A monoclonal antibody immunotherapy targeting MICA/MICB on tumor cells to enhance NKG2D-mediated immune recognition, reduce shedding of soluble MICA/MICB, and engage Fcγ receptors to promote ADCC/ADCP in relapsed/refractory multiple myeloma.
CLN-619 is a human IgG1 monoclonal antibody that binds the alpha3 domain of MICA/MICB on tumor cells, preventing their proteolytic shedding and reducing soluble MICA/MICB. This preserves and enhances NKG2D-mediated recognition by NK cells and cytotoxic T cells, activating antitumor immunity. Its Fc domain engages Fcγ receptors to promote antibody-dependent cell-mediated cytotoxicity and phagocytosis (ADCC/ADCP).
CLN-619 binds MICB on tumor cells and engages Fcγ receptors on effector cells to drive ADCC/ADCP; it also prevents MICB shedding, enhancing NKG2D-mediated NK/CTL cytotoxicity against the target-expressing cells.
TROP2-targeted antibody–drug conjugate delivering a topoisomerase I inhibitor payload to TROP2-expressing tumor cells.
TROP2-targeted antibody–drug conjugate that binds TROP2 on tumor cells, is internalized, and releases a topoisomerase I–inhibiting payload, causing DNA damage and apoptotic cell death (with potential bystander effect).
ADC binds TROP2 on tumor cells, is internalized, and releases a topoisomerase I inhibitor payload that causes DNA damage and apoptotic cell death (with possible bystander effect).
EGFR tyrosine kinase inhibitor targeting EGFR-mutant signaling in tumor cells.
Third‑generation, oral, irreversible EGFR tyrosine kinase inhibitor that covalently binds mutant EGFR (e.g., T790M, L858R, exon 19 deletions) at Cys797, selectively blocking EGFR signaling (MAPK/PI3K pathways) to inhibit proliferation and induce tumor cell death, with reduced activity against wild‑type EGFR.
Osimertinib irreversibly binds the EGFR T790M-mutant kinase (Cys797), inhibits EGFR signaling (MAPK/PI3K-AKT), leading to growth arrest and apoptosis of EGFR-mutant tumor cells.