Antibody-drug conjugate targeting a tumor-associated cell-surface antigen; internalizes and releases a cytotoxic payload (e.g., topoisomerase I or microtubule-targeting warhead) to kill cancer cells.
HER2-directed antibody-drug conjugate (trastuzumab rezetecan). The trastuzumab antibody binds HER2 on tumor cells, is internalized, and a cleavable linker releases a camptothecin-derived topoisomerase I inhibitor that stabilizes Topo I-DNA complexes, causing DNA strand breaks, blocking DNA replication, and inducing apoptosis in HER2-expressing cancer cells.
HER2-targeted ADC binds HER2, is internalized, and releases a camptothecin topoisomerase I inhibitor that causes DNA strand breaks, blocks replication, and induces apoptosis in HER2-expressing cells.
A trispecific T-cell engager (multispecific antibody biologic) that binds CD3 on T cells and CD19/CD20 on B cells to redirect T-cell cytotoxicity against malignant B cells in relapsed/refractory B-cell non-Hodgkin lymphoma; administered with step-up then maintenance IV or SC dosing on 21-day cycles.
IgG-like trispecific T-cell engager that simultaneously binds CD3 on T cells and CD19/CD20 on B cells, redirecting and activating cytotoxic T cells to kill CD19/CD20-expressing malignant B cells and reducing antigen-escape by dual B-cell targeting.
Trispecific T-cell engager bridges CD3 on T cells to CD20 on B cells, activating T-cell cytotoxicity (perforin/granzyme- and Fas/FasL-mediated killing) against CD20-expressing cells.
Bispecific T-cell engager (BiTE) antibody that links CD3 on T cells to CD19 on B cells to induce T cell–mediated cytotoxicity.
A bispecific T-cell engager (BiTE) antibody that binds CD3 on T cells and CD19 on B cells to form an immunologic synapse, redirecting and activating T cells to kill CD19+ B-lymphoblasts via perforin/granzyme-mediated cytotoxicity.
Blinatumomab links CD3+ T cells to CD19+ cells, forming an immunologic synapse that triggers T‑cell cytotoxicity via perforin/granzyme-mediated apoptosis of the CD19-expressing cells.
Chimeric IgG1 anti-EGFR monoclonal antibody that blocks EGFR ligand binding, inhibits EGFR signaling, promotes receptor internalization, and can induce ADCC.
Chimeric IgG1 monoclonal antibody against EGFR that blocks ligand binding and receptor dimerization, inhibits downstream EGFR→RAS/RAF/MEK/ERK signaling, promotes receptor internalization, and can mediate ADCC, leading to antiproliferative and antitumor effects.
Cetuximab binds EGFR on target cells and its IgG1 Fc engages Fcγ receptors on NK cells/macrophages to induce ADCC (and sometimes CDC), leading to lysis of EGFR+ cells; EGFR blockade also causes antiproliferative effects.
Anti-CD20 monoclonal antibody that depletes B cells via ADCC, complement activation, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20+ cells via Fc-mediated ADCC, complement-dependent cytotoxicity, and induction of apoptosis.
Rituximab binds CD20 and induces killing via Fc-mediated ADCC by NK cells/macrophages, complement-dependent cytotoxicity (CDC), and apoptosis triggered by CD20 crosslinking.