Autologous CAR T-cell gene therapy in which patient T cells are engineered to express two fully human CARs: anti-CD19 with CD28/CD3ζ signaling and anti-CD20 with 4-1BB/CD3ζ signaling to enhance activation and persistence and reduce antigen-loss escape.
Autologous T cells are genetically engineered to express two CARs: an anti‑CD19 CAR with CD28/CD3ζ signaling and an anti‑CD20 CAR with 4‑1BB/CD3ζ signaling. Upon binding CD19 or CD20 on B cells, the CARs activate T‑cell cytotoxicity and cytokine release to kill malignant B cells; CD28 promotes rapid activation/expansion and 4‑1BB enhances persistence. Dual antigen targeting is intended to reduce antigen‑loss escape and results in on‑target B‑cell aplasia.
YES
DIRECT
CAR T cells recognize CD20 via the anti‑CD20 CAR (4‑1BB/CD3ζ), become activated, and kill CD20+ cells through perforin/granzyme release and death‑receptor pathways (e.g., Fas/FasL).
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.
YES
DIRECT
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.
YES
DIRECT
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.
YES
DIRECT
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.
YES
DIRECT
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.