A bispecific EGFR/HER3-targeted antibody–drug conjugate that, after receptor binding and internalization, releases a camptothecin-class topoisomerase I inhibitor payload, causing DNA damage and apoptosis.
Bispecific EGFR/HER3-targeted antibody-drug conjugate that binds EGFR and HER3, undergoes receptor-mediated internalization, and releases a camptothecin-class topoisomerase I inhibitor payload, causing replication-associated DNA damage and apoptosis in tumor cells.
The bispecific ADC binds HER3 on target cells, is internalized, and releases a camptothecin-class topoisomerase I inhibitor that causes replication-associated DNA damage leading to apoptosis.
An oral third-generation, irreversible EGFR tyrosine kinase inhibitor selective for activating and T790M resistance mutations.
Third-generation, irreversible EGFR tyrosine kinase inhibitor that covalently binds and inhibits mutant EGFR (e.g., T790M, L858R, exon 19 deletions), suppressing EGFR signaling and thereby inhibiting proliferation and inducing cell death in EGFR-mutant tumors, with reduced activity on wild-type EGFR.
Irreversible inhibition of mutant EGFR (including T790M) suppresses EGFR signaling (e.g., MAPK/PI3K-AKT), causing growth arrest and apoptosis of EGFR-mutant cells.
An autologous BCMA-directed chimeric antigen receptor (CAR) T-cell therapy in which patient T cells are collected, engineered ex vivo to express a BCMA-targeted CAR, expanded, and reinfused to mediate antigen-dependent T-cell activation, proliferation, cytokine release, and cytotoxic killing of myeloma cells.
Autologous T cells are collected and genetically engineered ex vivo to express a chimeric antigen receptor targeting BCMA, then expanded and reinfused. Upon BCMA binding on myeloma cells, CAR signaling (CD3ζ with costimulation) drives T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing, with potential persistence for ongoing tumor control.
BCMA-specific CAR T cells bind BCMA on target cells, triggering T-cell activation and degranulation with perforin/granzyme to induce apoptosis/lysis (with possible Fas/FasL and cytokine-mediated killing).
An oral third-generation, irreversible EGFR tyrosine kinase inhibitor selective for activating and T790M resistance mutations.
Third-generation, irreversible EGFR tyrosine kinase inhibitor that covalently binds and inhibits mutant EGFR (e.g., T790M, L858R, exon 19 deletions), suppressing EGFR signaling and thereby inhibiting proliferation and inducing cell death in EGFR-mutant tumors, with reduced activity on wild-type EGFR.
Osimertinib irreversibly inhibits the mutant EGFR (L858R) kinase, shutting down EGFR signaling and inducing apoptosis of EGFR-dependent tumor cells.
An oral third-generation, irreversible EGFR tyrosine kinase inhibitor selective for activating and T790M resistance mutations.
Third-generation, irreversible EGFR tyrosine kinase inhibitor that covalently binds and inhibits mutant EGFR (e.g., T790M, L858R, exon 19 deletions), suppressing EGFR signaling and thereby inhibiting proliferation and inducing cell death in EGFR-mutant tumors, with reduced activity on wild-type EGFR.
Osimertinib irreversibly inhibits mutant EGFR (including exon 19 deletions), shutting down EGFR signaling and triggering apoptosis/cell death in EGFR-mutant tumor cells.