Jonathan Fletcher presented results showing that sorafenib has superior in vitro potency compared with imatinib or sunitinib against a panel of GIST-relevant mutant kinase cell lines and models. They found that unlike sunitinib, sorafenib is active against most imatinib-resistant secondary mutations involving the KIT activation loop (exon 17). In their abstract, Fletcher and Heinrich (Pictured left) suggest that sorafenib should be evaluated for clinical efficacy as a second-line treatment for GIST with a primary KIT exon 11 mutation that has become resistant to imatinib.
This research is funded in part by The Life Raft Group and the GIST Cancer Research Fund and results from collaboration between Oregon Health & Science University and Brigham and Women’s Hospital.
Abstract #: 10500