Oral third-generation irreversible EGFR tyrosine kinase inhibitor active against Exon 19 deletion/L858R and T790M mutations.
Oral third-generation irreversible EGFR tyrosine kinase inhibitor that selectively and covalently targets mutant EGFR (Exon 19 deletion, L858R, T790M), blocking downstream signaling and inducing death of EGFR-mutant tumor cells while sparing wild-type EGFR; penetrates the blood–brain barrier.
Irreversible inhibition of mutant EGFR kinase (e.g., Exon 19 del, L858R, T790M) blocks downstream survival signaling (PI3K/AKT, MAPK), leading to growth arrest and apoptosis of EGFR-mutant tumor cells; minimal effect on wild-type EGFR.
Bispecific monoclonal antibody (CD20×CD3) T‑cell engager that redirects T cells to kill CD20+ B cells.
Humanized bispecific CD20xCD3 monoclonal antibody that binds CD20 on B cells and CD3 on T cells, crosslinking them to activate TCR/CD3 signaling and form cytolytic synapses, leading to perforin/granzyme-mediated killing of CD20+ malignant B cells.
Bispecific CD20xCD3 T‑cell engager redirects T cells to CD20+ cells, forming a cytolytic synapse and inducing perforin/granzyme-mediated killing.
Type I anti-CD20 monoclonal antibody that depletes CD20-positive B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis; given intravenously or subcutaneously.
Chimeric type I anti-CD20 monoclonal antibody that binds CD20 on B cells and induces their depletion via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and direct apoptosis.
Rituximab binds CD20 on B cells and induces killing via Fc-mediated ADCC by NK cells/macrophages, complement-dependent cytotoxicity (MAC formation), and can trigger direct apoptotic signaling upon CD20 crosslinking.