Autologous dendritic cells ex vivo loaded with survivin peptides; administered intradermally and intravenously to prime/expand tumor-specific CD8+ and CD4+ T cells against survivin-expressing glioblastoma cells.
Autologous dendritic cells are ex vivo loaded with survivin peptides and, after intradermal/IV administration, present survivin epitopes on MHC I/II to activate and expand survivin-specific CD8+ cytotoxic T cells and CD4+ helper T cells, driving targeted immune-mediated killing of survivin-expressing glioblastoma cells.
YES
INDIRECT
Dendritic-cell vaccination primes survivin-specific T cells; activated CD8+ CTLs (and cytotoxic CD4+ T cells when tumor is HLA II+) recognize survivin peptides on tumor cells and kill via perforin/granzyme and Fas–FasL pathways.
Anti-CD20 chimeric monoclonal antibody that depletes B cells, lowering ANCA autoantibody production and antigen presentation.
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 ANCA autoantibody production and antigen presentation.
YES
DIRECT
Rituximab binds CD20 on B cells and induces complement-dependent cytotoxicity and Fc-mediated ADCC/phagocytosis by NK cells/macrophages; it can also trigger apoptosis of CD20+ cells.
Investigational antitumor agent for injection; specific target/mechanism not disclosed in the registry; dose exploration ongoing.
IgG1 monoclonal antibody targeting nectin-4 delivers a cleavable topoisomerase I inhibitor payload; after binding and internalization in nectin-4–expressing tumor cells, linker cleavage releases the payload to inhibit topoisomerase I, blocking DNA replication and inducing cell cycle arrest and apoptosis.
YES
DIRECT
ADC binds nectin-4 on tumor cells, is internalized, and releases a cleavable topoisomerase I inhibitor that blocks DNA replication and induces apoptosis.
Investigational antitumor agent for injection; specific target/mechanism not disclosed in the registry; dose exploration ongoing.
IgG1 monoclonal antibody targeting nectin-4 delivers a cleavable topoisomerase I inhibitor payload; after binding and internalization in nectin-4–expressing tumor cells, linker cleavage releases the payload to inhibit topoisomerase I, blocking DNA replication and inducing cell cycle arrest and apoptosis.
NO
INDIRECT
SHR-A2102 targets nectin-4, is internalized, and releases a topoisomerase I inhibitor that causes DNA damage and apoptosis in nectin-4–positive cells; expression of DNA topoisomerase I alone does not make cells a direct target.
A TCR-based bispecific ImmTAC biologic that uses a high-affinity TCR to bind a PIWIL1-derived peptide presented by HLA-A*02:01 on tumor cells and an anti-CD3 domain to recruit/activate T cells; administered IV.
IMC-R117C is a soluble TCR–CD3 bispecific (ImmTAC) that uses an affinity-enhanced TCR to bind a PIWIL1-derived peptide presented by HLA-A*02:01 on tumor cells and an anti-CD3 domain to recruit and activate polyclonal T cells, driving synapse formation, cytokine release, and targeted T‑cell cytotoxicity against PIWIL1+ HLA-A*02:01 tumor cells.
YES
DIRECT
The ImmTAC binds the PIWIL1 peptide–HLA-A*02:01 complex and CD3 on T cells, forming a synapse that activates T cells to kill the bound target cell via perforin/granzyme-mediated cytotoxicity.