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.
Teclistamab bridges CD3 on T cells to BCMA on target cells, activating T cells to form cytolytic synapses and kill BCMA+ cells via perforin/granzyme-mediated apoptosis.
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.
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.
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.
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.
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).
ADCC-enhanced monoclonal antibody targeting GPRC5D; Fc engineering increases binding to Fc gamma receptors (e.g., CD16) to activate NK cells and mediate antibody-dependent cellular cytotoxicity against malignant plasma cells.
Fc-engineered monoclonal antibody that binds GPRC5D on malignant plasma cells and has increased affinity for Fcγ receptors (e.g., CD16) to more effectively recruit NK cells (and other FcγR+ effector cells), triggering antibody-dependent cellular cytotoxicity (and potentially ADCP/CDC) to kill myeloma cells.
The antibody binds GPRC5D on myeloma cells and its Fc engages Fc gamma receptors (e.g., CD16) on NK cells to trigger ADCC (perforin/granzyme), with possible ADCP/CDC.