A conditionally replicative oncolytic adenovirus engineered with an RGD-modified fiber to retarget entry to αv integrins (e.g., αvβ3/αvβ5) on pancreatic tumor cells; COX-2–linked selectivity enables tumor-restricted replication, inducing oncolysis and immunogenic cell death after endoscopic ultrasound–guided intratumoral injection.
RGDCRAdCOX2F is a conditionally replicative adenovirus engineered with an RGD-modified fiber to enter tumor cells via alpha v integrins (e.g., alpha v beta 3/alpha v beta 5). E1 expression is driven by a COX-2 promoter to restrict replication to COX-2–overexpressing tumors, resulting in selective intratumoral viral amplification, direct oncolysis, and immunogenic cell death with release of tumor antigens that can elicit anti-tumor immune responses.
The RGD-modified adenovirus uses αvβ3 (integrin β3-containing) for entry; in COX-2–overexpressing cells it replicates and causes lytic oncolysis, directly killing the infected cells.
A conditionally replicative oncolytic adenovirus engineered with an RGD-modified fiber to retarget entry to αv integrins (e.g., αvβ3/αvβ5) on pancreatic tumor cells; COX-2–linked selectivity enables tumor-restricted replication, inducing oncolysis and immunogenic cell death after endoscopic ultrasound–guided intratumoral injection.
RGDCRAdCOX2F is a conditionally replicative adenovirus engineered with an RGD-modified fiber to enter tumor cells via alpha v integrins (e.g., alpha v beta 3/alpha v beta 5). E1 expression is driven by a COX-2 promoter to restrict replication to COX-2–overexpressing tumors, resulting in selective intratumoral viral amplification, direct oncolysis, and immunogenic cell death with release of tumor antigens that can elicit anti-tumor immune responses.
RGD-modified adenovirus binds alpha v beta 5 integrin for entry; in COX-2–overexpressing cells, COX-2–driven E1 expression enables viral replication and lytic oncolysis, directly killing the infected cell.
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.
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.
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.
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.