Autologous, gene-modified CD19-directed CAR T-cell therapy (also known as CNCT19) in which a patient’s T cells are engineered to express a CAR targeting CD19, leading to T-cell activation, cytotoxic killing of CD19+ B-cell malignancies, and B-cell aplasia.
Autologous T cells are genetically modified to express a CD19-directed chimeric antigen receptor; upon binding CD19 on B-cell malignancies, CAR signaling (CD3zeta with costimulation) activates T-cell cytotoxicity and cytokine release, resulting in perforin/granzyme-mediated killing of CD19+ cells and on-target B-cell aplasia.
CD19-directed CAR T cells bind CD19 and activate T-cell effector killing, primarily via perforin/granzyme-mediated apoptosis (and Fas–FasL).
Human IgG1 monoclonal antibody immune checkpoint inhibitor that binds PD-L1, blocking its interaction with PD-1 and B7.1 to restore T-cell antitumor activity; retains an intact Fc region enabling ADCC and engagement of NK cells.
Human IgG1 monoclonal antibody that binds PD-L1, blocking its interaction with PD-1 and B7.1 to inhibit PD-1 signaling and restore T-cell antitumor activity; the intact Fc region engages Fc receptors to mediate antibody-dependent cellular cytotoxicity against PD-L1-expressing cells.
Avelumab binds PD-L1 on target cells and, via its intact IgG1 Fc, engages Fc gamma receptors (e.g., CD16) on NK cells to trigger antibody-dependent cellular cytotoxicity (ADCC), killing PD-L1–expressing cells; it also blocks PD-1/PD-L1 to restore T-cell activity (indirect).
HER2-targeted antibody-drug conjugate (Enhertu, T-DXd) that delivers a topoisomerase I inhibitor (DXd) to HER2-expressing tumor cells, causing DNA damage and bystander killing.
HER2-targeted monoclonal antibody (trastuzumab) delivers a membrane-permeable topoisomerase I inhibitor payload (DXd) to HER2-expressing tumor cells. After HER2 binding and internalization, DXd inhibits Top1, causing DNA damage, replication blockade, and apoptosis; additional effects include bystander killing and antibody-dependent cell-mediated cytotoxicity (ADCC).
The ADC binds HER2, is internalized, and releases the DXd topoisomerase I inhibitor payload, causing DNA damage and apoptosis in HER2+ cells; it can also mediate ADCC and bystander killing.
Chimeric anti-CD20 monoclonal antibody that depletes B cells via ADCC, CDC, and apoptosis.
Chimeric anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells and induces B-cell depletion via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and direct apoptosis (and phagocytosis).
Anti-CD20 mAb binds CD20 on B cells and triggers Fc-mediated ADCC by NK/macrophages, complement-dependent cytotoxicity (MAC formation), direct apoptotic signaling, and antibody-dependent phagocytosis, leading to B-cell killing.
An anti-CD20 monoclonal antibody that binds CD20 on B lymphocytes and depletes B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis.
Anti-CD20 monoclonal antibody that binds CD20 on B lymphocytes and depletes B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis.
The anti-CD20 antibody binds CD20 on B cells and eliminates them via Fc-mediated ADCC and complement-dependent cytotoxicity, with additional direct apoptotic signaling upon receptor crosslinking.