A fully human anti-CD20 monoclonal antibody (immunotherapy) administered subcutaneously. It binds a membrane-proximal CD20 epitope on B lymphocytes and depletes circulating naïve and memory B cells via complement-dependent cytotoxicity and Fc-mediated ADCC/ADCP, sparing plasma cells and stem cells, thereby reducing B-cell antigen presentation, costimulation, and pro-inflammatory cytokines.
Fully human IgG1 anti-CD20 monoclonal antibody that binds a membrane-proximal CD20 epitope on B cells and depletes circulating naive and memory B cells via complement-dependent cytotoxicity and Fc-mediated ADCC/ADCP, sparing plasma cells and stem cells; this reduces B-cell antigen presentation, costimulation, and pro-inflammatory cytokine production.
YES
DIRECT
Antibody binds CD20 on B cells and triggers complement-dependent cytotoxicity and Fc-mediated effector killing (ADCC by NK cells and ADCP by macrophages), leading to lysis/phagocytosis of CD20+ cells.
A monoclonal antibody that targets the urokinase plasminogen activator receptor (uPAR); in this trial it serves as the targeting moiety for radioimmunotherapy when chelated and labeled with lutetium-177.
MNPR-101 is a uPAR-targeting monoclonal antibody chelated with PCTA and labeled with lutetium-177. Binding to uPAR on tumor and tumor-associated stromal cells localizes beta-emitting 177Lu to the lesion, delivering ionizing radiation that causes DNA double-strand breaks and cell death, with a crossfire effect to neighboring cells.
YES
DIRECT
uPAR-binding antibody delivers 177Lu beta radiation to bound cells, causing ionizing radiation–induced DNA double-strand breaks and cell death (with crossfire to nearby cells).
HER2-directed antibody–drug conjugate linking trastuzumab to a topoisomerase I inhibitor payload (deruxtecan).
HER2-targeted monoclonal antibody (trastuzumab) linked to a membrane-permeable topoisomerase I inhibitor payload (deruxtecan). After binding HER2 and internalization, the payload is released to inhibit Top1–DNA complexes, causing DNA damage, replication arrest, and apoptosis; the antibody can also mediate ADCC and the payload can induce a bystander killing effect.
YES
DIRECT
The ADC binds HER2, is internalized, and releases the deruxtecan topoisomerase I inhibitor that induces DNA damage and apoptosis in HER2-expressing cells; the antibody Fc can also trigger ADCC, with some bystander killing from the membrane-permeable payload.
HER2-directed antibody–drug conjugate linking trastuzumab to a topoisomerase I inhibitor payload (deruxtecan).
HER2-targeted monoclonal antibody (trastuzumab) linked to a membrane-permeable topoisomerase I inhibitor payload (deruxtecan). After binding HER2 and internalization, the payload is released to inhibit Top1–DNA complexes, causing DNA damage, replication arrest, and apoptosis; the antibody can also mediate ADCC and the payload can induce a bystander killing effect.
NO
INDIRECT
The ADC binds HER2, is internalized, and releases deruxtecan, which inhibits Top1 to cause DNA damage and apoptosis (with possible bystander effect); Top1 expression alone is not directly targeted.
Autologous CAR T-cell therapy engineered to express a STEAP2-specific chimeric antigen receptor; upon binding STEAP2 on prostate cancer cells, it activates T cells to proliferate, release cytokines, and lyse STEAP2-positive tumor cells. Administered intravenously after lymphodepleting chemotherapy.
Autologous T cells engineered to express a STEAP2-specific CAR and a dominant-negative TGF-β receptor II. Upon binding STEAP2 on prostate cancer cells, CAR signaling activates T cells to proliferate, secrete cytokines, and kill target cells via cytotoxic mechanisms, while the dnTGFBRII blocks immunosuppressive TGF-β signaling to enhance activity in the tumor microenvironment.
YES
DIRECT
STEAP2-specific CAR T cells bind STEAP2 on target cells and directly kill them via T-cell cytotoxic mechanisms (perforin/granzyme-mediated lysis and death receptor apoptosis); dnTGFBRII enhances activity by blocking TGF-β suppression.