Lung Cancer Patients
PORTLAND, OR, Dec 09, 2011 (MARKETWIRE via COMTEX) -- MolecularMD Corp. today announces the issuance of a patent titled "Methods and Compositions for Detecting a Drug Resistant EGFR Mutant." The newly issued U.S. Patent is based on the pioneering work of researchers at Memorial Sloan-Kettering Cancer Center to identify causes of resistance in patients treated with epidermal growth factor receptor (EGFR) targeted therapies erlotinib (Tarceva(TM)) or gefitinib (Iressa(TM))(1). MolecularMD has exclusively licensed the commercial rights to this intellectual property which covers methods for detecting the EGFR T790M mutation.
"A high proportion of non-small cell lung cancer (NSCLC) patients treated with erlotinib or gefitinib develop the gatekeeper EGFR T790M mutation. Identifying this mutation with our test will support development of promising next-generation EGFR-targeted therapies critical to overcoming resistance," commented Stephane Wong, Chief Scientific Officer of MolecularMD.
The new U.S. Patent, No. 8,067,175, describes methods of detecting the EGFR T790M mutation as it relates to acquired resistance in patients harboring activating EGFR mutations. Monitoring for the emergence of the EGFR T790M mutation will allow for early identification of acquired resistance and prompt treatment intervention.
About EGFR in Lung Cancer The epidermal growth factor receptor has been identified as a therapeutic target for treatment of solid tumors, as it is involved in proliferation and survival of cancer cells. EGFR is of particular significance in the most common form of lung cancer, non-small cell lung cancer (NSCLC), in which activating mutations of the EGFR gene are key drivers of the disease. Drugs directed at inhibiting the activated EGFR, the tyrosine kinase inhibitors (TKIs) gefitinib and erlotinib, have recently joined the arsenal of oncology therapeutics. Despite initial responses to TKI treatment, unfortunately the clinical utility of these first-generation EGFR inhibitors is short-lived due to acquired resistance. In approximately 50% of cases, this acquired resistance is a result of emergence of the T790M mutation in EGFR.