Autologous gene-modified T cells engineered to express a CAR targeting BCMA, depleting BCMA-positive plasma cells/plasmablasts to reduce pathogenic autoantibody production in MDR-SRNS.
Autologous T cells are genetically engineered to express a chimeric antigen receptor specific for BCMA. On recognizing BCMA on plasma cells/plasmablasts, the CAR-T cells become activated and kill these BCMA-positive cells via cytotoxic mechanisms, depleting antibody-secreting cells and reducing pathogenic autoantibody production in MDR-SRNS.
CAR-T cells bind BCMA on target cells and induce cytotoxic T-cell killing via perforin/granzyme-mediated lysis and apoptosis (and Fas–FasL pathways).
Autologous T cells genetically engineered to co-express a bispecific chimeric antigen receptor targeting CD19 and CD22, activating T-cell cytotoxicity against B-ALL blasts and reducing antigen-loss escape.
Autologous T cells are genetically engineered to co-express a bispecific chimeric antigen receptor that recognizes CD19 and CD22 on B-ALL cells. CAR engagement activates T-cell signaling, driving proliferation, cytokine release, and perforin/granzyme-mediated cytotoxicity, while dual targeting reduces antigen-loss escape compared with single-antigen CARs.
Bispecific CAR T cells bind CD19 on target cells, triggering T-cell activation and perforin/granzyme-mediated cytolysis (and Fas/FasL apoptosis) of CD19-expressing cells.
Autologous T cells genetically engineered to co-express a bispecific chimeric antigen receptor targeting CD19 and CD22, activating T-cell cytotoxicity against B-ALL blasts and reducing antigen-loss escape.
Autologous T cells are genetically engineered to co-express a bispecific chimeric antigen receptor that recognizes CD19 and CD22 on B-ALL cells. CAR engagement activates T-cell signaling, driving proliferation, cytokine release, and perforin/granzyme-mediated cytotoxicity, while dual targeting reduces antigen-loss escape compared with single-antigen CARs.
CAR T cells bind CD22 via the CAR, activating T-cell cytotoxicity and killing target cells through perforin/granzyme-mediated lysis and cytokine release.
An autologous anti-DLL3 chimeric antigen receptor (CAR) T-cell therapy composed of genetically engineered patient T cells expressing a CAR targeting Delta-like ligand 3 (DLL3). Binding of DLL3 triggers T-cell activation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of DLL3-positive tumor cells.
Autologous T cells are genetically engineered to express a chimeric antigen receptor targeting DLL3. CAR engagement of DLL3 on tumor cells activates the T cells, inducing cytokine release, expansion, and perforin/granzyme-mediated cytotoxic killing of DLL3-positive tumor cells.
Anti-DLL3 CAR T cells bind DLL3 on target cells, activate, and kill via perforin/granzyme-mediated cytotoxicity leading to apoptosis.
Anti‑CD20 monoclonal antibody that depletes malignant B cells via ADCC, CDC, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B lymphocytes and depletes malignant B cells via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), antibody-dependent cellular phagocytosis, and induction of apoptosis.
Anti-CD20 antibody binds CD20 on B cells, recruiting effector mechanisms to kill them: Fc-mediated ADCC by NK cells, complement activation (CDC) forming MAC, antibody-dependent phagocytosis by macrophages, and apoptosis upon crosslinking.