An investigational HER2-targeted antibody-drug conjugate (ADC). The monoclonal antibody binds HER2 (including low-HER2 expressers), is internalized, and releases a cytotoxic payload to induce tumor cell death and suppress proliferation; targets HER2/ERBB signaling pathways.
HER2-targeted monoclonal antibody (trastuzumab-based) binds HER2, including low-expressing cells, is internalized, and after linker cleavage releases a camptothecin-derived topoisomerase I–inhibiting payload that induces DNA damage, leading to cell-cycle arrest and apoptosis and suppression of HER2-driven tumor proliferation.
YES
DIRECT
The HER2-targeted ADC binds HER2 on tumor cells, is internalized, and releases a camptothecin-derived topoisomerase I inhibitor that induces DNA damage, leading to cell-cycle arrest and apoptosis.
Anti-CD20 monoclonal antibody given once on Cycle 1 Day 1.
Obinutuzumab is a glycoengineered, humanized type II anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells and depletes malignant B cells primarily via enhanced Fc-mediated effector functions (increased binding to FcγRIIIa leading to potent antibody‑dependent cellular cytotoxicity and phagocytosis) and by inducing direct, caspase‑independent cell death.
YES
DIRECT
Anti‑CD20 antibody binds CD20 on B cells and kills them via FcγRIIIa‑mediated ADCC and phagocytosis, and also induces direct, caspase‑independent cell death (with some complement involvement).
An investigational HER2-targeted antibody-drug conjugate (ADC). The monoclonal antibody binds HER2 (including low-HER2 expressers), is internalized, and releases a cytotoxic payload to induce tumor cell death and suppress proliferation; targets HER2/ERBB signaling pathways.
HER2-targeted monoclonal antibody (trastuzumab-based) binds HER2, including low-expressing cells, is internalized, and after linker cleavage releases a camptothecin-derived topoisomerase I–inhibiting payload that induces DNA damage, leading to cell-cycle arrest and apoptosis and suppression of HER2-driven tumor proliferation.
NO
INDIRECT
SHR-A1811 targets HER2 on the cell surface, is internalized, and then releases a camptothecin payload that inhibits topoisomerase I to cause DNA damage and apoptosis. Topoisomerase I is not the directly recognized antigen; killing depends on HER2 targeting and payload delivery.
Autologous BCMA-directed chimeric antigen receptor (CAR) T-cell therapy; engineered T cells bind BCMA on myeloma cells and trigger T-cell cytotoxicity and cytokine release to eliminate malignant plasma cells.
Autologous T cells engineered to express a BCMA-targeting chimeric antigen receptor (with 4-1BB costimulation) bind BCMA (TNFRSF17) on malignant plasma cells, triggering T-cell activation, cytokine release, and cytotoxic killing of BCMA-expressing myeloma cells.
YES
DIRECT
BCMA-directed CAR T cells bind BCMA on target cells, triggering T-cell activation and immune-synapse–mediated killing via perforin/granzyme release (and Fas–FasL), leading to apoptosis of BCMA-expressing cells.
Investigational intravenous bispecific antibody (anti-PSMA × CD28) T-cell co-stimulatory engager that binds PSMA on tumor cells and CD28 on T cells to deliver conditional CD28 agonist co-stimulation, enhancing T-cell activation and tumor cell killing in PSMA-positive lesions.
A bispecific antibody that binds PSMA on tumor cells and CD28 on T cells to provide conditional CD28 co-stimulation at PSMA-positive sites, enhancing T-cell activation, proliferation, cytokine release, and cytotoxic killing of PSMA-expressing tumor cells.
YES
DIRECT
Bispecific anti-PSMA×CD28 antibody provides localized CD28 co-stimulation on T cells at PSMA+ cells, activating/expanding T cells that then kill PSMA-expressing cells via cytotoxic T-cell mechanisms (perforin/granzyme, Fas–FasL).