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.
YES
DIRECT
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.
YES
DIRECT
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.
YES
DIRECT
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.
Autologous T cells genetically engineered to express chimeric antigen receptors that recognize tumor antigens and activate T cells via CD3 signaling to kill malignant cells.
Autologous T cells are engineered to express a chimeric antigen receptor that binds tumor-associated antigens independent of MHC and activates T-cell signaling (CD3ζ with costimulatory domains such as CD28 or 4-1BB), leading to proliferation and targeted cytotoxic killing of malignant cells via perforin/granzyme release and cytokine-mediated immune activation.
YES
DIRECT
CD19-targeted CAR T cells bind CD19 on target cells, triggering CAR (CD3ζ + costimulatory) signaling and killing via perforin/granzyme-mediated cytolysis and Fas–FasL apoptosis.