Autologous, gene-edited TCR-T cell therapy engineered to express an HLA-A*11:01–restricted TCR specific for the KRAS G12D neoantigen; administered as an infusion with dose escalation to mediate antigen-specific cytotoxicity against KRAS G12D–mutant tumors.
Autologous T cells are gene-edited to express an HLA-A*11:01–restricted TCR specific for the KRAS G12D neoantigen. After infusion, these engineered TCR-T cells recognize KRAS G12D peptide–MHC I complexes on tumor cells, activate via TCR signaling, and kill target cells through antigen-specific cytotoxic mechanisms (e.g., perforin/granzyme).
NO
INDIRECT
Engineered TCR-T cells kill only cells presenting the KRAS G12D peptide in HLA-A*11:01 (pMHC) via perforin/granzyme; HLA-A*11:01 expression alone is not sufficient.
Humanized anti-CD20 monoclonal antibody immunotherapy that depletes CD20+ B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis while sparing hematopoietic stem cells and plasma cells; targets peripheral and meningeal CD20+ B lymphocytes to modulate pathogenic adaptive immune signaling implicated in cortical demyelination.
Humanized anti-CD20 monoclonal antibody that binds CD20 on B lymphocytes and depletes them via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis while sparing hematopoietic stem cells and plasma cells; this reduces pathogenic B-cell antigen presentation, costimulation, and proinflammatory cytokine signaling implicated in demyelination.
YES
DIRECT
Ocrelizumab binds CD20 on B cells and induces killing via Fc-mediated ADCC (NK cells/macrophages), complement-dependent cytotoxicity, and can also trigger apoptosis of CD20+ cells.
An intravenous T-cell–engaging bispecific monoclonal antibody that binds CD3 on T cells and FcRH5/FCRL5 on myeloma cells to redirect T-cell cytotoxicity.
Cevostamab is an intravenous bispecific monoclonal antibody that simultaneously binds CD3 on T cells and FcRH5 (FCRL5) on myeloma cells, physically bridging T cells to FcRH5-expressing plasma cells. This crosslinking activates TCR/CD3 signaling, triggers cytokine release, and drives perforin/granzyme-mediated cytotoxicity leading to targeted lysis of FcRH5+ tumor cells.
YES
DIRECT
Bispecific antibody bridges CD3 on T cells and FcRH5 on target cells, activating TCR signaling and inducing perforin/granzyme-mediated lysis of FcRH5+ cells.
An intravenous T-cell–engaging bispecific monoclonal antibody that binds CD3 on T cells and FcRH5/FCRL5 on myeloma cells to redirect T-cell cytotoxicity.
Cevostamab is an intravenous bispecific monoclonal antibody that simultaneously binds CD3 on T cells and FcRH5 (FCRL5) on myeloma cells, physically bridging T cells to FcRH5-expressing plasma cells. This crosslinking activates TCR/CD3 signaling, triggers cytokine release, and drives perforin/granzyme-mediated cytotoxicity leading to targeted lysis of FcRH5+ tumor cells.
NO
INDIRECT
The drug binds CD3 on T cells to activate and redirect them to kill FcRH5+ myeloma cells via perforin/granzyme; CD3+ T cells themselves are not targeted for lysis.
Autologous chimeric antigen receptor T-cell therapy engineered to target BCMA on malignant plasma cells.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that recognizes BCMA on malignant plasma cells, triggering MHC-independent T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of the target cells.
YES
DIRECT
BCMA-specific CAR T cells bind BCMA on target cells, become activated, and directly kill via perforin/granzyme-mediated cytolysis (and death-receptor pathways).