Allogeneic, off-the-shelf adoptive T-cell therapy composed of donor CMV-specific T lymphocytes expanded ex vivo, stimulated with CMV pp65 peptide and selected via IFN-γ capture; exerts HLA-restricted, antigen-specific TCR recognition with CD4+ helper and CD8+ cytotoxic activity against CMV-infected cells.
Allogeneic donor-derived CMV-specific T lymphocytes expanded ex vivo and selected via IFN-γ capture after CMV pp65 peptide stimulation. These cells use their native, HLA-restricted TCRs to recognize CMV antigens on infected host cells; CD8+ T cells mediate perforin/granzyme cytotoxicity and CD4+ T cells provide helper functions, restoring antigen-specific antiviral immunity.
YES
DIRECT
CMV-specific donor T cells recognize the pp65 peptide–MHC I complex via their native, HLA-restricted TCRs and kill infected cells through CD8+ perforin/granzyme-mediated cytotoxicity (with CD4+ helper support).
Allogeneic, off-the-shelf adoptive T-cell therapy composed of donor CMV-specific T lymphocytes expanded ex vivo, stimulated with CMV pp65 peptide and selected via IFN-γ capture; exerts HLA-restricted, antigen-specific TCR recognition with CD4+ helper and CD8+ cytotoxic activity against CMV-infected cells.
Allogeneic donor-derived CMV-specific T lymphocytes expanded ex vivo and selected via IFN-γ capture after CMV pp65 peptide stimulation. These cells use their native, HLA-restricted TCRs to recognize CMV antigens on infected host cells; CD8+ T cells mediate perforin/granzyme cytotoxicity and CD4+ T cells provide helper functions, restoring antigen-specific antiviral immunity.
NO
INDIRECT
The product contains CMV-specific T cells whose CD4+ cells recognize pp65 peptide–MHC II and mainly provide helper cytokines; direct cytotoxicity is mediated by CD8+ T cells recognizing pp65 on MHC I via perforin/granzyme. Thus MHC II–presenting cells are not directly lysed.
Investigational anticancer agent from Hengrui; mechanism/target not specified in the registry. Studied in combination with rituximab-containing chemotherapy.
Monoclonal antibody targeting CD79b on B-cell lymphomas delivers a topoisomerase I inhibitor payload. After binding and internalization, the payload is released to inhibit DNA topoisomerase I, blocking DNA replication and inducing cell cycle arrest and apoptosis in CD79b-expressing tumor cells.
YES
DIRECT
ADC binds CD79b on B cells, is internalized, and releases a topoisomerase I inhibitor that blocks DNA replication, causing DNA damage, cell cycle arrest, and apoptosis of CD79b-expressing cells.
Investigational anticancer agent from Hengrui; mechanism/target not specified in the registry. Studied in combination with rituximab-containing chemotherapy.
Monoclonal antibody targeting CD79b on B-cell lymphomas delivers a topoisomerase I inhibitor payload. After binding and internalization, the payload is released to inhibit DNA topoisomerase I, blocking DNA replication and inducing cell cycle arrest and apoptosis in CD79b-expressing tumor cells.
NO
INDIRECT
SHR-A1912 targets CD79b on B cells, is internalized, and releases a topoisomerase I inhibitor that blocks DNA replication and triggers apoptosis in CD79b-positive cells; DNA topoisomerase I is the intracellular enzyme target of the payload, not the surface cytotoxic target.
Anti-CD20 monoclonal antibody that depletes CD20+ B cells via ADCC, complement-dependent cytotoxicity, and induction of apoptosis; component of the R-chemotherapy regimen.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on pre-B and mature B cells and depletes CD20+ cells via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and induction of apoptosis.
YES
DIRECT
Binding to CD20 triggers Fc-mediated ADCC by immune effector cells, complement-dependent cytotoxicity, and can induce apoptosis of CD20+ cells.