Roche’s investigational medicine cobimetinib, used in combination with Zelboraf (vemurafenib), helped people with advanced melanoma live significantly longer without their disease worsening

• Data from the coBRIM study will be presented at an upcoming medical meeting
• Roche plans to submit these data to health authorities around the world

Roche (SIX: RO, ROG; OTCQX: RHHBY) announced today that the Phase III coBRIM study met its primary endpoint. The study demonstrated that the investigational MEK inhibitor cobimetinib, used in combination with Roche’s BRAF inhibitor Zelboraf, helped patients with previously untreated BRAF V600 mutation-positive advanced melanoma live significantly longer without their disease worsening (progression-free survival; PFS) compared to Zelboraf alone.¹ Adverse events were consistent with those observed in a previous study of the combination.

“Despite great progress in our understanding and therapy in recent years, advanced melanoma remains a difficult and deadly disease that requires more treatment options,” said Sandra Horning, M.D., Chief Medical Officer and Head of Global Product Development. “These encouraging data support the potential combined use of cobimetinib with Zelboraf to block tumour growth longer than Zelboraf alone. We hope this combination therapy will lead to a new option for patients.”

Data from this pivotal study will be presented at an upcoming medical meeting. Additionally, Roche plans to submit these data to the U.S. Food and Drug Administration, European Medicines Agency, and other health authorities around the world for potential approval.

Cobimetinib is designed to selectively block the activity of MEK,² one of a series of proteins inside cells that make up a signaling pathway that helps regulate cell division and survival.³ Cobimetinib binds to MEK while Zelboraf binds to mutant BRAF, another protein on the pathway, to interrupt abnormal signaling that can cause tumours to grow.^4,5

References

1. Roche data on file
2. Johnston S. XL518, a potent, selective, orally bioavailable MEK1 inhibitor, downregulates the Ras/Raf/MEK/ERK pathway in vivo, resulting in tumor growth inhibition and regression in preclinical models. Poster presented at: AACR-NCI-EORTC Symposium on Molecular Targets and Cancer Therapeutics; October 22, 2007; San Francisco, CA. Abstract C209.
3. Khavari TA, Rinn J. Ras/Erk MAPK signaling in epidermal homeostasis and neoplasia. Cell Cycle. 2007;6:2928-31
4. Safaee Ardekani G, et al. The prognostic value of BRAF mutation in colorectal cancer and melanoma: a systematic review and meta-analysis. PLoS One 2012;7:e47054.
5. Haferkamp S, et al. Vemurafenib induces senescence features in melanoma cells. J Invest Dermatol 2013;133:1601-9