A lutetium-177–labeled anti–PD-L1 single-domain antibody (nanobody) radiopharmaceutical that binds PD-L1 on tumor and immunosuppressive cells to deliver targeted beta radiation causing DNA damage and cell death, with gamma emissions enabling SPECT/CT imaging.
A lutetium-177–labeled anti–PD-L1 single-domain antibody (nanobody) that binds PD-L1 on tumor and immunosuppressive cells and delivers targeted beta radiation, causing DNA damage and cell death; gamma emissions enable SPECT/CT imaging and dosimetry.
An anti–PD-L1 nanobody delivers Lu-177 beta radiation to PD-L1–expressing cells, causing DNA double-strand breaks and radiation-induced cell death (with possible crossfire to nearby cells).
Allogeneic anti-CD19 chimeric antigen receptor T-cell therapy; gene-modified donor T cells engineered to recognize and kill CD19+ B-lineage cells (B cells/plasmablasts) to induce B-cell aplasia and suppress autoantibody production in relapsed/refractory autoimmune hemolytic anemia/Evans syndrome.
Allogeneic donor T cells engineered with a CD19-specific chimeric antigen receptor bind CD19 on B-lineage cells and, upon engagement, activate cytotoxic effector functions to lyse these cells, inducing B-cell aplasia and reducing autoantibody production; TCR/CD3 disruption minimizes graft-versus-host risk.
CD19 CAR T cells bind CD19 on target B-lineage cells and kill them via T-cell cytotoxic mechanisms (perforin/granzyme-mediated lysis and death receptor pathways).
A trispecific T-cell engager (TriTE) given intravenously that binds CD19 on B cells, CD3 on T cells, and CD28 for co-stimulation, bridging T and B cells to trigger TCR activation and co-stimulation, leading to targeted cytotoxicity and depletion of CD19+ B cells/plasmablasts to reduce autoantibody production; carries cytokine release syndrome risk mitigated by a low priming dose.
Trispecific antibody that binds CD19 on B cells and CD3 plus CD28 on T cells, bridging T and B cells to provide TCR activation with CD28 co-stimulation, triggering T-cell–mediated cytotoxicity and depletion of CD19+ B cells/plasmablasts.
Tri-specific T-cell engager binds CD19 on target cells and CD3/CD28 on T cells, forming an immune synapse that activates and co-stimulates T cells to kill CD19+ cells via perforin/granzyme-mediated apoptosis.
Intravenous monoclonal antibody against endoglin (CD105) on proliferating endothelial cells; anti-angiogenic via blockade of TGF-β/BMP9/10–ALK1/endoglin signaling with potential ADCC.
Chimeric monoclonal antibody targeting endoglin (CD105) on proliferating endothelial cells; blocks TGF-β/BMP9/10–ALK1/endoglin signaling to inhibit angiogenesis and endothelial proliferation, with potential Fc-mediated ADCC, leading to anti-tumor effects via vascular targeting.
Anti-endoglin IgG engages Fc receptors to trigger ADCC against endoglin-positive endothelial cells; it also blocks TGF-β/ALK1 signaling to inhibit proliferation/angiogenesis.
A bispecific T‑cell–engaging IgG antibody that binds BCMA on myeloma plasma cells and CD3 on T cells, redirecting and activating T cells to kill BCMA-positive cells via TCR/CD3 signaling and cytotoxic effector functions.
Teclistamab is a bispecific IgG antibody that binds BCMA on malignant plasma cells and CD3 on T cells, cross-linking them to activate TCR/CD3 signaling and redirect polyclonal T-cell cytotoxicity to kill BCMA-positive myeloma cells.
Teclistamab bridges CD3 on T cells to BCMA on target cells, activating TCR/CD3 signaling and redirecting T-cell cytotoxicity (perforin/granzyme-mediated lysis) to kill BCMA-positive cells.