A chimeric anti-CD20 monoclonal antibody that depletes CD20+ B cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, thereby reducing pathogenic autoantibodies (e.g., anti-PLA2R/THSD7A) and downstream complement-mediated podocyte injury in idiopathic membranous nephropathy.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes them via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, reducing pathogenic autoantibodies and downstream complement-mediated tissue injury.
Rituximab binds CD20 on B cells and induces complement-dependent cytotoxicity (MAC-mediated lysis) and FcγR-mediated ADCC by NK cells/macrophages; it can also trigger apoptosis.
An intravenous anti-HER2 antibody–drug conjugate (trastuzumab linked via a cleavable linker to the topoisomerase I inhibitor payload deruxtecan [DXd]); binds HER2 (including HER2-low), internalizes, and releases DXd to inhibit topoisomerase I causing DNA damage and apoptosis; retains trastuzumab-mediated HER2 blockade and ADCC with bystander killing.
Anti-HER2 antibody–drug conjugate: trastuzumab targets HER2 (including HER2-low), is internalized, and releases the topoisomerase I–inhibiting payload deruxtecan (DXd), causing DNA damage, cell-cycle arrest, and apoptosis. Retains trastuzumab-mediated HER2 blockade and Fc-dependent ADCC, with a membrane-permeable payload enabling bystander killing.
The anti-HER2 ADC binds HER2, is internalized, and releases the topoisomerase I inhibitor DXd, causing DNA damage and apoptosis; it also engages Fc-mediated ADCC and can cause bystander killing.
Non-replicating, off-the-shelf gene therapy vector that delivers HSV-enhanced thymidine kinase (suicide gene) and human GM-CSF to tumors, making transduced cells susceptible to valganciclovir and enhancing antitumor immune activation via myeloid APC recruitment.
Non-replicating gene therapy vector that transduces tumor cells to express HSV-enhanced thymidine kinase and human GM-CSF. After vector delivery, oral valganciclovir is phosphorylated by HSV-tk in transduced cells to ganciclovir triphosphate, which inhibits DNA synthesis and kills those tumor cells. Resultant antigen release plus locally expressed GM-CSF recruits and activates myeloid antigen-presenting cells, enhances antigen presentation, and promotes cytotoxic T-cell (and NK)–mediated antitumor immunity.
Tumor cells transduced to express HSV‑enhanced thymidine kinase phosphorylate valganciclovir/ganciclovir to ganciclovir triphosphate, which inhibits DNA synthesis (DNA polymerase/chain elongation), causing death of those transduced cells.
Small-molecule antiviral prodrug of ganciclovir; in this study it is phosphorylated by HSV-eTK expressed from GEN2 to induce selective tumor cell death.
Valganciclovir is a prodrug of ganciclovir (a deoxyguanosine analogue). After phosphorylation by HSV-enhanced thymidine kinase (expressed by the GEN2 vector) and subsequent cellular kinases, the active triphosphate is incorporated into DNA, inhibiting DNA polymerase and causing DNA chain termination, leading to selective death of transduced tumor cells.
HSV-1 thymidine kinase in expressing cells phosphorylates valganciclovir (ganciclovir), which is further converted to the triphosphate that is incorporated into DNA, inhibits DNA polymerase, and causes chain termination, killing the expressing cells.
An intravenous antibody–drug conjugate (ADC) composed of an anti–Nectin-4 monoclonal antibody that binds Nectin-4 (PVRL4) on tumor cells, is internalized, and releases an intracellular cytotoxic payload to kill Nectin-4–expressing cells, with potential bystander effect.
LY4101174 is an intravenous anti–Nectin-4 IgG1 antibody–drug conjugate that binds Nectin-4 (PVRL4) on tumor cells, is internalized, and releases the topoisomerase I inhibitor exatecan via a cleavable linker, causing inhibition of DNA replication, cell‑cycle arrest, and apoptosis of Nectin‑4–expressing cells, with potential bystander effect.
The ADC binds Nectin-4 on target cells, is internalized, and releases the topoisomerase I inhibitor exatecan via a cleavable linker, inhibiting DNA replication and inducing cell-cycle arrest and apoptosis (with potential bystander effect).