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.
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.
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.
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.
TROP2-directed antibody–drug conjugate carrying a topoisomerase I inhibitor payload; binds TROP2 on tumor cells, is internalized, and releases the cytotoxic payload to induce DNA damage/replication stress with a bystander effect.
TROP2-targeted antibody–drug conjugate that binds TROP2 on tumor cells, is internalized, and releases a topoisomerase I inhibitor payload to induce DNA damage and replication stress, with a membrane-permeable bystander effect.
Anti-TROP2 antibody-drug conjugate binds TROP2, is internalized, and releases a topoisomerase I inhibitor payload that causes DNA damage/replication stress, killing the target cell (with a bystander effect).
Gene-modified natural killer (NK) cells engineered to express an NKG2D-based chimeric antigen receptor (CAR) that recognizes NKG2D ligands (MICA, MICB, ULBP family) on tumor cells, activating NK cytotoxicity for treatment of relapsed/refractory multiple myeloma.
Gene‑modified NK cells expressing an NKG2D‑based CAR recognize stress‑induced NKG2D ligands (MICA, MICB, ULBP family) on tumor cells. CAR signaling activates NK cytotoxic functions, inducing degranulation (perforin/granzyme), cytokine‑mediated killing, and apoptosis of malignant cells, targeting relapsed/refractory multiple myeloma.
NKG2D-CAR NK cells bind ULBP2 on target cells, triggering NK activation and degranulation (perforin/granzyme) leading to apoptotic cytolysis.