Autologous patient T cells genetically engineered to express a CD19-directed chimeric antigen receptor (CAR) incorporating CD3ζ with CD28 or 4-1BB co-stimulatory domains, enabling HLA-independent recognition and cytotoxic elimination of CD19-positive malignant B cells.
Autologous T cells are genetically engineered to express a CD19-specific chimeric antigen receptor containing CD3ζ and CD28 or 4-1BB co-stimulatory domains. The CAR enables HLA-independent binding to CD19 on B cells, triggering T-cell activation, proliferation, cytokine release, and cytotoxic killing of CD19-positive malignant B cells.
YES
DIRECT
CAR T cells recognize CD19 on target cells, activate, and induce cytotoxicity via perforin/granzyme release and Fas–FasL apoptosis.
Autologous patient T cells genetically engineered to express a BCMA-directed chimeric antigen receptor (CAR) incorporating CD3ζ with CD28 or 4-1BB co-stimulatory domains, enabling HLA-independent recognition and cytotoxic elimination of BCMA-positive malignant plasma cells.
Autologous T cells are genetically engineered to express a BCMA-directed chimeric antigen receptor containing CD3ζ signaling plus CD28 or 4-1BB co-stimulation. The CAR enables HLA-independent recognition of BCMA on malignant plasma cells, triggering T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of BCMA-positive cells.
YES
DIRECT
BCMA-targeted CAR T cells bind BCMA on tumor cells, triggering activation and degranulation with perforin/granzyme-mediated lysis (and Fas/FasL apoptosis) of BCMA-positive cells.
Type II, glycoengineered anti-CD20 monoclonal antibody that depletes CD20+ B cells via enhanced ADCC/ADCP and direct cell death (with some CDC).
Type II, glycoengineered humanized IgG1 anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes them via enhanced Fc gamma RIII (CD16)-mediated ADCC and ADCP and by inducing direct cell death/apoptosis, with some complement-dependent cytotoxicity (CDC). Afucosylated Fc glycosylation increases Fc receptor affinity and cytotoxic effector function.
YES
DIRECT
Binds CD20 on B cells and kills via enhanced FcγRIIIa-mediated ADCC by NK cells, ADCP by macrophages, direct type II cell death/apoptosis, and some complement-dependent cytotoxicity (CDC).
Fc-enhanced anti-CTLA-4 monoclonal antibody that promotes T-cell priming and depletes intratumoral Tregs via ADCC, boosting CD8+ T-cell responses.
Fc-enhanced anti-CTLA-4 monoclonal antibody that blocks CTLA-4 to promote T-cell priming/activation and leverages Fc-mediated ADCC to deplete intratumoral Tregs, boosting CD8+ T-cell responses.
YES
DIRECT
Antibody binds CTLA-4 on target cells; its Fc engages FcγR-bearing effectors (e.g., NK cells/macrophages) to mediate ADCC/ADCP, depleting CTLA-4+ cells such as intratumoral Tregs.
Autologous tumor-infiltrating lymphocyte (TIL) adoptive cell therapy administered intravenously after lymphodepleting chemotherapy to mediate TCR-dependent cytotoxicity against tumor cells.
Autologous TILs expanded ex vivo are reinfused after lymphodepleting chemotherapy. They recognize patient-specific tumor antigens via TCR-MHC and kill tumor cells through perforin/granzyme-mediated cytotoxicity and cytokine release, with IL-2 supporting T-cell activation, proliferation, and persistence.
YES
DIRECT
Autologous TILs recognize the tumor-associated peptide–MHC II complex via their TCRs and directly kill target cells through perforin/granzyme-mediated cytolysis (with possible Fas–FasL and cytokine-mediated effects).