Autologous CD19-directed CAR T-cell therapy with CD28 costimulation; gene-modified T cells recognize CD19 on malignant B cells to drive T-cell activation and cytotoxic killing.
Autologous T cells are genetically engineered to express a CD19-directed chimeric antigen receptor with CD28 costimulation. Upon binding CD19 on malignant B cells, CAR signaling activates and expands the T cells, triggering perforin/granzyme-mediated cytotoxicity and cytokine release to eliminate CD19+ B cells.
YES
DIRECT
CD19-directed CAR T cells bind CD19 on target cells, form an immune synapse, and induce apoptosis via perforin/granzyme (and Fas–FasL) after CAR activation.
T-cell–engaging bispecific antibody (CD20×CD3) that bridges CD3 on T cells to CD20 on B cells, inducing T-cell–mediated B-cell lysis; administered with step-up dosing.
CD20×CD3 bispecific antibody that binds CD20 on B cells and CD3 on T cells, crosslinking them to form an immune synapse and activate T cells for perforin/granzyme-mediated lysis of CD20+ B-cell malignancies; step-up dosing used to mitigate cytokine release.
YES
DIRECT
Bispecific antibody links CD3 on T cells to CD20 on target cells, forming an immune synapse and inducing perforin/granzyme-mediated T‑cell killing of CD20+ cells.
T-cell–engaging bispecific antibody (CD20×CD3) that bridges CD3 on T cells to CD20 on B cells, inducing T-cell–mediated B-cell lysis; administered with step-up dosing.
CD20×CD3 bispecific antibody that binds CD20 on B cells and CD3 on T cells, crosslinking them to form an immune synapse and activate T cells for perforin/granzyme-mediated lysis of CD20+ B-cell malignancies; step-up dosing used to mitigate cytokine release.
NO
INDIRECT
Glofitamab binds CD3 on T cells to activate them and bridge to CD20 on B cells, leading to T cell–mediated perforin/granzyme killing of CD20+ cells; CD3+ cells are effectors, not targets of killing.
Glycoengineered type II anti-CD20 monoclonal antibody used as pre-treatment to deplete peripheral B cells and mitigate CRS; mediates ADCC and direct cell death.
Glycoengineered type II anti-CD20 IgG1 that binds CD20 on B cells and, through enhanced Fc-gamma RIIIa (CD16a) engagement from afucosylated Fc glycans, induces strong ADCC (and phagocytosis) and triggers direct, caspase-independent cell death to deplete B cells.
YES
DIRECT
Binds CD20 on B cells; afucosylated Fc enhances FcγRIIIa engagement to trigger strong NK cell–mediated ADCC and macrophage phagocytosis, and the type II antibody also induces direct, caspase‑independent cell death.
Glycoengineered type II anti-CD20 monoclonal antibody used as pre-treatment to deplete peripheral B cells and mitigate CRS; mediates ADCC and direct cell death.
Glycoengineered type II anti-CD20 IgG1 that binds CD20 on B cells and, through enhanced Fc-gamma RIIIa (CD16a) engagement from afucosylated Fc glycans, induces strong ADCC (and phagocytosis) and triggers direct, caspase-independent cell death to deplete B cells.
NO
INDIRECT
Obinutuzumab binds CD20 on B cells; its afucosylated Fc engages Fc gamma receptor IIIa (CD16a) on NK cells/macrophages to trigger ADCC and phagocytosis, plus direct caspase-independent cell death of CD20+ B cells. CD16a-expressing effector cells are not killed by the drug.