Anti-CD79b antibody-drug conjugate that delivers the microtubule inhibitor MMAE (monomethyl auristatin E) to B cells.
Anti-CD79b monoclonal antibody linked via a protease-cleavable linker to the microtubule inhibitor MMAE. After binding CD79b on B cells and internalization, MMAE is released to inhibit tubulin polymerization, causing G2/M arrest and apoptosis of CD79b-expressing malignant B cells.
ADC binds CD79B on B cells, is internalized, linker is cleaved to release MMAE, which inhibits tubulin polymerization causing G2/M arrest and apoptosis of CD79B-expressing cells.
Anti-CD20 chimeric monoclonal antibody that depletes CD20-positive B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B lymphocytes and depletes CD20-positive cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
Rituximab binds CD20 on B cells and eliminates them via Fc-mediated ADCC (NK cells/macrophages), complement-dependent cytotoxicity, and direct induction of apoptosis.
Bispecific IgG1 monoclonal antibody targeting EGFR and MET; blocks EGFR/MET signaling, promotes receptor internalization/degradation, and mediates Fc-dependent cytotoxicity (ADCC/ADCP); administered IV.
Bispecific IgG1 monoclonal antibody targeting EGFR and MET; blocks EGFR/MET signaling, induces receptor internalization and degradation, and engages Fc receptors to mediate ADCC/ADCP against tumor cells.
Amivantamab binds EGFR on target cells and engages Fcγ receptors on NK cells/macrophages to trigger ADCC/ADCP, leading to killing of EGFR-expressing cells.
Bispecific IgG1 monoclonal antibody targeting EGFR and MET; blocks EGFR/MET signaling, promotes receptor internalization/degradation, and mediates Fc-dependent cytotoxicity (ADCC/ADCP); administered IV.
Bispecific IgG1 monoclonal antibody targeting EGFR and MET; blocks EGFR/MET signaling, induces receptor internalization and degradation, and engages Fc receptors to mediate ADCC/ADCP against tumor cells.
Amivantamab binds MET on target cells and engages Fcγ receptor–bearing effector cells via its Fc domain, inducing ADCC/ADCP to kill MET+ cells; receptor blockade/internalization may further promote apoptosis.
Investigational antibody–drug conjugate that targets TROP-2 on TNBC cells and, after internalization, releases a topoisomerase I inhibitor payload to induce DNA damage.
Targets TROP-2 on TNBC cells; after antibody-mediated binding and internalization, releases a topoisomerase I inhibitor payload that induces DNA damage and tumor cell death.
ADC binds TROP-2, is internalized, and releases a topoisomerase I inhibitor payload that causes DNA damage, leading to apoptosis/tumor cell death.