The FDA granted accelerated approval to encorafenib (Braftovi; Array BioPharma/Pfizer), a BRAF inhibitor, in combination with the anti-EGFR mAb cetuximab (Erbitux; Eli Lilly) and the chemotherapy regimen mFOLFOX6 for patients with metastatic colorectal cancer harboring a BRAFV600E mutation. The decision was based on results from the phase III BREAKWATER trial, in which 61% of patients with metastatic disease receiving encorafenib, cetuximab, and mFOLFOX6 responded to the drug regimen, compared with 40% of patients receiving chemotherapy with or without the anti-VEGF mAb bevacizumab (Avastin; Genentech). The approval is the first to be granted under Project FrontRunner, an FDA initiative that aims to encourage drugmakers to seek accelerated approval of drugs as first-line treatments for patients with advanced or metastatic disease. Encorafenib was originally approved to treat inoperable or metastatic melanoma and garnered approval for the treatment of metastatic non–small cell lung canc

The ALK tyrosine kinase inhibitor (TKI) ensartinib (Ensacove; Xcovery) was approved for patients with locally advanced or metastatic ALK-positive non–small cell lung cancer (NSCLC). The decision was based on results from the phase III eXALT3 trial, in which patients with NSCLC who had not already received an ALK TKI took either ensartinib or crizotinib (Xalkori; Pfizer). Median progression-free survival, the study’s primary outcome, was 25.8 months in the ensartinib group and 12.7 months in the crizotinib group. There was no statistically significant difference in overall survival between the two treatment groups.

The cereblon E3 ligase modulator cemsidomide showed activity against multiple myeloma and two types of non–Hodgkin lymphoma in a phase I study.

Interest is growing in the potential of genetically reprogramming B cells to pump out protein-based drugs in patients’ own bodies. An initial report from one company, Be Biopharma, at the American Society of Hematology Annual Meeting and Exposition, provides proof-of-concept, showing that B cells engineered to secrete a bispecific T-cell engager are active in mice with ALL.