A biologic antibody targeting CD20 that depletes CD20-positive B cells to reduce humoral sensitization prior to kidney transplantation.
Monoclonal antibody that binds CD20 on B cells and depletes CD20+ B-cell populations via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, thereby reducing humoral responses (e.g., anti-HLA antibody production) prior to transplantation.
Binding to CD20 triggers complement-dependent cytotoxicity and Fc-mediated effector killing (ADCC/ADCP by NK cells/macrophages), with possible direct apoptosis of B cells.
Autologous T cells genetically engineered to express a chimeric antigen receptor targeting STEAP1 on prostate cancer cells; CAR engagement activates T-cell cytotoxicity and cytokine signaling against STEAP1-positive tumor cells.
Autologous T cells are engineered to express a CAR that binds STEAP1 on tumor cells; CAR engagement activates T-cell signaling, cytokine release, and cytotoxic granule-mediated killing of STEAP1-positive cancer cells.
CAR binding to STEAP1 activates the engineered T cells to kill STEAP1+ cells via perforin/granzyme release and Fas–FasL–mediated apoptosis.
An antibody–drug conjugate (PADCEV) consisting of a human IgG1 monoclonal antibody targeting Nectin-4 linked to the microtubule-disrupting agent monomethyl auristatin E (MMAE), inducing internalization and apoptosis in Nectin-4–expressing urothelial cancer cells.
Enfortumab vedotin is an antibody-drug conjugate comprising a human IgG1 monoclonal antibody targeting Nectin-4 linked via a cleavable linker to the microtubule toxin monomethyl auristatin E (MMAE). After binding Nectin-4 on tumor cells and internalization, intracellular cleavage releases MMAE, which binds tubulin, inhibits microtubule polymerization, induces G2/M cell-cycle arrest, and triggers apoptosis in Nectin-4–expressing cancer cells.
The ADC binds Nectin-4 on target cells, is internalized, and releases MMAE, which inhibits tubulin polymerization, causing G2/M arrest and apoptosis in Nectin-4-expressing cells.
Autologous gene-modified T cells engineered to express a mesothelin-directed KIR-based CAR; given as a single IV infusion. The KIR-CAR binds mesothelin on tumor cells to activate the engineered T cells, inducing antigen-specific cytotoxicity and cytokine release against mesothelin-expressing ovarian cancer, cholangiocarcinoma, and mesothelioma.
Autologous T cells engineered with a mesothelin-directed KIR-based CAR (anti-MSLN scFv fused to KIR2DS2 signaling and DAP12). Binding to mesothelin on tumor cells triggers KIR-mediated activation, leading to antigen-specific T-cell cytotoxicity and cytokine release against mesothelin-expressing cancers; KIR-CAR design may reduce T-cell exhaustion and enhance persistence.
Mesothelin-targeted KIR-CAR T cells bind mesothelin on tumor cells, activate, and kill them via perforin/granzyme-mediated cytolysis and death receptor pathways, with cytokine release.
Anti-CD38 IgG1 monoclonal antibody that mediates complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity/phagocytosis, and apoptosis, depleting CD38-positive plasma and immunosuppressive cells.
Anti-CD38 IgG1 monoclonal antibody that binds CD38 on plasma/tumor and immunosuppressive cells, inducing complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity and phagocytosis, and apoptosis, leading to depletion of CD38+ cells.
Binds CD38 on target cells and triggers complement-dependent cytotoxicity, Fc-mediated ADCC and phagocytosis, and can induce apoptosis, leading to depletion of CD38+ cells.