Vebreltinib clinical study

Clinical studies involving Vebreltinib currently undergoing or planning consist of the following:

一、Non-small cell lung cancer clinical study involving MET Exon 14 mutation and intrinsic MET amplification:

MET Exon 14 mutation and intrinsic MET amplification have been proved to be some of the major causes for non-small cell lung cancer, as they can lead to activation of MET pathways. Phases I and II clinical studies have found that Vebreltinib - a highly-selective inhibitor - can inhibit tumor growth. More than 70% of patients in the clinical trials saw partial relief, with outstanding safety for the medication. Vebreltinib is found to be "Best-in-class" among MET inhibitors.

二、Clinical study for PTPRZ1-MET (ZM) fusion gene positive glioma:

Glioma is a type of malignant tumors. Secondary glioblastomas develop from lower level of glioma. Alternatively they are glioblastomas accompanied by IDH genetic mutation. As a small-molecule, highly-selective MET kinase inhibitor, Vebreltinib cuts off the downstream signal pathway for ZM fusion-genes through blood-brain barrier, thus achieving the suppression of tumor growth and invasion. Vebreltinib is the first targeted drug available internationally for secondary glioblastomas sub-types.

三、Clinical trial on non-small cell lung cancer involving EGFR inhibitor-resistant accompanied with MET amplification:

MET amplification is found in as high as 30% of patients suffering from non-small cell lung cancer with EGFR inhibitor resistance. Activation of MET gene is a major cause for drug-resistance by patients with non-small cell lung cancer involving EGFR mutation. Our company offers two highly-selective kinase inhibitors namely Vebreltinib and PLB1004, which respectively works on MET and EGFR targets. As such, they possess the condition precedent for undertaking joint drug-use research. For late-stage non-small cell lung cancer patient with recurrence after EFGR inhibitor treatment due to MET amplification, Vebreltinib can effectively inhibit the expression of MET signal pathways, while PLB1004 can continue to render effective inhibition of EGFR mutation. The joint drug-use treatment study is now at the frontier of international research.