Autologous patient T cells genetically engineered to express an anti-CD19 chimeric antigen receptor; targeting CD19+ B cells and plasmablasts to reduce AQP4-IgG autoantibody production in NMOSD.
Autologous T cells engineered with an anti‑CD19 chimeric antigen receptor recognize CD19 on B cells and plasmablasts, triggering T‑cell activation and cytotoxic killing (perforin/granzyme) to deplete the B‑cell lineage and reduce pathogenic AQP4‑IgG autoantibody production in NMOSD.
Anti-CD19 CAR-T cells bind CD19 on B-lineage cells, form an immune synapse, and induce cytotoxicity via perforin/granzyme release (and Fas–FasL apoptosis), leading to target cell death.
Autologous patient T cells genetically engineered to express a chimeric antigen receptor targeting CD7, administered as a single IV infusion after lymphodepletion to recognize and kill CD7-expressing malignant T cells in relapsed/refractory T-ALL/LBL.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that binds CD7. Upon engagement of CD7 on malignant T cells, CAR signaling (CD3ζ with co-stimulation) activates the T cells, driving proliferation, cytokine release, and perforin/granzyme‑mediated cytotoxic killing, leading to clearance of CD7‑expressing T‑lineage blasts in R/R T‑ALL/LBL.
CAR T cells recognize CD7 on target cells and, upon CAR signaling, directly kill them via perforin/granzyme-mediated cytolysis (and death receptor–mediated apoptosis).
Anti–CD20 monoclonal antibody that depletes B cells.
Rituximab is an anti‑CD20 monoclonal antibody that binds CD20 on pre‑B and mature B lymphocytes and induces B‑cell depletion via antibody‑dependent cellular cytotoxicity, complement‑dependent cytotoxicity, and apoptosis, eliminating CD20‑positive malignant and normal B cells.
Anti-CD20 antibody binds CD20 on B cells and triggers immune killing via Fc-mediated ADCC (NK cells/macrophages), complement-dependent cytotoxicity (MAC formation), and can induce apoptosis after crosslinking.
Antibody-drug conjugate targeting tumor antigens to deliver a cytotoxic payload.
An antibody targets a tumor-associated antigen, the conjugate is internalized, its linker is cleaved, and a potent cytotoxic payload is released within the cancer cell to cause cell death (e.g., via DNA damage or microtubule disruption), with potential bystander effect depending on linker/payload.
The ADC binds the tumor-associated antigen, is internalized, the linker is cleaved, and a potent cytotoxic payload is released inside the cell (e.g., DNA damage or microtubule disruption), leading to cell death; some payloads can also cause bystander killing.