Anti-HER2 monoclonal antibody that inhibits HER2 signaling and mediates ADCC.
Humanized IgG1 monoclonal antibody targeting HER2/ERBB2; binds the extracellular domain on HER2-overexpressing tumor cells to block receptor signaling and dimerization, promote receptor downregulation, and engage Fc receptors to mediate antibody-dependent cell-mediated cytotoxicity (ADCC).
After binding HER2, trastuzumab’s Fc engages Fcγ receptors on NK cells and other effectors to mediate ADCC (and some CDC), resulting in killing of HER2-expressing cells.
Autologous or allogeneic T cells transduced with a lentiviral vector to express a CD19-specific chimeric antigen receptor; IV infusion at 2×10^6–1×10^7 CAR-T/kg with dose escalation to define MTD; mediates MHC-independent cytotoxicity against malignant B cells.
Autologous or allogeneic T cells are lentivirally engineered to express a CD19-specific chimeric antigen receptor. Upon CAR binding to CD19 on B-lineage malignant cells, the T cells are activated in an MHC-independent manner, expand, and mediate cytotoxicity via perforin/granzyme release and cytokine signaling, leading to targeted depletion of CD19+ tumor cells.
CAR T cells bind CD19 on target cells, become activated, and kill them via perforin/granzyme-mediated cytolysis (MHC-independent), with additional death signals from cytokines/Fas–FasL.
A human IgG1 monoclonal antibody that binds PD-L1 to block interaction with PD-1, enhancing antitumor T‑cell responses.
Human IgG1 monoclonal antibody that binds PD-L1, blocking PD-L1/PD-1 interaction to release T-cell inhibition and restore antitumor activity; Fc engagement can induce ADCC against PD-L1-expressing tumor cells.
Avelumab binds PD-L1 on target cells and its IgG1 Fc engages Fcγ receptor–bearing effector cells (e.g., NK cells, macrophages) to trigger ADCC/ADCP, killing PD-L1–expressing cells; PD-L1/PD-1 blockade also indirectly restores CTL-mediated killing.
Autologous BCMA-directed chimeric antigen receptor (CAR) T-cell therapy. Patient T cells are gene-modified to express a CAR targeting BCMA (TNFRSF17) and, upon binding, kill BCMA-positive plasma cells to reduce pathogenic autoantibodies in SLE. Administered by IV infusion.
Autologous T cells are gene-modified to express a BCMA (TNFRSF17)-targeting chimeric antigen receptor. Upon engaging BCMA on plasma cells/late B cells, the CAR T cells become activated and kill these BCMA-positive cells, depleting autoantibody-secreting plasma cells and reducing pathogenic autoantibodies in SLE.
BCMA-directed CAR T cells bind BCMA on target cells and directly lyse them via T-cell cytotoxic pathways (perforin/granzyme release and death-receptor signaling).
An intravenous anti-CD19 antibody-drug conjugate (ADC) that delivers a pyrrolobenzodiazepine (PBD) dimer payload via a cleavable linker; after CD19 binding and internalization, it releases the payload to induce DNA interstrand cross-links, leading to cell-cycle arrest and apoptosis in malignant B cells.
Humanized anti-CD19 monoclonal antibody linked via a cleavable linker to a pyrrolobenzodiazepine (PBD) dimer payload; upon CD19 binding and internalization in malignant B cells, the payload is released to create DNA interstrand cross-links in the minor groove, inhibiting DNA replication and triggering cell-cycle arrest and apoptosis.
The anti-CD19 ADC binds CD19, is internalized, and releases a PBD dimer that creates DNA interstrand cross-links, inhibiting replication and inducing cell-cycle arrest and apoptosis in the target cell.