An antibody–drug conjugate where a trastuzumab-based anti-HER2 antibody targets HER2-expressing tumor cells and delivers a deruxtecan (DXd) topoisomerase I inhibitor payload, causing DNA damage and apoptosis; the membrane-permeable payload enables a bystander effect and the Fc region may mediate ADCC.
A trastuzumab-based anti-HER2 antibody binds HER2 on tumor cells, is internalized, and releases the deruxtecan (DXd) payload, a membrane-permeable topoisomerase I inhibitor that induces DNA damage and apoptosis; the payload can exert a bystander effect on neighboring cells, and the antibody Fc region may mediate ADCC.
The anti-HER2 ADC binds HER2, is internalized, and releases the DXd topoisomerase I inhibitor, causing DNA damage and apoptosis; Fc-mediated ADCC and a membrane-permeable bystander effect can add killing.
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.
Cetuximab binds EGFR on target cells and its IgG1 Fc engages Fcγ receptors on NK cells to mediate ADCC (and can trigger complement-dependent cytotoxicity), leading to lysis of EGFR-positive cells; EGFR blockade mainly inhibits proliferation.
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.
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).
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.
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.
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.
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).