Antibody–drug conjugate targeting CD79b; internalization releases MMAE (a microtubule inhibitor) causing mitotic arrest and apoptosis.
CD79b-directed monoclonal antibody linked via a protease-cleavable linker to the microtubule inhibitor MMAE; binding to CD79b on B cells triggers internalization and release of MMAE, which inhibits tubulin polymerization, leading to G2/M arrest and apoptosis of malignant B cells.
The ADC binds CD79b on B cells, is internalized, and releases MMAE, which inhibits tubulin polymerization leading to G2/M arrest and apoptosis of the target-expressing cells.
A humanized IgG1 kappa monoclonal antibody targeting HER2/ErbB2. It binds the HER2 extracellular domain to block receptor dimerization and downstream signaling (e.g., PI3K/AKT, MAPK) and mediates antibody-dependent cellular cytotoxicity (ADCC). In this trial, both Roche’s Herclon and a proposed Incepta biosimilar administer trastuzumab as a single 6 mg/kg IV dose.
Humanized IgG1 monoclonal antibody that binds the HER2/ErbB2 extracellular domain, preventing receptor dimerization and downstream PI3K/AKT and MAPK signaling; promotes receptor downregulation and mediates Fc-dependent ADCC against HER2-overexpressing tumor cells.
Fc-mediated ADCC: trastuzumab binds HER2 on tumor cells and its Fc engages FcγR-bearing effector cells (e.g., NK cells, macrophages) to lyse the target; may also contribute via CDC, while signaling blockade is mainly antiproliferative.
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.
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.
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 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.
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.