Humanized monoclonal antibody targeting HER2/ERBB2; binds the extracellular domain to inhibit downstream PI3K/AKT and MAPK signaling, promote receptor internalization, and mediate ADCC.
Humanized monoclonal antibody against HER2/ERBB2 that binds the extracellular domain to block receptor signaling (PI3K/AKT, MAPK), promote receptor internalization and reduced dimerization, and mediate antibody-dependent cellular cytotoxicity (ADCC) against HER2-overexpressing tumor cells.
Fc-mediated ADCC: trastuzumab binds HER2 and engages Fcγ receptors on NK cells/other effectors to kill target cells; signaling blockade can also induce apoptosis/growth arrest.
Autologous gene-modified T cells expressing a chimeric antigen receptor targeting CD56 (NCAM1) with a PD-1 signal-conversion module to overcome PD-1/PD-L1–mediated inhibition and enhance cytotoxicity against CD56-positive tumor cells.
Autologous T cells genetically engineered to express a chimeric antigen receptor that binds CD56 (NCAM1), triggering T‑cell activation and cytotoxic killing of CD56‑positive tumor cells; incorporates a PD‑1 signal‑conversion module that transforms PD‑1/PD‑L1 inhibitory signals into activating signals to enhance antitumor activity and persistence.
CAR T cells recognize CD56 (NCAM1) via the CAR and directly kill CD56+ cells through T‑cell effector mechanisms (perforin/granzyme and death receptor pathways); a PD‑1 signal‑conversion module enhances activation but does not change the direct cytolysis.
A BCMAxCD3 bispecific T-cell-engaging monoclonal antibody that redirects and activates T cells to kill BCMA-positive multiple myeloma cells; administered subcutaneously and intravenously.
Etentamig (ABBV-383) is a human IgG4 bispecific antibody that binds BCMA on malignant plasma cells and CD3 on T lymphocytes, forming an immune synapse that redirects and activates cytotoxic T cells to kill BCMA-positive myeloma cells via TCR/CD3 signaling and perforin/granzyme-mediated apoptosis, with preferential activation of effector over regulatory T cells.
Bispecific BCMA×CD3 antibody links T cells to BCMA+ cells, activating CD3/TCR signaling and inducing perforin/granzyme-mediated apoptosis of the BCMA-expressing cells.
Anti-CTLA-4 IgG1 monoclonal antibody that blocks CTLA-4 to enhance T-cell priming and can deplete tumor regulatory T cells via FcγR-mediated ADCC/ADCP.
Human IgG1 monoclonal antibody against CTLA-4 that blocks CTLA-4-mediated inhibition to enhance CD28 costimulation and T-cell priming/activation, promoting antitumor cytotoxic T-cell responses; the IgG1 Fc can engage Fc-gamma receptors to deplete intratumoral regulatory T cells via ADCC/ADCP.
Ipilimumab binds CTLA-4 on T cells (especially intratumoral Tregs); its IgG1 Fc engages Fc-gamma receptors on NK cells/macrophages to mediate ADCC/ADCP, depleting CTLA-4–expressing cells.
CD20×CD3 bispecific IgG T‑cell engager used with step‑up dosing to redirect T cells to kill CD20+ B cells; also given as post–CAR‑T maintenance.
CD20×CD3 bispecific antibody that binds CD20 on B cells and CD3 on T cells to crosslink them, activate T cells, and induce perforin/granzyme-mediated cytotoxic killing of CD20-positive B cells (step-up dosing used to mitigate CRS).
CD20×CD3 bispecific crosslinks CD20 on B cells with CD3 on T cells, activating T cells to deliver perforin/granzyme-mediated cytotoxic killing of CD20+ cells.