Autologous gene-modified T cells engineered to express a dual-target chimeric antigen receptor against CD19 and BCMA, intended to deplete CD19+ B cells and BCMA+ plasmablasts/plasma cells to suppress pathogenic autoantibody production in refractory immune thrombocytopenia.
Autologous T cells gene-modified to express dual chimeric antigen receptors targeting CD19 and BCMA. Upon binding CD19+ B cells and BCMA+ plasmablasts/plasma cells, CAR signaling activates T‑cell cytotoxicity and cytokine release, depleting B‑lineage cells and suppressing pathogenic autoantibody production; dual targeting reduces antigen escape.
BCMA-expressing cells are recognized by the BCMA CAR on the engineered T cells, triggering T‑cell activation and killing via perforin/granzyme release and death-receptor (Fas/FasL) apoptosis.
Glycoengineered chimeric IgG1 anti-CD20 monoclonal antibody (brand: BRIUMVI) that depletes CD20+ B cells via enhanced antibody-dependent cellular cytotoxicity and complement-dependent cytotoxicity, reducing antigen presentation, costimulation, and proinflammatory cytokine production driving MS relapses.
Glycoengineered chimeric IgG1 anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes them via enhanced antibody-dependent cellular cytotoxicity and complement-dependent cytotoxicity, reducing antigen presentation, costimulation, and proinflammatory cytokine production.
Binds CD20 on B cells and triggers Fc-mediated effector killing (ADCC by NK cells/macrophages) and complement-dependent cytotoxicity, causing lysis/apoptosis of CD20+ cells.
A HER2-targeted antibody-drug conjugate (brand name Enhertu) that binds HER2, is internalized, and releases a topoisomerase I inhibitor (DXd) to induce DNA damage and apoptosis; also inhibits HER2 signaling and can mediate ADCC with a bystander effect.
HER2-targeted antibody-drug conjugate: trastuzumab binds HER2 on tumor cells, is internalized, and releases the topoisomerase I inhibitor DXd to cause DNA damage, replication arrest, and apoptosis; also inhibits HER2 signaling and mediates ADCC with a bystander effect.
The ADC binds HER2, is internalized, and releases the DXd topoisomerase I inhibitor inside target cells, causing DNA damage, replication arrest, and apoptosis; it can also trigger Fc-mediated ADCC and a bystander effect.
TROP2-targeted antibody-drug conjugate delivering a topoisomerase I inhibitor payload; binds TROP2, internalizes, and releases cytotoxic payload causing DNA damage.
TROP2-directed antibody–drug conjugate that binds TROP2 on tumor cells, is internalized, and releases a topoisomerase I inhibitor payload to induce DNA damage and tumor cell death.
The ADC binds TROP2 on target cells, is internalized, and releases a topoisomerase I inhibitor payload that induces DNA damage, leading to cell death.
Autologous, gene-modified chimeric antigen receptor T cells engineered to target both CD19 and BCMA, administered as a single IV infusion to deplete B cells, plasmablasts, and plasma cells, aiming to suppress autoantibody production and B cell–driven inflammation.
Autologous T cells are gene-modified to express chimeric antigen receptors that recognize CD19 and BCMA. After IV infusion, CAR T cells bind CD19+ B cells and BCMA+ plasmablasts/plasma cells, become activated, and lyse these targets via cytotoxic pathways, depleting the B-lineage compartments responsible for autoantibody production and reducing B cell–driven inflammation.
CD19-directed CAR T cells bind CD19+ cells and kill them via T-cell cytotoxic pathways, primarily perforin/granzyme-mediated lysis and apoptosis (and Fas–FasL).