Bispecific T‑cell engager (BiTE) antibody that links CD3 on T cells to CD19 on B‑cell blasts to drive T‑cell–mediated cytotoxicity.
Bispecific T‑cell engager (BiTE) antibody that binds CD3 on T cells and CD19 on B‑cell blasts, bringing them into close proximity to activate T cells and induce cytotoxic killing of CD19+ B cells.
NO
INDIRECT
CD3 on T cells is engaged to activate and redirect T cells to kill CD19+ B cells; CD3+ T cells are effectors, not the killed cells.
Oral BH3‑mimetic that selectively inhibits BCL‑2 to restore intrinsic apoptosis in malignant lymphoid cells.
Selective, oral BH3-mimetic that inhibits BCL-2 by binding its hydrophobic groove, blocking its anti-apoptotic function and freeing pro-apoptotic effectors (e.g., BAX/BAK) to trigger intrinsic (mitochondrial) apoptosis in tumor cells; relatively spares BCL-XL.
YES
DIRECT
Venetoclax directly inhibits BCL-2, releasing pro-apoptotic effectors (BAX/BAK) to induce mitochondrial apoptosis (MOMP, cytochrome c release, caspase activation) in BCL-2–dependent cells.
Autologous gene-modified CAR T cells targeting B7-H3 (CD276) with an inducible caspase-9 safety switch; designed to kill B7-H3–positive tumor cells and allow on-demand elimination of the cells if needed.
Autologous T cells engineered to express a chimeric antigen receptor targeting B7-H3 (CD276). Antigen engagement triggers T-cell activation, cytokine release, and perforin/granzyme-mediated cytotoxicity to kill B7-H3–positive tumor cells. Incorporates an inducible caspase-9 safety switch for on-demand elimination of the CAR-T cells.
YES
DIRECT
Anti–B7-H3 CAR T cells bind B7-H3 on target cells, become activated, and kill them via perforin/granzyme-mediated cytotoxicity (apoptosis).
An anti-CLDN18.2 antibody–drug conjugate that binds Claudin 18.2 on tumor cells, internalizes, and releases a topoisomerase I–inhibitor payload to induce DNA damage and apoptosis; may also engage Fc-mediated ADCC/CDC.
Anti-CLDN18.2 monoclonal antibody linked to a topoisomerase I inhibitor; binds Claudin 18.2 on tumor cells, internalizes, and releases the cytotoxic payload to cause DNA damage and apoptosis, with potential Fc-mediated ADCC/CDC.
YES
DIRECT
The anti-CLDN18.2 ADC binds Claudin 18.2, is internalized, and releases a topoisomerase I inhibitor that causes DNA damage and apoptosis; its Fc can also trigger ADCC/CDC against target cells.
An anti-CLDN18.2 antibody–drug conjugate that binds Claudin 18.2 on tumor cells, internalizes, and releases a topoisomerase I–inhibitor payload to induce DNA damage and apoptosis; may also engage Fc-mediated ADCC/CDC.
Anti-CLDN18.2 monoclonal antibody linked to a topoisomerase I inhibitor; binds Claudin 18.2 on tumor cells, internalizes, and releases the cytotoxic payload to cause DNA damage and apoptosis, with potential Fc-mediated ADCC/CDC.
NO
INDIRECT
IBI343 is an anti-CLDN18.2 ADC; it binds CLDN18.2, internalizes, and releases a topoisomerase I inhibitor payload that causes DNA damage and apoptosis (±ADCC/CDC). Topoisomerase I is the intracellular payload target, not the antigen recognized by the drug, so cells expressing only topoisomerase I are not specifically targeted or directly killed.