An allogeneic cytokine-induced killer (CIK) cell therapy genetically engineered via transposon to express a CD19-directed chimeric antigen receptor (anti-CD19 scFv with CD3ζ signaling and CD28/OX40 costimulation) for treatment of relapsed/refractory CD19+ B-cell malignancies (NHL, CLL).
Allogeneic cytokine-induced killer (CIK) T cells engineered via transposon to express a CD19-targeted CAR with CD3ζ signaling and CD28/OX40 costimulation. CAR engagement of CD19 on B cells triggers T/CIK activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxicity to eliminate CD19+ malignant B cells.
NO
INDIRECT
CD28 is a costimulatory domain within the CAR T/CIK cells, not the targeted antigen. The therapy kills CD19+ cells via CAR engagement and perforin/granzyme-mediated cytotoxicity.
An intravenous HER2-targeted monoclonal antibody–drug conjugate (ADC) dosed 5.4 mg/kg every 3 weeks; binds HER2 (ERBB2) on tumor cells, is internalized, and releases a DNA-damaging cytotoxic payload that inhibits proliferation, leading to tumor cell death; designed for HER2-expressing and HER2-low solid tumors.
HER2-targeted monoclonal antibody–drug conjugate that binds HER2 (ERBB2) on tumor cells, is internalized, and releases a DNA-damaging cytotoxic payload, inhibiting proliferation and inducing tumor cell death in HER2-expressing and HER2-low solid tumors.
YES
DIRECT
HER2-targeted ADC binds HER2 on tumor cells, is internalized, and releases a DNA-damaging cytotoxic payload that causes cell cycle arrest and apoptosis/tumor cell death.
An allogeneic cytokine-induced killer (CIK) cell therapy genetically engineered via transposon to express a CD19-directed chimeric antigen receptor (anti-CD19 scFv with CD3ζ signaling and CD28/OX40 costimulation) for treatment of relapsed/refractory CD19+ B-cell malignancies (NHL, CLL).
Allogeneic cytokine-induced killer (CIK) T cells engineered via transposon to express a CD19-targeted CAR with CD3ζ signaling and CD28/OX40 costimulation. CAR engagement of CD19 on B cells triggers T/CIK activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxicity to eliminate CD19+ malignant B cells.
NO
INDIRECT
OX40 is a costimulatory domain within the CAR T cells, not the antigen target. The CAR recognizes CD19 on B cells, triggering perforin/granzyme-mediated killing of CD19+ cells; OX40-expressing cells are not specifically targeted.
Human anti-CD25 (IL-2 receptor alpha) monoclonal antibody immunotherapy that blocks IL-2/IL-2R signaling and can deplete CD25+ regulatory T cells via Fc-mediated effector functions (e.g., ADCC); administered intravenously as a single agent.
Human anti-CD25 (IL-2Rα) monoclonal antibody that binds CD25 on regulatory T cells, blocks IL-2/IL-2R signaling, and depletes CD25+ Tregs via Fc-mediated effector functions (e.g., ADCC), thereby reducing tumor-associated immunosuppression and enhancing effector T-cell activity.
YES
DIRECT
Anti-CD25 mAb binds CD25 on target cells and recruits FcγR-bearing effector cells to mediate ADCC (and potentially ADCP/CDC), depleting CD25+ cells.
Anti-CD20 monoclonal antibody that depletes malignant and normal B cells via CDC/ADCC and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20-positive malignant and normal B cells via complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity/phagocytosis (ADCC/ADCP), and induction of apoptosis.
YES
DIRECT
Binds CD20 on B cells and induces complement-dependent cytotoxicity and Fc-mediated ADCC/ADCP; CD20 crosslinking can also trigger direct apoptosis.