Autologous, humanized anti-CD22 chimeric antigen receptor (CAR) T-cell therapy using a humanized scFv against CD22 linked to CD3ζ signaling and a 4-1BB costimulatory domain to target and eliminate CD22-positive B-lineage malignant cells.
Autologous T cells are lentivirally transduced to express a humanized anti-CD22 CAR with a 4-1BB costimulatory domain and CD3ζ signaling. After infusion, the CAR T cells bind CD22 on B-lineage malignant cells, activate, expand, and mediate cytotoxic killing and cytokine release; 4-1BB supports activation, persistence, and antitumor activity.
YES
DIRECT
Anti-CD22 CAR T cells bind CD22 on target cells and, after CD3zeta signaling with 4-1BB costimulation, kill via perforin/granzyme-mediated cytolysis and death-receptor pathways.
Autologous, humanized anti-CD19 chimeric antigen receptor (CAR) T-cell therapy using a humanized scFv against CD19 linked to CD3ζ signaling and a 4-1BB costimulatory domain to target and eliminate CD19-positive B-lineage malignant cells.
Autologous T cells engineered to express a humanized anti‑CD19 CAR containing CD3ζ signaling and 4‑1BB costimulation. Upon binding CD19 on B‑lineage malignant cells, the CAR activates and co‑stimulates T cells to proliferate, persist, and mediate cytotoxic killing of CD19‑positive tumor cells.
YES
DIRECT
Anti-CD19 CAR T cells bind CD19 on target cells, become activated, and kill them via T-cell cytotoxic mechanisms (perforin/granzyme release and Fas–FasL–mediated apoptosis).
Genetically engineered natural killer (NK) cells expressing a chimeric antigen receptor targeting mesothelin to enable targeted cytotoxicity against mesothelin-positive ovarian epithelial carcinoma.
Genetically engineered NK cells express a mesothelin-specific chimeric antigen receptor that binds mesothelin on tumor cells and triggers NK-cell activation, leading to targeted cytotoxicity (perforin/granzyme release and cytokine secretion) and lysis of mesothelin-positive ovarian cancer cells.
YES
DIRECT
CAR-engineered NK cells bind mesothelin, activate, and kill target cells via perforin/granzyme-mediated cytotoxicity (with cytokine-mediated effects).
Anti-CD79b antibody–drug conjugate delivering MMAE to disrupt microtubules and induce B-cell apoptosis.
Anti-CD79b monoclonal antibody–drug conjugate; after binding CD79b on B cells it is internalized and linker cleavage releases MMAE, a microtubule inhibitor that blocks tubulin polymerization, leading to G2/M arrest and apoptosis of malignant B cells.
YES
DIRECT
ADC binds CD79b, is internalized, and releases MMAE that inhibits tubulin polymerization, causing G2/M arrest and apoptosis of the target-expressing B cells.
Anti-CD79b antibody–drug conjugate delivering MMAE to disrupt microtubules and induce B-cell apoptosis.
Anti-CD79b monoclonal antibody–drug conjugate; after binding CD79b on B cells it is internalized and linker cleavage releases MMAE, a microtubule inhibitor that blocks tubulin polymerization, leading to G2/M arrest and apoptosis of malignant B cells.
NO
INDIRECT
The ADC binds CD79b on B cells, is internalized, and releases MMAE; MMAE binds beta-tubulin to disrupt microtubules, causing G2/M arrest and apoptosis in CD79b-positive cells, not in cells merely expressing beta-tubulin.