Peptide receptor radionuclide therapy (PRRT); a radiolabeled somatostatin analog (DOTA-TATE) that binds SSTR2 on tumor cells and delivers beta radiation, causing DNA damage and tumor cell death (brand name Lutathera).
Radiolabeled somatostatin analog (DOTA-TATE) that binds somatostatin receptor 2 (SSTR2) on tumor cells, is internalized, and delivers beta radiation from Lu-177, causing DNA damage and tumor cell death in SSTR-positive cells.
The radiolabeled somatostatin analog binds SSTR2, is internalized, and Lu-177 emits beta radiation that causes DNA damage (double-strand breaks), leading to death of SSTR2-positive cells.
IV humanized anti-CD19 monoclonal antibody that binds CD19 on malignant B cells, inducing antibody-dependent cellular cytotoxicity/phagocytosis and direct cytotoxic signaling.
Humanized anti-CD19 monoclonal antibody that binds CD19 on malignant B cells, inducing antibody-dependent cellular cytotoxicity and phagocytosis and promoting direct cytotoxic/apoptotic signaling.
Binds CD19 on B cells and recruits FcγR-expressing immune effectors to kill via ADCC and antibody-dependent phagocytosis; can also trigger pro-apoptotic signaling in CD19+ cells.
Oral BCL-2 inhibitor (BH3 mimetic) that blocks BCL-2 to trigger mitochondrial apoptosis.
Selective oral BCL-2 inhibitor (BH3 mimetic) that binds the hydrophobic groove of BCL-2, neutralizes its anti-apoptotic function, restores mitochondrial outer membrane permeabilization, and triggers caspase-mediated apoptosis in BCL-2–dependent tumor cells; spares BCL-XL.
Venetoclax is a BH3-mimetic that binds and inhibits BCL-2, displacing pro-apoptotic factors to activate BAX/BAK, induce mitochondrial outer membrane permeabilization, and trigger caspase-dependent apoptosis in BCL-2–dependent cells.
Autologous CD7-directed chimeric antigen receptor (CAR) T-cell therapy in which patient T cells are genetically engineered to express a CAR targeting CD7, enabling TCR-independent activation and cytotoxic killing of CD7-positive T/NK-cell malignancies.
Autologous T cells are genetically engineered to express a chimeric antigen receptor targeting CD7. Upon binding CD7 on malignant T/NK cells, the CAR triggers TCR-independent activation and cytotoxic killing via perforin/granzyme release and cytokine-mediated effects, leading to elimination of CD7-positive tumor cells.
Anti-CD7 CAR-T cells bind CD7 on target cells, become activated, and kill via perforin/granzyme-mediated cytolysis (and death receptor/cytokine-dependent apoptosis).
Monoclonal IgG1 anti-HER2 antibody that binds the extracellular domain of HER2, inhibits HER2 signaling, and mediates antibody-dependent cellular cytotoxicity (ADCC).
Humanized IgG1 monoclonal antibody targeting the extracellular domain of HER2 (ERBB2); blocks HER2-driven signaling and proliferation, promotes receptor downregulation, and engages Fcγ receptor–bearing effector cells to mediate antibody-dependent cellular cytotoxicity (ADCC) against HER2-overexpressing tumor cells.
Trastuzumab binds HER2 on tumor cells and engages Fcγ receptor–bearing immune cells (e.g., NK cells, macrophages) to mediate antibody‑dependent cellular cytotoxicity; it also inhibits HER2 signaling, promoting apoptosis.