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Second targeted combination regime approved for metastatic melanoma
Researchers are increasingly looking to rational combinations of drugs to meet the challenge of resistance to molecularly targeted anticancer therapies. The treatment of metastatic melanoma was significantly advanced with the development of BRAF inhibitors, but is still limited by the short-lived nature of the responses to these drugs and the almost universal occurrence of tumor regrowth. More durable responses could be produced by targeting multiple points in the mitogen-activated protein kinase (MAPK) signaling pathway of which BRAF is a central component. In the fall of 2015, the MEK inhibitor cobimetinib and BRAF inhibitor vemurafenib became the second such combination to receive regulatory approval in the United States following positive results from the international, phase 3, randomized coBRIM trial, which demonstrated the superiority of the combination over single-agent BRAF inhibitor therapy. It also marked the first US approval for cobimetinib.1
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Issue
The Journal of Community and Supportive Oncology - 14(2)
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Page Number
51-53
Legacy Keywords
melanoma, cobimetinib, vemurafenib, molecularly targeted anticancer therapies, metastatic melanoma, BRAF inhibitors, mitogen-activated protein kinase, MAPK, MEK inhibitor
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Researchers are increasingly looking to rational combinations of drugs to meet the challenge of resistance to molecularly targeted anticancer therapies. The treatment of metastatic melanoma was significantly advanced with the development of BRAF inhibitors, but is still limited by the short-lived nature of the responses to these drugs and the almost universal occurrence of tumor regrowth. More durable responses could be produced by targeting multiple points in the mitogen-activated protein kinase (MAPK) signaling pathway of which BRAF is a central component. In the fall of 2015, the MEK inhibitor cobimetinib and BRAF inhibitor vemurafenib became the second such combination to receive regulatory approval in the United States following positive results from the international, phase 3, randomized coBRIM trial, which demonstrated the superiority of the combination over single-agent BRAF inhibitor therapy. It also marked the first US approval for cobimetinib.1
Click on the PDF icon at the top of this introduction to read the full article.
Researchers are increasingly looking to rational combinations of drugs to meet the challenge of resistance to molecularly targeted anticancer therapies. The treatment of metastatic melanoma was significantly advanced with the development of BRAF inhibitors, but is still limited by the short-lived nature of the responses to these drugs and the almost universal occurrence of tumor regrowth. More durable responses could be produced by targeting multiple points in the mitogen-activated protein kinase (MAPK) signaling pathway of which BRAF is a central component. In the fall of 2015, the MEK inhibitor cobimetinib and BRAF inhibitor vemurafenib became the second such combination to receive regulatory approval in the United States following positive results from the international, phase 3, randomized coBRIM trial, which demonstrated the superiority of the combination over single-agent BRAF inhibitor therapy. It also marked the first US approval for cobimetinib.1
Click on the PDF icon at the top of this introduction to read the full article.
Issue
The Journal of Community and Supportive Oncology - 14(2)
Issue
The Journal of Community and Supportive Oncology - 14(2)
Page Number
51-53
Page Number
51-53
Topics
Article Type
Display Headline
Second targeted combination regime approved for metastatic melanoma
Display Headline
Second targeted combination regime approved for metastatic melanoma
Legacy Keywords
melanoma, cobimetinib, vemurafenib, molecularly targeted anticancer therapies, metastatic melanoma, BRAF inhibitors, mitogen-activated protein kinase, MAPK, MEK inhibitor
Legacy Keywords
melanoma, cobimetinib, vemurafenib, molecularly targeted anticancer therapies, metastatic melanoma, BRAF inhibitors, mitogen-activated protein kinase, MAPK, MEK inhibitor
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JCSO 2016;14:51-53
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