Gene-modified autologous T cells engineered to express a CD19-directed chimeric antigen receptor, leading to T-cell activation and cytotoxic killing of CD19-positive B-cell lymphoma.
Autologous T cells are gene-modified ex vivo to express a CD19-directed chimeric antigen receptor. Upon binding CD19 on B cells, the CAR transmits activation signals (CD3ζ with costimulatory domains), driving T-cell expansion, cytokine release, and perforin/granzyme-mediated cytotoxic killing of CD19-positive malignant B cells.
YES
DIRECT
CD19-specific CAR T cells bind CD19 on target B cells, become activated via CD3zeta/co-stimulatory signaling, and kill by perforin/granzyme-mediated cytolysis (and Fas–FasL apoptosis).
CD20×CD3 bispecific IgG T-cell engager (2:1 format) that binds CD20 on B cells and CD3 on T cells to redirect T-cell cytotoxicity against malignant B cells.
Bispecific antibody that binds CD20 on B cells and CD3 on T cells, crosslinking them to activate and redirect T-cell cytotoxicity against CD20-positive malignant B cells.
YES
DIRECT
Bispecific antibody bridges CD3 on T cells to CD20 on B cells, forming an immune synapse and triggering T‑cell perforin/granzyme–mediated killing of CD20+ cells.
CD20×CD3 bispecific IgG T-cell engager (2:1 format) that binds CD20 on B cells and CD3 on T cells to redirect T-cell cytotoxicity against malignant B cells.
Bispecific antibody that binds CD20 on B cells and CD3 on T cells, crosslinking them to activate and redirect T-cell cytotoxicity against CD20-positive malignant B cells.
NO
INDIRECT
Glofitamab engages CD3 on T cells to redirect them to kill CD20+ B cells via T‑cell cytotoxicity; CD3+ T cells themselves are not targeted for killing.
Glycoengineered type II anti-CD20 monoclonal antibody used as pre-treatment to deplete B cells and mitigate cytokine release syndrome before glofitamab.
Glycoengineered humanized IgG1 type II anti‑CD20 monoclonal antibody that binds CD20 on B cells and depletes them primarily via enhanced FcγRIIIa‑mediated ADCC and ADCP due to afucosylated Fc, and by inducing direct, caspase‑independent apoptosis; used as pre‑treatment to reduce B‑cell burden and mitigate cytokine release prior to CD20×CD3 bispecific therapy.
YES
DIRECT
Obinutuzumab binds CD20 on B cells and induces FcγRIIIa‑enhanced ADCC by NK cells and ADCP by macrophages, and also triggers direct, caspase‑independent cell death characteristic of type II anti‑CD20 antibodies.
Anti-CD38 IgG1 monoclonal antibody that depletes CD38+ myeloma plasma cells via ADCC, CDC, ADCP, and apoptosis; also modulates the immune microenvironment.
Human IgG1k monoclonal antibody targeting CD38 on myeloma cells; induces tumor cell death via ADCC, CDC, ADCP, and apoptosis, and depletes CD38+ immunosuppressive cells (Tregs, Bregs, MDSCs), thereby modulating the immune microenvironment.
YES
DIRECT
Anti-CD38 IgG1 binds CD38 on target cells and induces Fc-mediated ADCC (NK cells), CDC (complement), ADCP (macrophages), and can trigger apoptosis upon cross-linking.