Subcutaneous bispecific IgG antibody (CD3xCD20) that redirects T cells to kill CD20-positive B cells.
Bispecific IgG antibody that binds CD3 on T cells and CD20 on B cells, crosslinking T cells to malignant B cells to activate cytotoxic T-lymphocyte responses and induce perforin/granzyme-mediated killing of CD20-positive cells.
YES
DIRECT
Bispecific antibody links CD3+ T cells to CD20+ cells, activating T-cell cytotoxicity and perforin/granzyme-mediated killing of the CD20-expressing cells.
Off-the-shelf, allogeneic cord blood–derived natural killer (NK) cell therapy that provides cytotoxic NK cells mediating CD16 (FcγRIIIa)–dependent ADCC against anti-CD20–opsonized B cells.
Off-the-shelf allogeneic cord blood–derived NK cells that, via CD16 (FcγRIIIa), mediate antibody-dependent cellular cytotoxicity against anti-CD20–opsonized B cells (with rituximab/obinutuzumab), with additional innate NK cytotoxicity and cytokine effects.
YES
INDIRECT
CD20+ cells are killed when coated with anti-CD20 antibodies; the infused allogeneic NK cells bind antibody Fc via CD16 and mediate ADCC (perforin/granzyme-mediated lysis).
Subcutaneous bispecific IgG antibody (CD3xCD20) that redirects T cells to kill CD20-positive B cells.
Bispecific IgG antibody that binds CD3 on T cells and CD20 on B cells, crosslinking T cells to malignant B cells to activate cytotoxic T-lymphocyte responses and induce perforin/granzyme-mediated killing of CD20-positive cells.
NO
INDIRECT
Epcoritamab binds CD3ε on T cells to activate them and simultaneously binds CD20 on B cells, directing perforin/granzyme-mediated killing of CD20+ B cells; CD3ε+ T cells are not the killed targets.
Adoptive cellular immunotherapy using T cells engineered with chimeric antigen receptors to target B-cell antigens.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that recognizes B-cell antigens (e.g., CD19/CD20). Antigen engagement triggers CAR signaling (CD3zeta plus costimulatory domains), leading to T-cell activation, proliferation, cytokine release, and MHC-independent cytotoxic killing of antigen-expressing B cells.
YES
DIRECT
CAR T cells bind CD19 via the CAR, become activated, and kill CD19+ cells through perforin/granzyme-mediated cytolysis and apoptosis (and death-receptor pathways), independent of MHC.
Adoptive cellular immunotherapy using T cells engineered with chimeric antigen receptors to target B-cell antigens.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that recognizes B-cell antigens (e.g., CD19/CD20). Antigen engagement triggers CAR signaling (CD3zeta plus costimulatory domains), leading to T-cell activation, proliferation, cytokine release, and MHC-independent cytotoxic killing of antigen-expressing B cells.
YES
DIRECT
CAR T cells recognizing CD20 bind the antigen and, upon CAR signaling, directly lyse CD20+ cells via perforin/granzyme release and death-receptor pathways (MHC-independent).