Pipeline of c-Met-Targeted Immunotherapies

This competitive intelligence report about c-Met-Targeted Immunotherapies provides a competitor evaluation in the field of product candidates in research and development targeting c-Met. This report will be prepared on demand within one working day upon order placement. The report lists c-Met-targeted R&D programs by R&D phase in a tabular format and describes in brief the profile of c-Met-targeted immunotherapies by drug modality. The report will be provided in pdf format and sent by e-mail to the customer.

As an example of this category of on demand reports please see our free sample report of “Pipeline of 5T4-Targeted Immunotherapies”.

The c-MET signalling pathway consists of the mesenchymal epithelial transition factor (c-MET) transmembrane receptor tyrosine kinase receptor (RTK) and its ligand hepatocyte growth factor (HGF) or scatter factor (SF). Binding of HGF/SF to c-MET activates downstream signalling pathways such as Rho, focal adhesion kinase (FAK) and PI3K. These pathways regulate cancer cell growth, survival angiogenesis, invasion and metastasis. Thus, prevention of c-MET dependent neoplastic processes may provide a means for managing invasive tumors of high metastatic potential. c-Met is a well-characterized oncogene that is associated with poor prognosis in many solid tumor types.

In fact, c-MET/HGF has evolved as an attractive target for the pharmaceutical industry. Several c-Met RTK inhibitors have made it to the market to treat non-small cell lung cancer with specific MET mutations—Novartis’ Tabrecta (capmatinib), Merk KGaA’s Tepmetko (tepotinib) and AstraZeneca and HutchMed’s Orpathys (savolitinib) in China—validating c-Met as a viable target. While responses to c-Met RTK inhibitors have been observed in clinical trials, activity appears to be limited to those with MET gene amplifications or exon 14-skipping mutations, representing only small subsets of patients with tumors driven by signaling through the c-Met pathway, thereby necessitating selection of patients with MET amplification and/or c-Met activation most likely to respond.

As a cell surface receptor, c-Met is highly expressed in solid tumors, including non-small cell lung cancer (NSCLC) and head and neck squamous cell carcinoma (HNSCC), and, thus, may be well suited as a binding target for delivery of payloads.