Humanized anti-EGFR monoclonal antibody that blocks ligand binding and receptor activation, downregulating MAPK/ERK and PI3K/AKT signaling; inhibits proliferation and can enhance radio/chemosensitivity and mediate ADCC.
Humanized anti-EGFR IgG1 monoclonal antibody that binds the EGFR extracellular domain, blocking ligand binding and receptor activation, thereby suppressing downstream MAPK/ERK and PI3K/AKT signaling; inhibits proliferation and survival of EGFR-overexpressing tumor cells and can enhance radio/chemosensitivity and mediate ADCC.
YES
DIRECT
Binds EGFR on tumor cells and engages Fcγ receptors on immune effectors to trigger antibody‑dependent cellular cytotoxicity (ADCC), leading to target cell lysis.
An antibody–drug conjugate (Enhertu) consisting of an anti‑HER2 IgG1 monoclonal antibody linked to a topoisomerase I inhibitor (deruxtecan). It binds HER2 to deliver the DXd payload intracellularly, causing DNA damage and cell death with potential bystander effect.
HER2‑targeting IgG1 antibody (trastuzumab) binds HER2 on tumor cells and is internalized, where a cleavable linker releases the deruxtecan (DXd) payload, a topoisomerase I inhibitor that induces DNA damage leading to cell cycle arrest and apoptosis. The membrane‑permeable payload enables bystander killing of adjacent cells, and the antibody component can also mediate ADCC.
YES
DIRECT
The HER2-targeting ADC binds HER2, is internalized, and releases the DXd topoisomerase I inhibitor, causing DNA damage, cell-cycle arrest, and apoptosis; Fc-mediated ADCC can also contribute, with possible bystander killing.
An antibody–drug conjugate (Enhertu) consisting of an anti‑HER2 IgG1 monoclonal antibody linked to a topoisomerase I inhibitor (deruxtecan). It binds HER2 to deliver the DXd payload intracellularly, causing DNA damage and cell death with potential bystander effect.
HER2‑targeting IgG1 antibody (trastuzumab) binds HER2 on tumor cells and is internalized, where a cleavable linker releases the deruxtecan (DXd) payload, a topoisomerase I inhibitor that induces DNA damage leading to cell cycle arrest and apoptosis. The membrane‑permeable payload enables bystander killing of adjacent cells, and the antibody component can also mediate ADCC.
NO
INDIRECT
The ADC binds HER2 (not Top1), is internalized, and releases the DXd topoisomerase I inhibitor that causes DNA damage and apoptosis. DNA topoisomerase I is the intracellular enzymatic target of the payload, not the targeting antigen; any killing of Top1-expressing cells occurs only after HER2-mediated delivery or bystander diffusion.
An intravenous, novel asymmetric trivalent, tri-specific humanized antibody (biologic immunotherapy) designed to bind three targets simultaneously to enhance immune-mediated killing of malignant plasma cells in relapsed/refractory multiple myeloma; specific antigen targets and precise mechanism are not disclosed.
Asymmetric trispecific humanized antibody that binds BCMA and GPRC5D on multiple myeloma cells and CD3 on T cells, crosslinking to redirect and activate cytotoxic T cells to form an immune synapse and kill BCMA/GPRC5D-expressing malignant plasma cells.
YES
DIRECT
The trispecific T-cell engager binds BCMA on tumor cells and CD3 on T cells, crosslinking to form an immune synapse and activate T cells to kill BCMA+ cells via perforin/granzyme-mediated cytolysis.
An intravenous, novel asymmetric trivalent, tri-specific humanized antibody (biologic immunotherapy) designed to bind three targets simultaneously to enhance immune-mediated killing of malignant plasma cells in relapsed/refractory multiple myeloma; specific antigen targets and precise mechanism are not disclosed.
Asymmetric trispecific humanized antibody that binds BCMA and GPRC5D on multiple myeloma cells and CD3 on T cells, crosslinking to redirect and activate cytotoxic T cells to form an immune synapse and kill BCMA/GPRC5D-expressing malignant plasma cells.
YES
DIRECT
The trispecific T-cell engager binds GPRC5D on tumor cells and CD3 on T cells, crosslinking to activate T cells that form an immune synapse and kill GPRC5D+ cells via perforin/granzyme-mediated apoptosis.