Humanized IgG1 monoclonal antibody immunotherapy targeting CSF1R; blocks CSF1R to inhibit CSF1/M-CSF signaling and depletes CSF1R+ macrophages via receptor blockade and Fc-mediated clearance, reducing macrophage-driven tumor burden in TGCT.
Humanized IgG1 monoclonal antibody against CSF1R that blocks CSF1/M-CSF binding and downstream signaling, and engages Fc effector functions to deplete CSF1R+ macrophages (e.g., tumor-associated macrophages/giant cells), thereby reducing macrophage-driven pathology in TGCT.
YES
DIRECT
Emactuzumab (IgG1) binds CSF1R on target cells and engages Fcγ receptor–bearing effector cells to induce ADCC/ADCP (and potentially CDC), depleting CSF1R+ macrophages/giant cells.
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.
YES
DIRECT
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.
YES
DIRECT
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.
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.
NO
INDIRECT
The bispecific antibody binds CD3 on T cells to engage and activate them against DLL3-expressing tumor cells; activated T cells kill DLL3+ cells via cytotoxic mediators. CD3+ T cells themselves are not targeted for killing.
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.
YES
DIRECT
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).