Autologous, retroviral-transduced anti-BCMA (TNFRSF17) chimeric antigen receptor T-cell therapy that targets BCMA-expressing B-lineage cells (plasmablasts and long-lived plasma cells) to deplete autoantibody-producing cells in refractory B cell–mediated autoimmune diseases; administered as a single IV infusion following lymphodepletion.
Autologous T cells are retrovirally transduced to express an anti-BCMA chimeric antigen receptor with a 4-1BB costimulatory domain; upon infusion, these CAR-T cells recognize BCMA (TNFRSF17) on plasmablasts and long-lived plasma cells and mediate cytotoxic killing, depleting BCMA-positive B-lineage cells and reducing autoantibody production.
Anti-BCMA CAR-T cells bind BCMA on target cells, activate, and kill them via T-cell cytotoxic pathways (perforin/granzyme and Fas–FasL apoptosis).
An investigational antibody-drug conjugate administered intravenously every 2–3 weeks. It uses a monoclonal antibody to bind an unspecified tumor-associated antigen on malignant solid tumor cells, is internalized, and releases an intracellular cytotoxic payload to kill cancer cells; pharmacokinetics and immunogenicity are evaluated.
Monoclonal antibody–drug conjugate that binds a tumor-associated cell-surface antigen on malignant solid tumor cells, is internalized, and releases an intracellular cytotoxic payload (via linker cleavage) to kill the cancer cell.
ADC binds the tumor-associated cell-surface antigen, is internalized, and releases an intracellular cytotoxic payload after linker cleavage, directly killing the target-expressing cell.
A humanized monoclonal antibody targeting the IL-2 receptor alpha subunit (CD25); blocks IL-2 binding and downstream JAK/STAT5 signaling to inhibit T-cell activation/proliferation and alloreactivity, and may deplete CD25+ cells via Fc effector functions. Used here to reduce GVHD and potentially affect CD25-expressing EBV-infected T/NK cells after allo-HSCT.
Humanized monoclonal antibody against IL-2 receptor alpha (CD25) that blocks IL-2 binding and downstream JAK/STAT5 signaling, suppressing activation and proliferation of T cells (including alloreactive cells). May also deplete CD25+ cells through Fc-mediated effector functions such as ADCC/CDC.
The anti-CD25 IgG binds CD25 on target cells and recruits immune effectors via its Fc domain, triggering ADCC (NK/macrophage-mediated) and complement-dependent cytotoxicity (CDC) to deplete CD25+ cells; IL-2 blockade itself is non-cytotoxic.
Humanized afucosylated IgG1 monoclonal antibody targeting interleukin‑5 receptor alpha (IL‑5Rα); blocks IL‑5/IL‑5R signaling and induces Fc-mediated ADCC to deplete eosinophils (and basophils), reducing type 2 eosinophilic inflammation. Administered 30 mg subcutaneously q4w ×3 then q8w.
Humanized afucosylated IgG1 monoclonal antibody against IL‑5 receptor alpha (IL‑5Rα) that blocks IL‑5/IL‑5R signaling and leverages enhanced Fc‑mediated ADCC to deplete IL‑5Rα–expressing eosinophils (and basophils), thereby reducing type 2 eosinophilic inflammation.
Benralizumab binds IL-5Rα on eosinophils/basophils and, via its afucosylated IgG1 Fc, engages FcγRIIIa on NK cells to trigger potent ADCC, inducing apoptosis and depletion of IL-5Rα–expressing cells.
A bispecific IgG1 monoclonal antibody targeting EGFR and MET; blocks ligand binding and signaling, promotes receptor internalization/degradation, and mediates immune effector killing (ADCC/trogocytosis).
Bispecific IgG1 monoclonal antibody against EGFR and MET (c-Met) that blocks ligand binding and receptor phosphorylation, suppressing downstream signaling (e.g., MAPK/ERK, PI3K/AKT); promotes receptor internalization and degradation; and mediates Fc-dependent immune effector killing (ADCC/trogocytosis) of tumor cells.
Amivantamab binds EGFR on target cells and engages Fcγ receptor–bearing immune cells, inducing antibody-dependent cellular cytotoxicity (NK-cell killing) and trogocytosis/phagocytosis, leading to death of EGFR-expressing cells.