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.
BCMA-targeted CAR T cells bind BCMA+ cells, activate, and kill them via perforin/granzyme-mediated cytolysis and apoptotic pathways (e.g., Fas/FasL).
Antibody-drug conjugate targeting TROP2 (also known as iza-bren; izalontamab brengitecan; BMS-986507). Humanized IgG1 mAb linked via a cleavable linker to a camptothecin/topoisomerase-I inhibitor payload, leading to DNA damage and apoptosis; may have Fc-mediated effector and bystander effects.
Humanized IgG1 antibody-drug conjugate that binds TROP2 on tumor cells, is internalized, and releases a cleavable camptothecin/topoisomerase I–inhibitor payload to induce DNA damage and apoptosis; may also elicit Fc-mediated effector functions and bystander killing.
ADC binds TROP2 on tumor cells, is internalized, and releases a cleavable topoisomerase I inhibitor payload causing DNA damage and apoptosis; Fc-mediated effector and bystander killing may also contribute.
A CD3xCD20 bispecific T-cell–engager antibody that binds CD3 on T cells and CD20 on malignant B cells, activating cytotoxic T cells to kill CD20+ CLL/SLL cells via perforin/granzyme release and caspase-dependent apoptosis.
Bispecific CD3xCD20 antibody that bridges CD3 on T cells to CD20 on malignant B cells, activating cytotoxic T cells to kill CD20+ cells via perforin/granzyme release and caspase-dependent apoptosis.
CD3xCD20 bispecific antibody crosslinks T cells to CD20+ cells, activating T-cell cytotoxicity with perforin/granzyme release and caspase-dependent apoptosis of the CD20-expressing cells.
A cellular immunotherapy in which natural killer (NK) cells are genetically engineered to express a chimeric antigen receptor (CAR) targeting CD19 on B cells; CAR engagement activates NK cytotoxic pathways (perforin/granzyme and death receptor signaling) to eliminate CD19+ B cells/plasmablasts and suppress autoantibody-driven inflammation in immune nephropathies.
Natural killer cells are genetically engineered to express a CD19-targeted chimeric antigen receptor. Upon binding CD19 on B cells, the CAR activates NK cytotoxic pathways (perforin/granzyme release and death receptor signaling), depleting CD19+ B cells/plasmablasts and reducing autoantibody-driven inflammation in immune nephropathies.
CAR-engineered NK cells bind CD19 on target cells and trigger NK cytotoxic pathways, killing CD19+ cells via perforin/granzyme-mediated lysis and death receptor (e.g., Fas/TRAIL) signaling.
Patient-derived T cells genetically engineered ex vivo to express a chimeric antigen receptor targeting BCMA (TNFRSF17) on myeloma cells; infused after lymphodepletion to expand and mediate antigen-specific cytotoxicity.
Autologous T cells are collected and genetically engineered ex vivo to express a chimeric antigen receptor that recognizes BCMA (TNFRSF17) on myeloma cells. Following lymphodepletion, the CAR‑T cells are infused; antigen binding activates the CAR signaling domains (CD3ζ with costimulation), driving T‑cell expansion, cytokine release, and perforin/granzyme‑mediated cytotoxic killing of BCMA‑expressing malignant plasma cells.
BCMA-directed CAR-T cells bind BCMA on target cells, activate, and kill via perforin/granzyme-mediated cytolysis (and Fas–FasL apoptosis).