Trop-2–directed antibody–drug conjugate that delivers SN-38 (a topoisomerase I inhibitor) to tumor cells, causing DNA damage and cell death with a potential bystander effect.
TROP-2–targeted antibody–drug conjugate (humanized anti–TROP-2 mAb linked to SN-38). After binding TROP-2 and internalization, the linker is cleaved to release SN-38, a topoisomerase I inhibitor that stabilizes topo I–DNA complexes, causing DNA damage and apoptosis; extracellular payload can produce a bystander effect.
YES
DIRECT
ADC binds TROP-2, is internalized, and releases SN-38; the topoisomerase I inhibitor induces DNA damage leading to apoptosis (with possible bystander killing from extracellular SN-38).
Trop-2–directed antibody–drug conjugate that delivers SN-38 (a topoisomerase I inhibitor) to tumor cells, causing DNA damage and cell death with a potential bystander effect.
TROP-2–targeted antibody–drug conjugate (humanized anti–TROP-2 mAb linked to SN-38). After binding TROP-2 and internalization, the linker is cleaved to release SN-38, a topoisomerase I inhibitor that stabilizes topo I–DNA complexes, causing DNA damage and apoptosis; extracellular payload can produce a bystander effect.
NO
INDIRECT
The ADC binds TROP-2 (not topoisomerase I) on tumor cells, is internalized, and releases SN-38, which inhibits DNA topoisomerase I to cause DNA damage and apoptosis; extracellular SN-38 can also cause a bystander effect.
Intravenous anti‑CD20 monoclonal antibody that depletes CD20+ B cells via antibody‑dependent cellular cytotoxicity, complement‑dependent cytotoxicity, and direct apoptosis.
Anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20+ cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
YES
DIRECT
Rituximab binds CD20 on B cells and triggers Fc-mediated ADCC (NK cells/macrophages), activates complement for CDC/lysis, and can induce apoptosis via CD20 crosslinking.
Rabbit polyclonal anti-thymocyte globulin that depletes T cells to prevent rejection and GVHD.
Rabbit polyclonal anti-thymocyte IgG that binds multiple T-cell surface antigens and depletes T cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, producing immunosuppression to prevent rejection and GVHD.
YES
DIRECT
Rabbit anti-thymocyte IgG binds CD4 on T cells and induces complement-dependent lysis, Fc-mediated ADCC by effector cells, and apoptosis, depleting CD4+ T cells.
Lipid nanoparticle–encapsulated mRNA therapeutic vaccine encoding HPV16/18 antigens, administered intramuscularly (25/75/150 µg; three doses every 2 weeks). It promotes dendritic-cell antigen presentation (MHC I/II) and robust CD8+ and CD4+ T-cell responses to clear HPV-infected dysplastic cervical epithelial cells and drive lesion regression.
Lipid nanoparticle–encapsulated mRNA encoding HPV16/18 antigens is taken up by host cells, translated into viral proteins, and presented on MHC I/II by dendritic and other antigen-presenting cells. This primes and expands HPV16/18-specific CD8+ cytotoxic and CD4+ helper T cells, promoting immune-mediated clearance of HPV-infected dysplastic cervical epithelial cells and lesion regression.
YES
INDIRECT
The mRNA vaccine primes HPV16 E6–specific CD8+ T cells via APC presentation; these CTLs recognize E6 peptides on MHC I of infected epithelial cells and kill them via perforin/granzyme-mediated apoptosis (with CD4+ T-cell help).