Autologous, fully human anti-CD19 chimeric antigen receptor T-cell therapy that depletes CD19+ B-lineage cells to reduce pathogenic autoantibodies in generalized myasthenia gravis.
Autologous T cells are engineered with a lentiviral vector to express an anti-CD19 chimeric antigen receptor (scFv-CD19 with CD8α hinge/transmembrane, CD28 costimulatory, and CD3ζ signaling domains). After infusion, the CAR T cells recognize CD19 on B-lineage cells (B cells and plasmablasts), become activated, and mediate cytotoxic lysis, depleting CD19+ cells and reducing pathogenic autoantibody production in generalized myasthenia gravis.
YES
DIRECT
Anti-CD19 CAR T cells bind CD19 on B-lineage cells and, upon activation, kill them via T cell cytotoxic mechanisms (perforin/granzyme release and death-receptor signaling), leading to lysis/apoptosis of CD19+ cells.
Bispecific antibody–drug conjugate (aka iza-bren; izalontamab brengitecan; BMS-986507) targeting EGFR and HER3. After binding, it is internalized and releases a camptothecin-class topoisomerase I inhibitor payload (brengitecan) to induce DNA damage; it also blocks EGFR/HER3 signaling.
Bispecific ADC that binds EGFR and HER3 on tumor cells; after receptor-mediated internalization it releases a camptothecin-class topoisomerase I inhibitor payload (brengitecan) to induce DNA damage and cell death, while concurrently inhibiting EGFR/HER3 signaling.
NO
INDIRECT
BL-B01D1 targets EGFR/HER3 on tumor cells, is internalized, and releases a camptothecin-class topoisomerase I inhibitor (brengitecan) that causes DNA damage; topoisomerase I is the intracellular enzymatic target of the payload, not the antigen used for cell targeting.
Anti-EGFR IgG1 monoclonal antibody that inhibits EGFR-driven signaling (RAS–RAF–MAPK, PI3K–AKT) and induces antibody-dependent cellular cytotoxicity (ADCC).
Cetuximab is an IgG1 monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding and receptor dimerization to inhibit downstream RAS–RAF–MAPK and PI3K–AKT signaling, suppressing tumor cell proliferation and survival; its Fc region also engages immune effector cells to induce antibody-dependent cellular cytotoxicity (ADCC).
YES
DIRECT
Cetuximab binds EGFR on target cells and its IgG1 Fc engages FcγR-expressing effector cells (e.g., NK cells) to induce antibody-dependent cellular cytotoxicity; it can also activate complement (CDC). EGFR signaling blockade may further promote apoptosis.
Anti-EGFR IgG1 monoclonal antibody that inhibits EGFR-driven signaling (RAS–RAF–MAPK, PI3K–AKT) and induces antibody-dependent cellular cytotoxicity (ADCC).
Cetuximab is an IgG1 monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding and receptor dimerization to inhibit downstream RAS–RAF–MAPK and PI3K–AKT signaling, suppressing tumor cell proliferation and survival; its Fc region also engages immune effector cells to induce antibody-dependent cellular cytotoxicity (ADCC).
NO
INDIRECT
Cetuximab binds EGFR on tumor cells; its Fc engages CD16a on NK cells to trigger ADCC, which kills EGFR-expressing cells. CD16a+ effector cells are not killed.
Chimeric anti-CD20 monoclonal antibody that depletes CD20-expressing B cells and may affect CD20+ T cells to preserve beta-cell function in recent-onset type 1 diabetes.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B lymphocytes (and a subset of CD20+ T cells) and depletes these cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, thereby dampening autoimmunity and aiming to preserve beta-cell function.
YES
DIRECT
Rituximab binds CD20 on target cells and eliminates them via complement-dependent cytotoxicity and Fc-mediated effector functions (ADCC/ADCP), and can also induce apoptosis.