Anti-CD33 antibody–drug conjugate that delivers calicheamicin; after binding CD33 and internalization, releases calicheamicin to induce DNA double-strand breaks and apoptosis in AML blasts.
Humanized anti-CD33 monoclonal antibody linked to calicheamicin; after CD33 binding and internalization, calicheamicin is released to bind the DNA minor groove, inducing double-strand breaks and apoptosis in CD33-positive AML cells.
The anti-CD33 ADC binds CD33, is internalized, and releases calicheamicin, which binds the DNA minor groove to cause double-strand breaks and apoptosis in CD33+ cells.
Bispecific T-cell–engager antibody immunotherapy that bridges CD19+ B cells and T cells, binding CD19 on B cells and engaging T cells to activate a cytotoxic response against CD19-expressing cells; administered IV once weekly; evaluated as monotherapy in relapsed/refractory CD19+ B-ALL.
Bispecific antibody that links CD19+ B-lineage leukemia cells to T cells—binding CD19 on tumor cells and engaging T cells (via CD3) to trigger T-cell activation and cytotoxic killing of CD19-expressing cells.
The bispecific antibody binds CD19 on target cells and CD3 on T cells, forming an immune synapse that activates T cells to kill CD19+ cells via perforin/granzyme-mediated cytotoxicity.
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).
Engineered TCR-T cells recognize KRAS G12D peptide–HLA-A*11:01 on target cells via their TCR and kill them through cytotoxic granule release (perforin/granzymes) and death-receptor signaling.
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.
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.
Bispecific antibody bridges CD3 on T cells and FcRH5 on target cells, activating TCR signaling and inducing perforin/granzyme-mediated lysis of FcRH5+ cells.