An intravenously administered tetra-specific antibody (biologic immunotherapy) engineered to engage CD3 on T cells and recognize multiple B-cell-associated antigens to redirect and activate T cells against B-cell lymphoma, aiming to enhance cytotoxicity, provide costimulation/checkpoint modulation, and reduce antigen escape.
Tetra-specific T-cell–redirecting antibody that binds CD3 on T cells, CD19 on B-cell lymphomas, PD-L1 to block PD-1–mediated inhibition, and 4-1BB to provide costimulation. By crosslinking T cells to CD19+ tumor cells, it induces CTL-mediated killing while concurrently enhancing activation and persistence and reducing antigen escape.
NO
INDIRECT
4-1BB binding provides T-cell costimulation; cytotoxicity is mediated when the antibody links CD3+ T cells to CD19+ tumor cells, leading to perforin/granzyme killing of CD19-expressing cells. 4-1BB+ cells are not targeted for killing.
Rabbit polyclonal anti-thymocyte globulin that depletes T cells to prevent rejection and GVHD.
Rabbit polyclonal anti-thymocyte IgG that binds multiple T-cell surface antigens and depletes T cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, producing immunosuppression to prevent rejection and GVHD.
YES
DIRECT
ATG contains antibodies that can bind HLA-DR; bound cells are killed via complement-dependent lysis, Fc-mediated ADCC, and apoptosis.
Autologous CD19-directed CAR T-cell therapy. Patient T cells are engineered ex vivo to express a chimeric antigen receptor targeting CD19 and are administered as a single intravenous infusion (0.2–2 million cells/kg) after lymphodepleting chemotherapy to promote expansion. The CAR engages CD19 on B-lineage cells to trigger T-cell activation, proliferation, and cytotoxic killing of malignant CD19+ cells, with expected on-target B-cell aplasia.
Autologous T cells are engineered ex vivo to express a chimeric antigen receptor that binds CD19 on B‑lineage cells. Upon engagement, CAR signaling (CD3ζ with costimulatory domains) activates the T cells, driving proliferation and cytotoxic killing of CD19+ malignant cells, resulting in tumor cell lysis and on‑target B‑cell aplasia; lymphodepleting chemotherapy is used to enhance CAR T‑cell expansion and persistence.
YES
DIRECT
CD19-directed CAR T cells bind CD19 on target cells, activate, and directly kill CD19+ cells via T-cell cytotoxic mechanisms (perforin/granzyme release and Fas–FasL–mediated apoptosis).
An IgG1 monoclonal antibody targeting Claudin 18.2 (CLDN18.2) on gastric/GEJ tumor cells, mediating immune effector functions including Fcγ receptor–driven antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and potential antibody-dependent cellular phagocytosis (ADCP).
A tumor-targeting IgG1 monoclonal antibody that binds Claudin 18.2 on gastric/GEJ cancer cells and induces immune-mediated killing via Fcγ receptor–dependent ADCC, complement-dependent cytotoxicity (CDC), and antibody-dependent cellular phagocytosis (ADCP).
YES
DIRECT
The antibody binds Claudin 18.2 on tumor cells and recruits immune effectors to kill via FcγR-mediated ADCC, complement-dependent cytotoxicity (CDC/MAC), and antibody-dependent cellular phagocytosis (ADCP).
An IgG1 monoclonal antibody targeting Claudin 18.2 (CLDN18.2) on gastric/GEJ tumor cells, mediating immune effector functions including Fcγ receptor–driven antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and potential antibody-dependent cellular phagocytosis (ADCP).
A tumor-targeting IgG1 monoclonal antibody that binds Claudin 18.2 on gastric/GEJ cancer cells and induces immune-mediated killing via Fcγ receptor–dependent ADCC, complement-dependent cytotoxicity (CDC), and antibody-dependent cellular phagocytosis (ADCP).
NO
INDIRECT
The antibody binds CLDN18.2 on tumor cells; its Fc engages CD16A on NK cells to trigger ADCC (and can also enable CDC/ADCP), killing CLDN18.2-positive tumor cells, not CD16A-expressing cells.