Autologous, non–genetically engineered, ex vivo–expanded polyclonal multi–tumor-associated antigen (multiTAA)–specific T-cell therapy that recognizes multiple shared TAAs on pancreatic adenocarcinoma via native, MHC-restricted TCRs to mediate cytotoxic killing and cytokine-driven immune activation.
Autologous, ex vivo-expanded polyclonal CD4+/CD8+ T cells with native, MHC-restricted TCRs specific for multiple shared tumor-associated antigens on pancreatic adenocarcinoma. After infusion, these T cells recognize antigen-MHC complexes on tumor cells and mediate cytotoxic killing (perforin/granzyme) and cytokine-driven immune activation; multi-antigen targeting reduces antigen-loss escape and may improve durability.
Autologous T cells recognize SSX2-derived peptide presented on MHC via native TCRs and directly kill target cells through perforin/granzyme-mediated cytotoxicity, with cytokine-driven immune activation.
Intravenous bispecific T-cell engager antibody that binds DLL3 on tumor cells and CD3 on T cells to redirect and activate T cells to kill DLL3-positive cells.
Obrixtamig (BI 764532) is an intravenous bispecific T‑cell engager antibody that binds DLL3 on tumor cells and CD3 on T cells, physically bringing them together to form an immune synapse and activate T cells to release cytotoxic mediators and kill DLL3‑positive cells.
The bispecific T‑cell engager links CD3 on T cells to DLL3 on target cells, forming an immune synapse that activates T cells to release perforin/granzymes and kill DLL3-positive cells.
Autologous CD79b-targeted chimeric antigen receptor (CAR) T-cell therapy. Patient T cells are genetically engineered to express a CAR recognizing CD79b (Igβ) on B cells; CAR engagement activates T cells to proliferate, release cytokines, and mediate perforin/granzyme-dependent cytotoxicity against CD79b-positive malignant B cells. Administered intravenously after leukapheresis for relapsed/refractory B-cell lymphomas.
Autologous T cells engineered to express an anti-CD79b chimeric antigen receptor bind CD79b on malignant B cells, triggering T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of CD79b-positive cells.
Anti-CD79b CAR T cells bind CD79b on target B cells, become activated, and kill them via perforin/granzyme–mediated cytotoxicity (with apoptosis of CD79b-positive cells).
CD20×CD3 bispecific monoclonal antibody (T‑cell engager) that redirects patient T cells via CD3 to kill CD20+ malignant B cells.
A CD20×CD3 bispecific monoclonal antibody that binds CD3 on T cells and CD20 on B cells, crosslinking them to activate and redirect cytotoxic T cells to kill CD20-positive malignant B cells.
Bispecific T-cell engager binds CD20 on target cells and CD3 on T cells, crosslinking and activating T cells to kill CD20+ cells via perforin/granzyme-mediated cytotoxicity.
Type II anti‑CD20 monoclonal antibody that depletes B cells and enhances ADCC; used as pretreatment to reduce tumor burden and mitigate CRS risk.
Glycoengineered humanized IgG1 type II anti‑CD20 monoclonal antibody that binds CD20 on B cells; enhanced Fc glycosylation increases FcγRIIIa affinity to boost ADCC/ADCP, and type II engagement triggers direct, caspase‑independent apoptosis (with limited CDC), resulting in potent B‑cell depletion.
Obinutuzumab binds CD20 on B cells; its Fc is glycoengineered to enhance FcγRIIIa engagement, driving ADCC/ADCP by NK cells/macrophages, and type II binding induces direct caspase‑independent apoptosis (with limited CDC), leading to B‑cell killing.