Autologous T lymphocytes genetically engineered to express a chimeric antigen receptor targeting carcinoembryonic antigen (CEA) for MHC-independent recognition and killing of CEA-positive tumor cells.
Autologous T cells are engineered to express a chimeric antigen receptor with an anti-CEA scFv, enabling MHC-independent recognition of CEA-positive tumor cells and inducing T-cell activation, expansion, cytokine release, and cytotoxic killing via perforin/granzyme pathways.
CEA-targeted CAR-T cells bind CEA on tumor cells, become activated, and kill targets via perforin/granzyme-mediated cytolysis (with T cell effector mechanisms).
A humanized anti-TROP2 IgG1 antibody-drug conjugate that, after binding TROP2 on tumor cells and internalization, releases a membrane-permeable topoisomerase I inhibitor (DXd) via a cleavable linker to induce DNA damage, replication stress, and tumor cell death with a bystander effect.
Humanized anti-TROP2 IgG1 antibody-drug conjugate; after binding TROP2 and internalization, a cleavable linker releases the DXd topoisomerase I inhibitor payload, inducing DNA damage and replication stress to kill tumor cells, with a membrane-permeable bystander effect.
The anti-TROP2 ADC binds TROP2, is internalized, and a cleavable linker releases the DXd topoisomerase I inhibitor inside the cell, causing DNA damage and replication stress that kills the target cell; the payload can also cause bystander killing.
A bispecific antibody immunotherapy evaluated in a Phase 1 dose-escalation/expansion study for relapsed/refractory B-cell non-Hodgkin lymphoma. It is designed to bind two targets and redirect immune effector activity to malignant B cells. Dosed across 0.3-500 mg for up to 12 months. Specific antigens and effector mechanisms are not disclosed.
Bispecific antibody that links T cells to malignant B cells—binding CD3 on T cells and a B‑cell antigen—to form an immunologic synapse and trigger T‑cell–mediated cytotoxic killing; specific targets are not disclosed.
The bispecific antibody bridges CD3 on T cells to the B‑cell antigen on target cells, forming an immunologic synapse and triggering T‑cell–mediated cytotoxicity (perforin/granzyme and Fas–FasL apoptosis).
TROP2-directed antibody-drug conjugate; a humanized anti-TROP2 monoclonal antibody that is internalized upon binding and releases a topoisomerase I inhibitor payload to induce DNA damage and cell death.
Humanized anti-TROP2 monoclonal antibody binds TROP2 on tumor cells, is internalized, and releases a topoisomerase I inhibitor payload that induces DNA damage and tumor cell death.
The anti-TROP2 antibody–drug conjugate binds TROP2, is internalized, and releases a topoisomerase I inhibitor payload that induces DNA damage and apoptosis in the target cell.
Rabbit-derived polyclonal IgG immunosuppressant that depletes and functionally modulates T lymphocytes via complement-dependent cytotoxicity, apoptosis, and Fc-mediated clearance; preferentially reduces autoreactive effector/memory T cells and may spare or promote regulatory T cells to attenuate islet autoimmunity.
Rabbit-derived polyclonal IgG (anti-thymocyte globulin) that binds multiple T-cell surface antigens (e.g., CD2/CD3/CD4/CD8), inducing T-cell depletion via complement-dependent cytotoxicity, apoptosis, and Fc receptor–mediated clearance; preferentially reduces autoreactive effector/memory T cells while relatively sparing or promoting regulatory T cells, thereby suppressing TCR-driven and cytokine-mediated immune responses and attenuating islet autoimmunity.
Polyclonal antibodies bind CD2 on T cells, triggering complement-dependent cytotoxicity and Fc-mediated effector functions (ADCC/phagocytosis) and apoptosis, leading to depletion of CD2+ cells.