PSMA-targeted radioligand therapy: the small-molecule ligand PSMA-617 chelated to the beta-emitter lutetium-177; binds PSMA (FOLH1) on prostate cancer cells, is internalized, and delivers beta radiation causing DNA double-strand breaks with crossfire killing.
A PSMA-targeted small-molecule ligand (PSMA-617) chelated to lutetium-177 binds PSMA (FOLH1) on prostate cancer cells, is internalized, and emits beta particles that cause DNA double-strand breaks with a crossfire effect, leading to tumor cell death.
PSMA-617 binds PSMA on tumor cells, is internalized, and 177Lu beta emissions cause DNA double-strand breaks (with crossfire to nearby cells), leading to cell death.
Humanized anti-CD19 monoclonal antibody that depletes CD19+ B-lineage cells (pre-B, naive, memory, plasmablasts, some plasma cells) via antibody-dependent cellular cytotoxicity and complement, reducing pathogenic anti–aquaporin-4 autoantibodies in NMOSD.
Humanized afucosylated IgG1 anti‑CD19 monoclonal antibody that depletes CD19+ B‑lineage cells (pre‑B, naive, memory, plasmablasts, and some plasma cells) via antibody‑dependent cellular cytotoxicity and complement, thereby reducing pathogenic anti–aquaporin‑4 autoantibody production in NMOSD.
Anti-CD19 IgG1 binds CD19 on B cells; its Fc engages effector cells to mediate ADCC/ADCP and activates complement (CDC), resulting in lysis/depletion of CD19+ cells.
Autologous gene-modified CAR T-cell therapy targeting B-cell maturation antigen (BCMA) to eliminate BCMA-positive plasma cells and reduce anti-HLA antibody production.
Autologous T cells engineered to express an anti-BCMA CAR with 4-1BB and CD3z signaling domains recognize BCMA on plasma cells, activate, and kill BCMA-expressing cells via cytotoxic effector functions, depleting long-lived antibody-secreting cells and reducing anti-HLA antibody production.
Anti-BCMA CAR T cells recognize BCMA on target cells via the CAR, activate (4-1BB/CD3ζ), and kill BCMA+ cells through cytotoxic effector functions, primarily perforin/granzyme-mediated apoptosis.
Autologous humanized anti-CD19 CAR T-cell therapy that depletes CD19-positive B-lineage cells (naive, memory, plasmablasts) to suppress humoral alloimmunity.
Autologous humanized anti-CD19 chimeric antigen receptor T cells that bind CD19 on B-lineage cells and, upon engagement, activate cytotoxic pathways to eliminate CD19+ naive and memory B cells and plasmablasts, reducing antibody production and suppressing humoral alloimmunity.
Anti-CD19 CAR T cells bind CD19 on target cells, form an immunologic synapse, and kill via perforin/granzyme-mediated cytolysis and death-receptor pathways (e.g., Fas/FasL).
Chimeric anti-CD20 monoclonal antibody that depletes B cells via complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC), and induction of apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20-positive cells via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and induction of apoptosis.
Binding to CD20 triggers complement-dependent cytotoxicity and Fc-mediated ADCC by immune effectors, and can directly induce apoptosis of CD20+ B cells.