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.
YES
DIRECT
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.
YES
DIRECT
Osimertinib irreversibly inhibits mutant EGFR (including exon 19 deletions), shutting down EGFR signaling and triggering apoptosis/cell death in EGFR-mutant tumor cells.
A chimeric (mouse/human) anti-CD20 monoclonal antibody that depletes CD20-positive B cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis; used as a biologic DMARD in rheumatoid arthritis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on pre‑B and mature B lymphocytes (not plasma cells) and depletes them via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, thereby reducing autoantibody production and B-cell–mediated immune activation.
YES
DIRECT
Rituximab binds CD20 on B cells and induces complement-dependent cytotoxicity (CDC), Fc-mediated antibody-dependent cellular cytotoxicity (ADCC) by NK cells/macrophages, and can trigger apoptosis of the bound cells.
Anti-HER2 antibody-drug conjugate (RC48) that delivers MMAE to HER2-expressing tumor cells, causing microtubule disruption; may also induce ADCC and bystander killing.
Anti-HER2 antibody-drug conjugate that binds HER2 on tumor cells; upon internalization, delivers the microtubule inhibitor MMAE, leading to microtubule disruption, G2/M arrest, and apoptosis; may also trigger ADCC and bystander killing.
YES
DIRECT
ADC binds HER2 on tumor cells, is internalized, and releases MMAE, which inhibits microtubule polymerization causing G2/M arrest and apoptosis; can also induce ADCC and bystander killing.
Anti-HER2 antibody-drug conjugate (RC48) that delivers MMAE to HER2-expressing tumor cells, causing microtubule disruption; may also induce ADCC and bystander killing.
Anti-HER2 antibody-drug conjugate that binds HER2 on tumor cells; upon internalization, delivers the microtubule inhibitor MMAE, leading to microtubule disruption, G2/M arrest, and apoptosis; may also trigger ADCC and bystander killing.
YES
INDIRECT
Disitamab vedotin binds HER2 on tumor cells, is internalized, and releases MMAE, which binds the beta-tubulin vinca site to inhibit microtubule polymerization, causing G2/M arrest and apoptosis.