Autologous, gene-modified T cells engineered to express a chimeric antigen receptor that binds CD19; administered as a single IV infusion to activate cytotoxic T-cell killing of CD19+ B-lineage cells, leading to B-cell depletion and reduced autoantibody production.
Autologous T cells are gene-modified to express a chimeric antigen receptor that binds CD19 on B-lineage cells. Upon engagement, CAR-T cells activate and mediate cytotoxic killing (perforin/granzyme and cytokines), leading to profound depletion of CD19+ B cells/plasmablasts, reduction of autoantibody production, and functional resetting of humoral immunity.
CD19 CAR-T cells bind CD19 on B-lineage cells, form an immune synapse, and kill targets via perforin/granzyme-mediated cytolysis (and death-receptor pathways), depleting CD19+ cells.
Autologous T cells engineered ex vivo to express a chimeric antigen receptor targeting BCMA (TNFRSF17); upon BCMA engagement, CAR signaling activates T-cell cytotoxicity and cytokine release to eliminate BCMA-expressing myeloma cells.
Autologous T cells are engineered to express a chimeric antigen receptor that binds BCMA (TNFRSF17); upon BCMA engagement on myeloma cells, CAR signaling activates T-cell cytotoxicity and cytokine release, leading to perforin/granzyme-mediated lysis of BCMA-expressing cells.
BCMA-specific CAR T cells engage BCMA on target cells, become activated, and kill via immunologic synapse with perforin/granzyme release (and Fas–FasL), inducing apoptosis/lysis.
An antibody–drug conjugate comprising a humanized anti–Trop-2 IgG monoclonal antibody linked to SN-38 (the active metabolite of irinotecan), a topoisomerase I inhibitor; after binding Trop-2 on tumor cells, it is internalized and releases SN-38 to induce DNA damage and apoptosis, with a hydrolyzable linker enabling bystander killing.
Humanized anti-Trop-2 IgG monoclonal antibody linked via a hydrolyzable linker to SN-38 (topoisomerase I inhibitor). After binding Trop-2 on tumor cells and internalization, SN-38 is released, stabilizes Topo I-DNA complexes, induces DNA damage and replication stress, leading to cell death; the linker enables bystander killing.
Anti-TROP2 ADC binds TROP2 and is internalized; the linker is cleaved to release SN-38, a topoisomerase I inhibitor that stabilizes Topo I–DNA complexes, causing DNA damage and apoptosis (with additional bystander killing).
Autologous gene-modified T lymphocytes expressing a chimeric antigen receptor targeting Fc receptor–like 5 (FcRL5/CD307e) on multiple myeloma cells to mediate antigen-directed cytotoxicity.
Autologous T cells engineered to express a chimeric antigen receptor that binds FcRL5 (CD307e) on multiple myeloma cells; CAR engagement triggers CD3z/costimulatory signaling, leading to T-cell activation, expansion, cytokine release, and perforin/granzyme-mediated cytotoxic killing of FcRL5-positive plasma cells.
CAR-T cells recognize FcRL5 on target cells; CAR engagement activates CD3ζ/costimulatory signaling, triggering perforin/granzyme-mediated cytolysis (and death receptor pathways) of FcRL5-positive cells.
Anti-HER2 IgG1 monoclonal antibody that blocks HER2 signaling and mediates antibody-dependent cellular cytotoxicity (ADCC).
Humanized IgG1 monoclonal antibody targeting HER2; binds the extracellular domain to block HER2 signaling and tumor cell proliferation, and recruits immune effector cells via Fc gamma receptors to mediate antibody-dependent cellular cytotoxicity (ADCC).
HER2+ cells are killed via antibody-dependent cellular cytotoxicity (ADCC) when trastuzumab-bound cells are lysed by FcγR-expressing effector cells (e.g., NK cells); signaling blockade may also promote apoptosis.