(Health Korea News / Yoo Ji-in) ‘VERT-002’, a new drug candidate that decomposes the c-MET gene, known as one of the carcinogenic promoters of non-small cell lung cancer (NSCLC), is entering clinical trials in Korea.
c-MET is one of the proteins that transmit signals to cells and is considered a representative cancer-causing gene. It is known that overexpressed c-MET protein is detected in approximately 20% of all NSCLC. To date, none of the drugs that selectively target the c-MET protein have been approved by regulatory agencies.
The Ministry of Food and Drug Safety announced on the 27th, ‘First-in-human (FIH), phase 1/2 public, multicenter, phase 1/2 public trial of VERT-002 targeting patients with locally advanced or metastatic solid tumors, including non-small cell lung cancer (NSCLC) with MET mutation. , phase 1/2 of ‘dose escalation and expansion trial’ was approved. This clinical trial will be conducted at Seoul Asan Medical Center and Severance Hospital.
VERT-002 was developed by Vertical Bio, a Swiss biotechnology company specializing in the development of antibodies for cancer treatment, but the company was acquired by French pharmaceutical company Pierre Fabre Laboratories last year and the candidate was added to the anticancer drug discovery pipeline. did it
Pierre Fabre Laboratories announced last October that it had administered PFL-002/VERT-002, a monoclonal antibody that acts as a c-MET degrader, to its first overseas patient.
This trial will evaluate the safety, tolerability, pharmacokinetics, pharmacodynamics, and preliminary clinical efficacy of PFL-002/VERT-002 as monotherapy in patients with MET-dependent tumors, especially those resistant to other treatments. This is an open multicenter study that aims to
Non-small cell lung cancer (NSCLC) is the most common form of lung cancer, accounting for approximately 85% of newly diagnosed lung cancer cases. MET, also known as hepatocyte growth factor receptor (HGFR), is a factor that regulates oncogenes in a subset of patients with NSCLC. 1-4 MET exon 14 skipping mutations and MET amplification are found to be major oncogenes, and MET amplification appears to be a mechanism of resistance to selected targeted treatments.
VERT-002 has a mechanism to trigger the degradation of the c-MET oncogene by targeting clinically proven tumor-causing factors with a unique and differentiated mechanism of action.
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