A CD20×CD3 bispecific monoclonal antibody (T‑cell engager) that binds CD20 on B cells and CD3 on T cells to activate cytotoxic T cells and eliminate CD20+ lymphoma cells.
A CD20xCD3 bispecific monoclonal antibody that binds CD20 on B cells and CD3 on T cells, cross-linking and activating cytotoxic T cells to form immune synapses and lyse CD20-positive malignant B cells.
NO
INDIRECT
Glofitamab binds CD3 epsilon on T cells and CD20 on B cells to crosslink and activate T cells; the activated T cells kill CD20-positive B cells via immune synapse and perforin/granzyme release, not the CD3 epsilon–expressing T cells.
A glycoengineered type II anti‑CD20 monoclonal antibody that depletes B cells via ADCC and direct cell death; used as a lead‑in to debulk disease and reduce cytokine‑release risk.
Obinutuzumab is a glycoengineered humanized IgG1 type II anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes them via enhanced Fc gamma RIIIa–mediated ADCC and direct, caspase-independent apoptosis; it is often used as a lead-in to debulk disease and reduce cytokine-release risk.
YES
DIRECT
Binds CD20 on B cells and induces killing via enhanced FcγRIIIa-mediated ADCC by NK cells/macrophages and by direct, caspase‑independent apoptosis (with minimal CDC).
Lentivirally modified T cells expressing a CAR against CD79b (BCR component); IV infusion with dose escalation; intended for MHC-independent elimination of CD79b+ B-cell malignancies.
Gene-modified T cells express a chimeric antigen receptor that recognizes CD79b on B-cell malignancies; CAR engagement activates T cells in an MHC-independent manner, inducing proliferation, cytokine release, and perforin/granzyme-mediated killing of CD79b-positive tumor cells.
YES
DIRECT
CD79b-specific CAR T cells recognize CD79b on B cells and directly kill them via T‑cell activation and perforin/granzyme-mediated cytolysis (MHC‑independent).
Autologous gene-modified T cells engineered with an EGFRvIII synNotch receptor that induces expression of a CAR targeting EphA2 and IL-13Rα2; administered IV as cellular immunotherapy for EGFRvIII+ glioblastoma.
Autologous T cells engineered with an EGFRvIII-directed synNotch receptor that, upon binding EGFRvIII on tumor cells, induces expression of a CAR targeting EphA2 and IL-13Ralpha2. This logic-gated activation confines CAR expression to EGFRvIII+ tumors, enabling targeted T-cell cytotoxicity and cytokine release against EphA2- and IL-13Ralpha2-expressing glioblastoma cells.
NO
INDIRECT
EGFRvIII is a synNotch priming cue; binding to EGFRvIII induces CAR expression, after which T cells kill cells bearing EphA2 or IL-13Rα2 via CAR-mediated cytotoxicity (perforin/granzymes and cytokines).
Autologous gene-modified T cells engineered with an EGFRvIII synNotch receptor that induces expression of a CAR targeting EphA2 and IL-13Rα2; administered IV as cellular immunotherapy for EGFRvIII+ glioblastoma.
Autologous T cells engineered with an EGFRvIII-directed synNotch receptor that, upon binding EGFRvIII on tumor cells, induces expression of a CAR targeting EphA2 and IL-13Ralpha2. This logic-gated activation confines CAR expression to EGFRvIII+ tumors, enabling targeted T-cell cytotoxicity and cytokine release against EphA2- and IL-13Ralpha2-expressing glioblastoma cells.
YES
DIRECT
Upon EGFRvIII-triggered synNotch activation, the T cells express an anti‑EphA2 CAR; CAR engagement with EphA2 on tumor cells drives T‑cell cytotoxicity via perforin/granzyme release and apoptosis-inducing pathways.