Chimeric IgG1 monoclonal antibody targeting GD2 on neuroblastoma cells; mediates ADCC and complement-dependent cytotoxicity.
Chimeric IgG1 monoclonal antibody that binds GD2 on tumor cells and induces immune-mediated killing via antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC), leading to lysis of GD2-expressing cells.
Dinutuximab binds GD2 on target cells; its Fc engages FcγR-expressing effector cells to mediate ADCC and activates complement to induce CDC, causing lysis of GD2+ cells.
Humanized, afucosylated IgG1 monoclonal antibody targeting IL-5 receptor alpha (IL-5Rα); blocks IL-5 signaling and induces ADCC-mediated depletion of eosinophils to control severe eosinophilic asthma.
Afucosylated humanized IgG1 monoclonal antibody targeting IL-5 receptor alpha on eosinophils and basophils; blocks IL-5 signaling and, via enhanced FcγRIIIa engagement, induces strong NK cell–mediated ADCC to deplete eosinophils, thereby reducing eosinophilic inflammation and asthma exacerbations.
Afucosylated IgG1 binds IL-5Rα and engages FcγRIIIa on NK cells to induce strong ADCC, leading to apoptosis/depletion of IL-5Rα-expressing eosinophils and basophils.
Autologous T cells engineered with chimeric antigen receptors (typically targeting CD19/CD20) to redirect T-cell cytotoxicity against malignant B cells.
Autologous T cells are engineered to express a chimeric antigen receptor (typically targeting B‑cell antigens such as CD19 or CD20). CAR binding to the tumor antigen triggers CD3ζ and costimulatory signaling (e.g., CD28 or 4‑1BB), leading to T‑cell activation, proliferation, cytokine release, and targeted cytotoxic killing of malignant B cells independent of MHC.
CAR T cells bind CD19 via the CAR, activate through CD3ζ/costimulatory domains, and kill CD19+ cells via perforin–granzyme cytolysis (and Fas–FasL), independent of MHC.
Autologous T cells engineered with chimeric antigen receptors (typically targeting CD19/CD20) to redirect T-cell cytotoxicity against malignant B cells.
Autologous T cells are engineered to express a chimeric antigen receptor (typically targeting B‑cell antigens such as CD19 or CD20). CAR binding to the tumor antigen triggers CD3ζ and costimulatory signaling (e.g., CD28 or 4‑1BB), leading to T‑cell activation, proliferation, cytokine release, and targeted cytotoxic killing of malignant B cells independent of MHC.
CAR T cells bind CD20 on target cells, triggering CD3ζ and costimulatory signaling that activates T-cell cytotoxicity, leading to perforin/granzyme-mediated killing (and death receptor pathways) of CD20+ cells.
Off-the-shelf dual-binding antibodies (commonly CD3×CD20) that redirect T cells to kill CD20-positive B cells.
Off‑the‑shelf bispecific antibody that simultaneously binds CD3 on T cells and CD20 on B cells, forming an immunologic synapse to activate and redirect cytotoxic T cells for MHC‑independent lysis of CD20‑positive malignant B cells via perforin/granzyme release and cytokine‑mediated killing.
The CD3×CD20 bispecific links T cells to CD20+ cells, forming an immunologic synapse that activates T-cell cytotoxicity, causing MHC-independent perforin/granzyme-mediated and cytokine-mediated lysis of CD20-expressing cells.