Trastuzumab coats HER2+ cells and engages Fcγ receptor–bearing effector cells (e.g., NK cells) to induce antibody‑dependent cellular cytotoxicity (ADCC), leading to lysis of the target cells; signaling blockade contributes but ADCC is the primary killing mechanism.
HER2-targeted antibody–drug conjugate delivering MMAE to HER2-positive tumor cells, causing microtubule disruption and apoptosis; may also mediate ADCC.
HER2-targeted antibody–drug conjugate that binds HER2 on tumor cells and is internalized; a cleavable linker releases the MMAE payload intracellularly to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; the antibody Fc may also mediate ADCC and enable a bystander effect.
ADC binds HER2 and is internalized; a cleavable linker releases MMAE, inhibiting tubulin and causing G2/M arrest and apoptosis. Fc engagement can also mediate ADCC; a bystander effect may occur.
Type II anti-CD20 monoclonal antibody that depletes malignant B cells via ADCC/ADCP and direct cell death.
Glycoengineered humanized IgG1 type II anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes malignant CD20+ B cells primarily via enhanced FcγRIIIa-mediated ADCC and ADCP, with additional direct (caspase-independent) cell death; limited reliance on complement activation.
Obinutuzumab binds CD20 on B cells and kills them via enhanced FcγRIIIa-mediated ADCC by NK cells and ADCP by macrophages, plus induction of direct caspase-independent cell death; limited complement involvement.
A subcutaneous bispecific T-cell–engaging monoclonal antibody that binds BCMA (TNFRSF17) on malignant plasma cells and CD3 on T cells to activate T-cell receptor/CD3 signaling, induce cytotoxic T-cell killing, and trigger apoptosis of BCMA-positive plasma cells.
Bispecific monoclonal antibody that binds BCMA on malignant plasma cells and CD3 on T cells, crosslinking them to activate T-cell receptor/CD3 signaling, drive cytotoxic T-cell killing, and induce apoptosis of BCMA-positive plasma cells.
Elranatamab bridges CD3 on T cells to BCMA on target cells, activating T cells to deliver perforin/granzymes and induce apoptosis of BCMA-positive cells.
Bispecific T-cell engager (BiTE) antibody construct that binds CD19 on B-cell blasts and CD3 on T cells, redirecting T-cell cytotoxicity to eliminate CD19+ leukemia and minimal residual disease.
CD19xCD3 bispecific (BiTE) antibody that simultaneously binds CD19 on B cells and CD3 on T cells, recruiting and activating T cells to form an immunologic synapse and mediate perforin/granzyme-dependent lysis of CD19-positive leukemia cells, independent of MHC.
Blinatumomab links CD3 on T cells to CD19 on target cells, inducing an immunologic synapse and T‑cell activation that kills CD19+ cells via perforin/granzyme-dependent cytolysis (MHC-independent).