BCMA x CD3 bispecific IgG4 antibody that redirects T cells to kill BCMA-expressing myeloma cells.
Humanized bispecific IgG4 antibody that binds CD3 on T cells and BCMA on malignant plasma cells, cross-linking T cells to BCMA+ myeloma cells to activate cytotoxic T-cell responses and induce targeted tumor cell killing.
NO
INDIRECT
Teclistamab binds CD3ε on T cells to recruit/activate them; it does not target CD3ε+ cells for killing. Activated T cells then kill BCMA-expressing tumor cells via perforin/granzyme-mediated cytotoxicity.
GPRC5D x CD3 bispecific IgG4 antibody that redirects T cells to kill GPRC5D-expressing myeloma cells.
Humanized bispecific IgG4 antibody that binds CD3 on T cells and GPRC5D on myeloma cells, crosslinking T cells to tumor cells to activate cytotoxic T-lymphocyte responses (perforin/granzyme release) and kill GPRC5D-expressing cells.
YES
DIRECT
Talquetamab crosslinks CD3 on T cells to GPRC5D on target cells, activating T cells to form an immunologic synapse and kill GPRC5D+ cells via perforin/granzyme release.
GPRC5D x CD3 bispecific IgG4 antibody that redirects T cells to kill GPRC5D-expressing myeloma cells.
Humanized bispecific IgG4 antibody that binds CD3 on T cells and GPRC5D on myeloma cells, crosslinking T cells to tumor cells to activate cytotoxic T-lymphocyte responses (perforin/granzyme release) and kill GPRC5D-expressing cells.
NO
INDIRECT
Talquetamab binds CD3 on T cells to activate and redirect them to GPRC5D+ tumor cells; the T cells then kill GPRC5D-expressing cells via perforin/granzyme release, not the CD3+ cells.
Recombinant humanized anti-EGFR monoclonal antibody that blocks EGFR ligand binding and receptor activation, suppressing RAS/RAF/MEK/ERK and PI3K/AKT signaling to inhibit tumor cell proliferation and survival.
Recombinant humanized anti-EGFR monoclonal antibody that binds the EGFR extracellular domain to block ligand binding and receptor dimerization/activation, suppressing RAS/RAF/MEK/ERK and PI3K/AKT signaling to inhibit tumor cell proliferation and survival; glycoengineering enhances Fc-mediated ADCC.
YES
DIRECT
Anti-EGFR IgG binds EGFR on tumor cells and engages FcγR+ immune effectors (e.g., NK cells) to trigger ADCC, killing target cells; EGFR signaling blockade is primarily cytostatic.
Also known as RC48, an antibody–drug conjugate targeting HER2 (ERBB2) that delivers the microtubule inhibitor MMAE via a cleavable linker, leading to internalization, microtubule disruption, apoptosis, and bystander killing.
Anti-HER2 (ERBB2) antibody–drug conjugate that binds HER2 on tumor cells, is internalized, and via a cleavable linker releases monomethyl auristatin E (MMAE). MMAE binds tubulin and inhibits microtubule polymerization, inducing G2/M arrest and apoptosis, with potential bystander killing due to the membrane-permeable payload.
YES
DIRECT
The ADC binds HER2 on tumor cells, is internalized, the cleavable linker releases MMAE, which inhibits tubulin polymerization causing microtubule disruption, G2/M arrest, and apoptosis (with possible bystander killing from membrane-permeable MMAE).