An IgG-based bispecific T-cell–engaging antibody that binds CD276 (B7-H3) on tumor and tumor vasculature and CD3 on T cells; includes an attenuated CD3 binder and YTE Fc modification to extend half-life, designed to redirect T cells to CD276+ targets and provide anti-angiogenic effects.
IgG-based bispecific antibody that binds CD276 (B7-H3) on tumor and tumor vasculature and CD3 on T cells to redirect and activate T cells for cytotoxic killing of CD276+ targets; incorporates an attenuated CD3 binder to reduce off-target activation/CRS risk and a YTE Fc modification to extend half-life, with potential anti-angiogenic effects via CD276 on tumor endothelium.
NO
INDIRECT
The antibody binds CD3 on T cells to recruit/activate them; these T cells then kill CD276-positive tumor/endothelial cells via T-cell cytotoxicity (perforin/granzyme). CD3+ cells are not the targets of killing.
Anti-EGFR monoclonal antibody that inhibits EGFR-mediated activation of RAS signaling.
Cetuximab is a chimeric monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding and receptor dimerization, preventing EGFR activation and downstream RAS-MAPK and PI3K-AKT signaling, thereby inhibiting tumor cell proliferation; it can also trigger antibody-dependent cellular cytotoxicity.
YES
DIRECT
Cetuximab coats EGFR+ cells and engages Fcγ receptors on NK cells/macrophages to induce antibody-dependent cellular cytotoxicity (and some complement-mediated lysis), while also blocking EGFR signaling (antiproliferative).
Fc-mediated ADCC: trastuzumab binds HER2 on tumor cells and its Fc engages Fcγ receptors on NK cells/macrophages, triggering cytolytic degranulation and lysis of HER2-positive cells (with minimal complement involvement).
Humanized IgG1 monoclonal antibody targeting HER2; binds domain II to block HER2 heterodimerization with HER3/EGFR, suppress ligand-dependent signaling, and enhance ADCC.
Humanized IgG1 monoclonal antibody against HER2 that binds extracellular domain II to prevent HER2 heterodimerization (especially with HER3/EGFR), blocking ligand‑dependent HER signaling (PI3K/AKT, MAPK), inhibiting tumor growth and promoting apoptosis; Fc region mediates antibody‑dependent cellular cytotoxicity (ADCC).
YES
DIRECT
Pertuzumab binds HER2 and its Fc engages Fcγ receptor–bearing immune cells to mediate ADCC against HER2+ cells; blockade of HER2 heterodimerization also inhibits survival signaling and can induce apoptosis.
A HER2-targeted antibody–drug conjugate (RC48) that binds HER2 on tumor cells, is internalized, and releases the cytotoxic microtubule inhibitor MMAE via a cleavable linker to disrupt mitosis and induce apoptosis.
HER2-targeted antibody-drug conjugate: Disitamab binds HER2 on tumor cells, is internalized, and a cleavable linker releases monomethyl auristatin E (MMAE), which inhibits microtubule polymerization, causing G2/M arrest and apoptosis.
YES
DIRECT
An ADC binds HER2 on tumor cells, is internalized, and releases MMAE via a cleavable linker; MMAE inhibits microtubule polymerization, causing G2/M arrest and apoptosis (with potential bystander effect).