Autologous T cells genetically modified to express a chimeric antigen receptor that targets BAFFR (TNFRSF13C) on malignant B cells, leading to T-cell activation and cytotoxic killing.
Autologous T cells are gene-modified to express a chimeric antigen receptor that binds BAFFR (TNFRSF13C) on malignant B cells; CAR engagement triggers T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of BAFFR-expressing B cells.
YES
DIRECT
BAFFR-specific CAR T cells bind BAFFR on target B cells and, upon engagement, activate cytotoxic pathways (perforin/granzyme-mediated killing and death receptor signaling) to induce apoptosis.
Off-the-shelf allogeneic CD19-directed chimeric antigen receptor natural killer (CAR-NK) cell therapy designed to deplete CD19+ B-lineage cells to reduce pathogenic autoantibodies.
Off-the-shelf allogeneic NK cells engineered with a CD19-targeted CAR containing OX40 and CD3ζ signaling domains and membrane-bound IL-15. Upon binding CD19 on B-lineage cells, the CAR-NK cells are activated to release cytotoxic mediators and pro-inflammatory cytokines, leading to depletion of CD19+ B cells and reduction of pathogenic autoantibodies.
YES
DIRECT
CAR-NK cells bind CD19 on target cells, become activated, and kill via degranulation with perforin/granzymes leading to lysis/apoptosis of CD19+ cells.
Human IgG1κ anti-CD38 monoclonal antibody (DARZALEX) given IV weekly for 8 doses (4, 8, or 16 mg/kg); depletes CD38+ cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity/phagocytosis, and apoptosis; inhibits CD38 ectoenzyme (NADase) activity affecting adenosine signaling.
Human IgG1κ anti-CD38 monoclonal antibody that binds CD38 on plasma cells and other CD38+ immune cells, inducing complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC), antibody-dependent cellular phagocytosis (ADCP), and apoptosis to deplete target cells; also inhibits CD38 ectoenzyme (NADase) activity, modulating NAD/adenosine signaling.
YES
DIRECT
Anti-CD38 IgG1 mAb binds CD38 on target cells and induces complement-mediated lysis (CDC), Fc-mediated ADCC/ADCP by immune effectors, and apoptosis, depleting CD38+ cells.
Type II anti-CD20 glycoengineered monoclonal antibody that depletes CD20+ B cells via enhanced ADCC, CDC, and direct apoptosis.
Glycoengineered type II humanized anti-CD20 IgG1 that binds CD20 on B cells; afucosylated Fc enhances FcγRIIIa engagement, driving potent antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and direct (caspase-independent) apoptosis to deplete CD20+ B cells.
YES
DIRECT
Obinutuzumab binds CD20 on B cells; its afucosylated Fc engages Fc gamma RIIIa on effector cells to trigger ADCC, activates complement for CDC, and also induces direct caspase-independent apoptosis of CD20+ cells.
Type II anti-CD20 glycoengineered monoclonal antibody that depletes CD20+ B cells via enhanced ADCC, CDC, and direct apoptosis.
Glycoengineered type II humanized anti-CD20 IgG1 that binds CD20 on B cells; afucosylated Fc enhances FcγRIIIa engagement, driving potent antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and direct (caspase-independent) apoptosis to deplete CD20+ B cells.
NO
INDIRECT
Obinutuzumab binds CD20 on B cells; its afucosylated Fc engages CD16A on NK cells/macrophages to drive ADCC, plus CDC and direct apoptosis of CD20+ cells. CD16A-expressing effector cells are not killed.