Anti‑CD20 monoclonal antibody that depletes CD20+ B cells via ADCC, CDC, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20+ cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
Rituximab binds CD20 on B cells and eliminates them via Fc-mediated ADCC (NK cells/macrophages), complement-dependent cytotoxicity (CDC), and induction of apoptosis.
Autologous, lentiviral-engineered chimeric antigen receptor T-cell therapy with a bicephalic APRIL/BAFF ligand domain enabling dual recognition of BCMA and TACI (and possibly BAFF-R) on malignant plasma cells to trigger T-cell activation and cytotoxicity.
Autologous T cells are lentivirally engineered to express a chimeric antigen receptor with a bicephalic APRIL/BAFF ligand domain that binds BCMA and TACI (and possibly BAFF-R) on malignant plasma cells. Receptor engagement activates CAR signaling (CD3ζ with costimulation), leading to T‑cell activation, expansion, cytokine release, and perforin/granzyme-mediated cytotoxic killing. Dual targeting is intended to reduce antigen escape compared with single-antigen CARs.
CAR-T cells bind BCMA via the APRIL/BAFF ligand domain, triggering CAR signaling and T‑cell effector functions that kill BCMA+ cells by perforin/granzyme-mediated cytolysis (and death-receptor pathways).
Autologous, lentiviral-engineered chimeric antigen receptor T-cell therapy with a bicephalic APRIL/BAFF ligand domain enabling dual recognition of BCMA and TACI (and possibly BAFF-R) on malignant plasma cells to trigger T-cell activation and cytotoxicity.
Autologous T cells are lentivirally engineered to express a chimeric antigen receptor with a bicephalic APRIL/BAFF ligand domain that binds BCMA and TACI (and possibly BAFF-R) on malignant plasma cells. Receptor engagement activates CAR signaling (CD3ζ with costimulation), leading to T‑cell activation, expansion, cytokine release, and perforin/granzyme-mediated cytotoxic killing. Dual targeting is intended to reduce antigen escape compared with single-antigen CARs.
CAR‑T cells use the APRIL/BAFF ligand domain to bind TACI, triggering CAR signaling and T‑cell cytolytic activity that kills TACI‑expressing cells via perforin/granzyme (and death‑receptor) pathways.
Autologous, lentiviral-engineered chimeric antigen receptor T-cell therapy with a bicephalic APRIL/BAFF ligand domain enabling dual recognition of BCMA and TACI (and possibly BAFF-R) on malignant plasma cells to trigger T-cell activation and cytotoxicity.
Autologous T cells are lentivirally engineered to express a chimeric antigen receptor with a bicephalic APRIL/BAFF ligand domain that binds BCMA and TACI (and possibly BAFF-R) on malignant plasma cells. Receptor engagement activates CAR signaling (CD3ζ with costimulation), leading to T‑cell activation, expansion, cytokine release, and perforin/granzyme-mediated cytotoxic killing. Dual targeting is intended to reduce antigen escape compared with single-antigen CARs.
CAR-T cells bind BAFF-R via the BAFF ligand domain of the bicephalic CAR, triggering CD3ζ costimulatory signaling and T-cell–mediated lysis through perforin/granzyme release.
Adoptive cellular gene therapy using T cells engineered with a chimeric antigen receptor (e.g., anti-CD19) to target and eliminate malignant B cells in DLBCL.
Autologous T cells are genetically engineered to express a chimeric antigen receptor (e.g., anti-CD19) that binds antigen on malignant B cells independent of MHC, activating the T cells to proliferate, release cytokines, and kill target cells via perforin/granzyme-mediated cytotoxicity, resulting in elimination of the tumor.
CAR-T cells bind CD19 on target cells, form an immune synapse, and kill via perforin/granzyme-mediated cytotoxicity (and Fas–FasL apoptosis).