An intravenous bispecific T‑cell engager antibody that binds DLL3 on tumor cells and CD3 on T cells to redirect T cells and induce cytotoxic killing in DLL3‑expressing neuroendocrine cancers.
Obrixtamig (BI 764532) is an intravenous bispecific antibody that binds DLL3 on tumor cells and CD3 on T cells, physically bridging them to activate CD3/TCR signaling and redirect T‑cell cytotoxicity (perforin/granzyme and cytokines) to kill DLL3‑expressing neuroendocrine cancer cells.
DLL3×CD3 bispecific antibody redirects T cells to DLL3+ cells, activating CD3/TCR and inducing perforin/granzyme-mediated cytolysis (and cytokine effects) of target cells.
Etentamig (ABBV-383; TNB-383B) is an intravenous bispecific T-cell–redirecting antibody that binds BCMA on plasma cells and CD3 on T cells to activate cytotoxic T cells and eliminate BCMA+ plasma cells, reducing amyloidogenic light chains.
Bispecific IgG4 antibody that binds BCMA on plasma cells and CD3 on T cells, creating an immune synapse that activates and redirects cytotoxic T cells to kill BCMA-expressing cells, thereby reducing amyloidogenic light-chain production (with low CD3 activation to limit cytokine release).
Bispecific antibody binds BCMA on target cells and CD3 on T cells, forming an immune synapse that activates cytotoxic T cells to kill BCMA+ cells via perforin/granzyme-mediated apoptosis.
Autologous peripheral blood T cells engineered with the Sleeping Beauty transposon/transposase to express patient-specific TCRs recognizing mutated neoantigens; adoptive cellular gene therapy mediating HLA-restricted tumor cell killing.
Autologous peripheral blood T cells are genetically modified using the Sleeping Beauty transposon/transposase system to express patient-specific TCRs that recognize mutated neoantigen peptides presented by HLA on tumor cells. Upon infusion, TCR–HLA engagement activates the T cells to mediate targeted, HLA-restricted tumor cell killing via cytotoxic effector mechanisms (perforin/granzyme) and cytokine release.
Engineered TCR-T cells recognize the patient-specific mutated neoantigen peptide presented by HLA on target cells and induce HLA-restricted killing via perforin/granzyme–mediated apoptosis (and related cytotoxic pathways).
TROP2-directed antibody–drug conjugate; the monoclonal antibody binds TROP2 on tumor cells, is internalized, and releases a camptothecin-class topoisomerase I–inhibiting payload causing DNA replication stress, single-strand breaks, and apoptosis (with potential bystander effect).
TROP2-targeted monoclonal antibody that is internalized and releases a camptothecin-class topoisomerase I–inhibiting payload, inducing DNA replication stress and single-strand breaks that trigger apoptosis, with potential bystander killing of neighboring tumor cells.
An anti-TROP2 antibody–drug conjugate binds TROP2, is internalized, and releases a camptothecin-class topoisomerase I inhibitor that induces DNA damage/replication stress, leading to apoptosis (with potential bystander effect).
Autologous gene-modified T-cell therapy: patient T cells are collected, transduced ex vivo with a lentiviral vector encoding the EB103 transgene, then reinfused to redirect and activate T cells against malignant B-cell non-Hodgkin lymphoma (CAR-like signaling) leading to antigen-specific proliferation and cytotoxic killing.
Autologous T cells are transduced ex vivo with a lentiviral vector to express an anti‑CD19 antibody‑TCR (AbTCR) and a costimulatory molecule, enabling MHC‑independent recognition of CD19 on B‑cell malignancies. Upon reinfusion, engagement of CD19 triggers CAR‑like activation, proliferation, and T‑cell–mediated cytotoxic killing of tumor cells.
Engineered autologous T cells recognize CD19 in an MHC-independent, CAR-like manner and kill CD19+ cells via T-cell cytotoxic mechanisms (perforin/granzyme-mediated lysis and apoptosis).