Company will work with BMS on a melanoma drug and with Clovis on a companion diagnostic.
Roche inked two deals today with Bristol-Myers Squibb (BMS) for development of a melanoma treatment and separately with Clovis Oncology to develop a companion diagnostic for Clovis’ non-small-cell lung cancer (NSCLC) drug candidate.
BMS and Roche will conduct a Phase I/II study to evaluate the combination of BMS’ approved melanoma drug called Yervoy and Roche’s investigational vemurafenib in patients with a specific type of late-stage melanoma. “If appropriate, the companies may conduct further development of the combination,” according to BMS.
Vemurafenib is an oral BRAF inhibitor. Yervoy is a recombinant, human mAb that blocks the cytotoxic T-lymphocyte antigen-4 (CTLA-4) by binding to it and blocking the interaction of CTLA-4 with its ligands, CD80/CD86. Blockade of CTLA-4 has been shown to augment T-cell activation and proliferation.
On March 25, FDA approved Yervoy for patients with unresectable or metastatic melanoma, at a dosage of 3 mg/kg administered intravenously over 90 minutes every three weeks, for a total of four doses. According to BMS, Yervoy is the first and only therapy approved for unresectable or metastatic melanoma to demonstrate a significant improvement in overall survival based on results from a randomized, double-blind Phase III study that included 676 patients with unresectable or metastatic melanoma who were previously treated with one or more of the following: aldesleukin, dacarbazine, temozolomide, fotemustine, or carboplatin.
Separately with Clovis Oncology, Roche will work to develop an in vitro PCR-based companion diagnostic to identify activating epidermal growth factor receptor (EGFR) mutations in patients with NSCLC, including the EGFR T790M mutation. The EGFR mutation assay will run on Roche’s cobas 4800 clinical laboratory system.
Clovis has a preclinical stage NSCLC candidate called CO-1686, which is being developed under a license from Avila Therapeutics. It is designed to target and covalently bind to the activating and T790M mutant forms of EGFR, while also sparing wild-type EGFR and may thus treat refractory NSCLC while minimizing dose-limiting side effects.