Cotellic (cobimetinib)

P1, N=70, Completed, F. Hoffmann-La Roche AG | Recruiting --> Completed

She was initially treated with Vemurafenib and Cobimetinib, achieving complete remission. However, due to cumulative toxicities, therapy was switched to Encorafenib and Binimetinib in February 2023...Management included Binimetinib dose reduction and topical ketorolac, resulting in initial improvement, although the CME recurred several months later...The patient ultimately began immunotherapy with Nivolumab and Ipilimumab, but died in February 2024 due to refractory abdominal septic shock. This case highlights the importance of early ophthalmologic monitoring and interdisciplinary collaboration in patients receiving MEK inhibitors.

P2, N=720, Recruiting, Canadian Cancer Trials Group | Trial primary completion date: Jan 2026 --> Dec 2026

P2, N=45, Recruiting, Hanmi Pharmaceutical Company Limited

Therefore, this study aimed to examine the protein composition of the secretome of cells resistant to vemurafenib (a BRAF inhibitor) and cobimetinib (a MEK inhibitor) and to compare it with that of nonresistant cells. Proteins secreted by resistant melanoma cells can undoubtedly influence the surrounding microenvironment in a way that promotes the formation of a pro-tumor niche. Among the proteins secreted in significantly higher amounts by resistant cells (compared to the control group), which may be potential biomarkers or therapeutic targets in melanoma, plasminogen activator inhibitor 1, thymosin beta-4, clusterin, interleukin-6, superoxide dismutase, and selected matrix metalloproteinases can be distinguished.

P1, N=70, Recruiting, F. Hoffmann-La Roche AG | -> Recruiting | Phase classification: PN/A --> P1

P2, N=29, Active, not recruiting, University of Utah | Trial primary completion date: Jan 2026 --> Apr 2025

P1, N=65, Active, not recruiting, Genentech, Inc. | Trial completion date: Dec 2025 --> Jun 2027 | Trial primary completion date: Dec 2025 --> Jun 2027

ABM-1310 showed a favorable safety profile and encouraging intracranial activity. These findings support continued evaluation for CNS tumors and in cancer patients with prior BRAF inhibitor exposure.

P2, N=29, Active, not recruiting, University of Utah | Recruiting --> Active, not recruiting

P1, N=51, Completed, InxMed (Shanghai) Co., Ltd. | Active, not recruiting --> Completed | N=120 --> 51

Data from this study provides provocative evidence that, while BRAF+/-MEK inhibitor therapy produces an increase in overall and clonal T cell infiltrates, there is limited evidence for generation of new or persistent tumor immunity. Thus, BRAFi/MEKi therapy may enable tumor-reactive T cells to infiltrate tumors but tumor control does not appear to depend on priming new immune responses.