Autologous anti‑CD19 CAR T‑cell therapy with a 4‑1BB co‑stimulatory domain and CD3ζ signaling, engineered to recognize and kill CD19‑positive B cells.
Autologous T cells engineered to express an anti-CD19 chimeric antigen receptor with a 4-1BB co-stimulatory domain and CD3ζ signaling; upon binding CD19 on B cells, they activate, proliferate, and mediate cytotoxic killing of CD19-positive malignant B cells.
YES
DIRECT
Anti-CD19 CAR T cells bind CD19 on B cells, activate via CD3z/4-1BB signaling, and kill targets through T-cell cytotoxicity (perforin/granzyme-mediated apoptosis, and potentially Fas-FasL).
Chimeric IgG1 monoclonal antibody against EGFR; blocks ligand-induced EGFR signaling (RAS/RAF/MEK/ERK; PI3K/AKT) and opsonizes tumor cells to enhance NK cell ADCC.
Cetuximab is a chimeric IgG1 monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding, receptor activation and dimerization, thereby inhibiting downstream RAS/RAF/MEK/ERK and PI3K/AKT signaling to suppress tumor proliferation. Its Fc region also opsonizes EGFR-expressing tumor cells to promote NK cell–mediated ADCC.
NO
INDIRECT
Cetuximab binds EGFR on tumor cells and its Fc engages CD16a on NK cells to trigger ADCC against EGFR+ targets; CD16a-expressing cells serve as effectors and are not killed by the drug.
Humanized, afucosylated IgG1 monoclonal antibody targeting IL-5 receptor alpha (IL-5Rα); blocks IL-5 signaling and induces NK cell–mediated ADCC, leading to near-complete eosinophil depletion and reduced basophil activity; administered subcutaneously (e.g., 60 mg at weeks 0, 4, and 8) to suppress type 2/eosinophilic inflammation.
Humanized, afucosylated IgG1 monoclonal antibody targeting IL-5 receptor alpha (IL-5Rα); blocks IL-5–IL-5R signaling and engages FcγRIIIa on NK cells to drive potent ADCC, leading to near-complete eosinophil depletion and reduced basophil activity, thereby suppressing type 2/eosinophilic inflammation.
YES
DIRECT
Benralizumab binds IL-5Rα on eosinophils/basophils and, via its afucosylated Fc, engages FcγRIIIa on NK cells to induce strong ADCC (and ADCP), depleting target-expressing cells.
Humanized, afucosylated IgG1 monoclonal antibody targeting IL-5 receptor alpha (IL-5Rα); blocks IL-5 signaling and induces NK cell–mediated ADCC, leading to near-complete eosinophil depletion and reduced basophil activity; administered subcutaneously (e.g., 60 mg at weeks 0, 4, and 8) to suppress type 2/eosinophilic inflammation.
Humanized, afucosylated IgG1 monoclonal antibody targeting IL-5 receptor alpha (IL-5Rα); blocks IL-5–IL-5R signaling and engages FcγRIIIa on NK cells to drive potent ADCC, leading to near-complete eosinophil depletion and reduced basophil activity, thereby suppressing type 2/eosinophilic inflammation.
NO
INDIRECT
Benralizumab targets IL-5Rα on eosinophils; its afucosylated Fc engages CD16a on NK cells to drive ADCC against IL-5Rα+ cells. CD16a-expressing cells (NK cells) are effectors, not killed.
Autologous T cells lentivirally engineered to express an anti-CD38 chimeric antigen receptor with CD3ζ activation and 4-1BB (TNFRSF9) costimulatory domains; targets CD38 on malignant cells to induce T-cell activation, proliferation, and cytotoxic killing.
Autologous T cells are lentivirally engineered to express an anti-CD38 chimeric antigen receptor with CD3-zeta activation and 4-1BB costimulatory domains. Binding to CD38 on malignant cells triggers T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing, while 4-1BB enhances T-cell persistence and survival.
YES
DIRECT
Anti-CD38 CAR-T cells bind CD38, become activated via CD3-zeta and 4-1BB costimulation, and kill CD38+ cells through perforin/granzyme-mediated cytolysis (and associated apoptotic pathways).