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.
YES
INDIRECT
After HER2 binding and internalization, the ADC releases DXd, which inhibits topoisomerase I, causing DNA damage and apoptotic cell death; the membrane-permeable payload can also kill neighboring cells (bystander effect).
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.
YES
DIRECT
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).
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.
NO
INDIRECT
Teclistamab engages CD3ε on T cells to activate and redirect them to BCMA+ myeloma cells; the T cells kill the BCMA-expressing cells (perforin/granzyme), while CD3ε+ cells are not targeted for lysis.
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.
YES
DIRECT
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.
YES
DIRECT
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.