Allogeneic (off-the-shelf) UCAR-T cell therapy engineered with a mesothelin (MSLN)-specific chimeric antigen receptor; upon antigen engagement, CAR T cells activate cytotoxic programs (immune synapse formation, perforin/granzyme release, cytokine secretion) to lyse MSLN-expressing tumor cells. Administered by arterial infusion for MSLN-positive advanced pancreatic cancer.
Allogeneic (off‑the‑shelf) T lymphocytes engineered to express a mesothelin (MSLN)-specific chimeric antigen receptor. CAR engagement of MSLN on tumor cells triggers T‑cell activation and cytotoxic effector functions (immune synapse formation, perforin/granzyme release, cytokine secretion), leading to targeted lysis of MSLN‑expressing cancer cells.
MSLN-specific CAR T cells bind mesothelin on target cells, form an immune synapse, and kill via perforin/granzyme-mediated cytolysis (with supportive cytokine effects).
Allogeneic chimeric antigen receptor–engineered natural killer cell therapy (0.5–3×10^9 cells) designed to recognize a disease-relevant antigen and kill antigen-expressing cells; evaluated after lymphodepleting conditioning to enhance engraftment/expansion.
Allogeneic natural killer cells engineered with a chimeric antigen receptor that binds a disease-relevant antigen and induces killing of antigen-expressing cells via NK effector mechanisms (e.g., perforin/granzyme) triggered by CAR signaling; administered after lymphodepletion to enhance engraftment and expansion.
CAR-engineered NK cells bind the target antigen and directly kill antigen-expressing cells via NK effector mechanisms (perforin/granzyme-mediated cytolysis, apoptosis) upon CAR activation.
Autologous, fully human anti-CD19 CAR T-cell therapy that reprograms a patient’s T cells to express a CD19-directed CAR, enabling depletion of CD19+ B-lineage cells to reset B cell–driven immune dysregulation in non-relapsing progressive MS.
Autologous T cells are transduced to express a fully human anti-CD19 chimeric antigen receptor (CD8α hinge/transmembrane, CD28 costimulatory, CD3ζ signaling). On binding CD19 on B-lineage cells, the CAR T cells activate and mediate cytotoxic killing and depletion of CD19+ B cells (including naive/memory B cells and plasmablasts), aiming to reset B cell–driven immune dysregulation in multiple sclerosis.
Anti-CD19 CAR T cells bind CD19 on B cells, activate, and kill targets via perforin/granzyme-mediated cytolysis and Fas–FasL apoptosis, depleting CD19+ cells.
Chimeric anti-CD20 monoclonal antibody that depletes CD20+ B cells to reduce pathogenic autoantibodies and immune-driven neuroinflammation; used here to mitigate antibody-mediated disruption of NMDA receptor signaling. Adult dose 1 g or pediatric 375 mg/m2, repeated after ~14 days.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on pre-B and mature B lymphocytes and depletes them via Fc-mediated ADCC, complement-dependent cytotoxicity, and apoptosis, reducing pathogenic autoantibody production and immune-driven inflammation (e.g., NMDA receptor autoimmunity).
Anti-CD20 antibody binds CD20 on B cells and kills them via Fc-mediated ADCC (NK/macrophages) and complement-dependent cytotoxicity; can also induce apoptosis.
Humanized IgG1 monoclonal antibody against EGFR; inhibits EGFR signaling and mediates antibody-dependent cellular cytotoxicity (ADCC).
Humanized IgG1 monoclonal antibody targeting EGFR; binds the receptor’s extracellular domain to block ligand binding and receptor activation, suppressing downstream signaling (e.g., RAS/MAPK, PI3K/AKT) and tumor cell proliferation/survival. The IgG1 Fc also engages immune effector cells to mediate ADCC against EGFR-expressing tumor cells.
IgG1 anti-EGFR antibody binds EGFR on target cells and its Fc engages Fcγ receptors on NK cells/macrophages to mediate ADCC (and some CDC), leading to lysis/apoptosis of EGFR+ cells; signaling blockade is antiproliferative.