Actiza Pharmaceutical Private Limited

We are engaged in offering this product to our clients. Our range of all products is widely appreciated by our clients.

We are engaged in offering this product to our clients. Our range of all products is widely appreciated by our clients.

We are engaged in offering this product to our clients. Our range of all products is widely appreciated by our clients.

We are engaged in offering this product to our clients. Our range of all products is widely appreciated by our clients.

We are engaged in offering this product to our clients. Our range of all products is widely appreciated by our clients.

We are engaged in offering this product to our clients. Our range of all products is widely appreciated by our clients.

We are engaged in offering this product to our clients. Our range of all products is widely appreciated by our clients.

We are engaged in offering this product to our clients. Our range of all products is widely appreciated by our clients.

We are engaged in offering this product to our clients. Our range of all products is widely appreciated by our clients.

Capmatinib is a kinase inhibitor that targets MET, including mutants resulting from exon 14 skipping. MET exon 14 skipping results in the loss of regulatory domains in the protein, thereby reducing its negative regulation, resulting in increased downstream MET signaling. Capmatinib inhibits the growth of cancer cells driven by mutant MET variants lacking clinically achievable exon 14 concentrations and exhibits antitumor activity in a murine tumor xenograft model derived from human lung tumors that cause MET Exon 14 skipping or MET amplification. Capmatinib inhibits MET phosphorylation triggered by hepatocyte growth factor binding or by MET amplification, as well as MET-mediated phosphorylation of downstream signaling proteins and MET-dependent cancer cell proliferation and survival.

 

Indications

For the treatment of adult patients with metastatic non-small cell lung cancer (NSCLC) whose tumors have mutations that cause mesenchymal-to-epithelial transition (MET) exon 14 skipping.