Anti-CD20 monoclonal antibody that depletes B cells to reduce ANCA autoantibody production.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on pre‑B and mature B lymphocytes and depletes them via antibody‑dependent cellular cytotoxicity, complement‑dependent cytotoxicity, and apoptosis, thereby reducing ANCA autoantibody production.
Rituximab binds CD20 on B cells and triggers killing via Fc-mediated ADCC (e.g., NK cells), complement-dependent cytotoxicity, and can directly induce apoptosis.
Allogeneic BCMA-directed UCAR-T cells; genetically modified T cells engineered with a CAR targeting B-cell maturation antigen (BCMA). Administered by cell infusion to recognize BCMA+ malignant plasma cells and induce T-cell cytotoxicity and cytokine release.
Allogeneic T cells engineered with a chimeric antigen receptor targeting BCMA bind BCMA on malignant plasma cells, triggering CAR-mediated T‑cell activation, perforin/granzyme‑dependent cytotoxicity, and cytokine release to lyse BCMA‑positive myeloma/plasma cell leukemia cells; designed as an off‑the‑shelf (UCAR) product.
BCMA-directed CAR T cells bind BCMA on target cells and, upon CAR activation, kill via perforin/granzyme-dependent cytolysis (and related apoptosis/cytokine-mediated mechanisms).
Allogeneic CD9-directed UCAR-T cells; genetically modified T cells engineered with a CAR targeting CD9. Administered by cell infusion to recognize CD9+ malignant plasma cells and induce T-cell cytotoxicity and cytokine release.
Allogeneic, gene-edited T cells engineered with a CD9-specific chimeric antigen receptor bind CD9 on malignant plasma cells, triggering CAR signaling that activates T-cell cytotoxicity and cytokine release to lyse target cells.
CD9-specific CAR-T cells bind CD9 on target cells, triggering T-cell activation and killing via perforin/granzyme release and Fas–FasL–mediated apoptosis, with supportive cytokine effects.
Chimeric IgG1 anti-EGFR monoclonal antibody administered IV (100 mg) preoperatively to bind EGFR on tumor cells, inhibit ligand-induced signaling, and aid targeting for imaging.
Cetuximab is a chimeric IgG1 monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding and receptor dimerization/activation. This inhibits downstream EGFR signaling (e.g., MAPK and PI3K–AKT), reducing tumor cell proliferation and survival; its IgG1 Fc can also mediate ADCC. In this trial it additionally functions as a targeting carrier for an IRDye800 fluorophore to enable intraoperative imaging.
Cetuximab binds EGFR on target cells and its IgG1 Fc engages Fcγ receptors on immune effectors (e.g., NK cells), inducing ADCC (and potentially CDC), leading to lysis of EGFR+ cells; EGFR signaling blockade is antiproliferative.
Anti–IL-5Rα monoclonal antibody that induces antibody-dependent cellular cytotoxicity to deplete eosinophils and basophils.
Afucosylated humanized monoclonal antibody targeting IL-5 receptor alpha (IL-5Rα). By binding IL-5Rα on eosinophils and basophils, it enhances FcγRIIIa-mediated antibody-dependent cellular cytotoxicity (ADCC), leading to rapid depletion of these cells and consequent suppression of IL-5–driven type 2 inflammation.
Benralizumab binds IL-5Ralpha on eosinophils/basophils and, via its afucosylated Fc, engages Fc-gamma RIIIa on NK cells to trigger ADCC, depleting IL-5Ralpha+ cells.