An antibody-drug conjugate comprising an anti-HER2 IgG1 (trastuzumab) linked to a membrane-permeable topoisomerase I inhibitor payload (DXd). It binds HER2 (including low expression), is internalized, releases DXd to inhibit TOP1 and induce DNA damage/apoptosis with bystander effect; the trastuzumab component can inhibit HER2 signaling and mediate ADCC.
Anti-HER2 IgG1 (trastuzumab) linked to a membrane‑permeable topoisomerase I inhibitor payload (DXd). After binding HER2 (including low expression) and internalization, the linker is cleaved to release DXd, which inhibits TOP1, causing DNA damage and apoptotic cell death with a bystander effect; the antibody component can also inhibit HER2 signaling and mediate ADCC.
ADC binds HER2, is internalized, and releases the DXd topoisomerase I inhibitor, causing DNA damage and apoptotic death of HER2+ cells; trastuzumab component can also mediate ADCC and bystander killing.
A bispecific T-cell–engaging monoclonal antibody that binds CD3 on T cells and BCMA on myeloma plasma cells to redirect cytotoxic T cells against BCMA-positive cells.
Bispecific antibody that binds CD3 on T cells and BCMA on malignant plasma cells, crosslinking them to activate and redirect cytotoxic T cells to kill BCMA-positive myeloma cells.
Teclistamab bridges CD3+ T cells to BCMA-expressing cells, activating T cells to form an immunologic synapse and kill the target via perforin/granzyme-mediated cytotoxicity (apoptosis).
Oral small‑molecule BCL‑2 inhibitor that restores apoptosis in BCL‑2–dependent malignant B cells.
Selective BCL-2 inhibitor (BH3 mimetic) that binds the BCL-2 hydrophobic groove to block its anti-apoptotic function, displacing pro-apoptotic proteins and restoring mitochondrial apoptosis in BCL-2–dependent malignant B cells; minimal BCL-XL inhibition.
Venetoclax binds and inhibits BCL-2 (BH3 mimetic), releasing pro-apoptotic factors to activate BAX/BAK, causing mitochondrial outer membrane permeabilization, caspase activation, and apoptosis of BCL-2–dependent cells.
Chimeric anti‑CD20 monoclonal antibody that depletes CD20+ B cells via antibody‑dependent cellular cytotoxicity, complement activation, and direct apoptotic signaling.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and mediates B-cell depletion via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and direct apoptotic signaling.
Rituximab binds CD20 on B cells and kills them via Fc-mediated ADCC by NK/macrophages, complement-dependent cytotoxicity, and direct pro-apoptotic signaling upon CD20 cross-linking.
Humanized IgG1 monoclonal antibody immunotherapy targeting CSF1R; blocks CSF1R to inhibit CSF1/M-CSF signaling and depletes CSF1R+ macrophages via receptor blockade and Fc-mediated clearance, reducing macrophage-driven tumor burden in TGCT.
Humanized IgG1 monoclonal antibody against CSF1R that blocks CSF1/M-CSF binding and downstream signaling, and engages Fc effector functions to deplete CSF1R+ macrophages (e.g., tumor-associated macrophages/giant cells), thereby reducing macrophage-driven pathology in TGCT.
Emactuzumab (IgG1) binds CSF1R on target cells and engages Fcγ receptor–bearing effector cells to induce ADCC/ADCP (and potentially CDC), depleting CSF1R+ macrophages/giant cells.