Autologous anti-CD19 CAR T-cell therapy; gene-modified T cells that recognize and eliminate CD19+ B-lineage cells (naive/memory B cells, plasmablasts, some plasma cells) to reset humoral autoimmunity and reduce profibrotic signaling. Administered as a single infusion after lymphodepletion.
Autologous T cells genetically engineered to express an anti-CD19 chimeric antigen receptor. After infusion (post-lymphodepletion), the CAR T cells recognize CD19 on B-lineage cells and trigger T-cell activation and cytotoxic killing, resulting in depletion of CD19+ B cells (including naive/memory B cells and plasmablasts, some plasma cells). This resets humoral autoimmunity and, in oncology settings, eliminates CD19+ malignant cells.
Anti-CD19 CAR T cells recognize CD19 on target cells and kill them via T‑cell cytotoxic mechanisms (perforin/granzyme release and Fas–FasL–mediated apoptosis).
Anti-CD20 monoclonal antibody that depletes CD20+ B cells via ADCC/CDC, largely sparing long-lived plasma cells, aiming to reduce autoantibody production and downstream inflammation/fibrosis.
Chimeric anti‑CD20 monoclonal antibody that binds CD20 on pre‑B and mature B cells and depletes them primarily via ADCC and CDC (and apoptosis), reducing naive/memory B cells while largely sparing long‑lived plasma cells; this decreases autoantibody production and downstream inflammatory/fibrotic signaling.
Rituximab binds CD20 on B cells and recruits effector functions via its Fc: NK cell/macrophage ADCC and complement-dependent cytotoxicity (CDC), with some direct apoptosis signaling.
An intravenous antibody–drug conjugate targeting Trop-2 (TACSTD2); the monoclonal antibody binds Trop-2 on tumor cells, is internalized, and releases a cytotoxic payload intracellularly to induce cancer cell death. Dosed every 21 days; being evaluated in a first-in-human Phase I study for MTD/DLT, PK, safety, and preliminary antitumor activity in advanced solid tumors.
Humanized IgG1 anti–TROP-2 antibody–drug conjugate that binds TROP-2 on tumor cells, is internalized, and via a cleavable linker releases a topoisomerase I inhibitor payload intracellularly, inhibiting DNA replication and inducing cell cycle arrest and apoptosis in TROP-2–expressing cancers.
The ADC binds TROP-2, is internalized, and releases a cleavable topoisomerase I inhibitor payload intracellularly, inhibiting DNA replication and causing cell cycle arrest and apoptosis of TROP-2–expressing cells.
Autologous CD19-directed chimeric antigen receptor T cells (gene-modified cellular immunotherapy) administered as a single IV infusion; engineered T cells recognize CD19 on B-lineage cells to induce cytotoxic depletion and deep B-cell aplasia, reducing autoantibody production and B cell–T cell costimulation in autoimmune diseases.
Autologous T cells genetically engineered to express an anti‑CD19 chimeric antigen receptor bind CD19 on B-lineage cells and trigger T-cell cytotoxicity, leading to profound depletion of CD19+ B cells and plasmablasts, resulting in B‑cell aplasia and reduced autoantibody production and B cell–T cell costimulation.
Anti-CD19 CAR T cells bind CD19 on target cells and kill them via perforin/granzyme-mediated cytolysis and Fas–FasL apoptosis, causing B-cell depletion.
An IgG-based bispecific T-cell–engaging antibody that binds CD276 (B7-H3) on tumor and tumor vasculature and CD3 on T cells; includes an attenuated CD3 binder and YTE Fc modification to extend half-life, designed to redirect T cells to CD276+ targets and provide anti-angiogenic effects.
IgG-based bispecific antibody that binds CD276 (B7-H3) on tumor and tumor vasculature and CD3 on T cells to redirect and activate T cells for cytotoxic killing of CD276+ targets; incorporates an attenuated CD3 binder to reduce off-target activation/CRS risk and a YTE Fc modification to extend half-life, with potential anti-angiogenic effects via CD276 on tumor endothelium.
IgG-based bispecific T‑cell engager crosslinks CD276 on target cells with CD3 on T cells, forming an immune synapse and activating T cells to kill CD276+ cells via perforin/granzyme (and apoptotic) pathways; may also eliminate CD276+ tumor endothelium.