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MET Targeting

Oncogenic Signaling

MET targeting

MET signaling is critical in normal biological processes. It activates downstream signaling pathways, including RAS/ERK/MAPK, PI3K/AKT, and JAK/STAT, which drive cell proliferation, motility, and apoptosis. Dysregulation of the MET pathway (for example MET mutations and amplifications) can drive cancer cell proliferation, survival, invasion, and metastasis.¹

Tepotinib – MET kinase inhibitor

Tepotinib is a small-molecule inhibitor of the MET receptor tyrosine kinase. Alterations of the MET signaling pathway are found in various cancer types, and are thought to correlate with aggressive tumor behavior and poor clinical prognosis.¹

Read more about Tepotinib here

Learn more about oncogenic signaling

We are investigating the role that acquired resistance due to MET amplification may have across tumor types, and how that can potentially be targeted through combination therapies.

INSIGHT 2

For more information on the INSIGHT 2 clinical trial, please see the video below.

The investigational compound combinations in the INSIGHT 2 trial are not approved by any health authority. Safety and efficacy have not been established.

AKT, protein kinase B; EGFR, epidermal growth factor receptor; ERK, extracellular signal-regulated kinase; JAK, Janus kinase; MAPK, mitogen-activated protein kinase; MET, mesenchymal epithelial transition factor; NSCLC, non-small cell lung cancer, PI3K; phosphatidylinositol 3 kinase; RAS; rat sarcoma, STAT; signal transducers and activators of transcription.

Wu Y-L, Soo RA, Locatelli G, Stammberger U, Scagliotti G, Park K. Does c-Met remain a rational target for therapy in patients with EGFR TKI-resistant non-small cell lung cancer? Cancer Treat Rev. 2017;61:70-81.

GL-MULO-00164 | January 2024

GL-MULO-00232 | December 2025

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