Colon Pharmaceuticals (002422.SZ): First-line clinical study of lucansastuzumab (saC-TMT) combined with pabolizumab in the first-line treatment of PD-L1 negative locally advanced or metastatic non-squamous non-small cell lung cancer reached the main end

Zhitong Financial App News, Colon Pharmaceutical (002422.SZ) announced that the company's holding subsidiary Collonbotai's antibody-conjugate drug (ADC) targeting human nourishing cell surface antigen 2 (TROP2) (Sac-TMT) (Cathailai®) in combination with MSD's anti-programmed cell death protein-1 (PD-1) monoclonal antibody pavolizumab (Krida®) first-line treatment of programmed cell death ligand-1 (PD-L1) is negative locally advanced or non-squamous nonsquamous Phase 3 clinical study of small cell lung cancer (NSCLC) (OptiTrop-Lung06), the primary end point of progression-free survival (PFS) was confirmed by the Independent Data Monitoring Committee (IDMC) in a predetermined mid-term analysis.

This is the world's first phase 3 clinical study of ADC combined with an immune checkpoint inhibitor to reach the primary endpoint in first-line treatment of negative PD-L1 negative non-squamous NSCLC.

As the core product of Collumbotai, Lucan Satuzumab (Sac-TMT) is a novel TROP2ADC with independent intellectual property rights for advanced solid tumors such as NSCLC, breast cancer (BC), gastric cancer (GC), gynecological tumors, and urogenital tumors. Lucan satuzumab (Sac-TMT) was developed using a unique bifunctional connector. On the one hand, the ligand forms irreversible binding with the anti-TROP2 monoclonal antibody satuzumab, and on the other hand, it can pH-sensitively lyse the payload from the belotecan derivative topoisomerase I inhibitor in the lysosome, thereby maximizing the delivery of the payload to tumor cells, and the drug-antibody ratio (DAR) reaches 7.4. Lucan satuzumab (Sac-TMT) specifically identifies TROP2 on the surface of tumor cells through recombinant anti-TROP2 humanized monoclonal antibodies, which are then endocytosed by tumor cells and release the payload KL610023 within the cell. As a topoisomerase I inhibitor, KL610023 can induce DNA damage in tumor cells, which in turn leads to cell cycle blockade and apoptosis. Furthermore, it also releases KL610023 in the tumor microenvironment. Since KL610023 is permeable to cell membranes, it can achieve a bystander effect, that is, kill neighboring tumor cells.