Intravenous chimeric IgG1 monoclonal antibody against EGFR; blocks ligand binding and receptor activation and can elicit ADCC.
Chimeric IgG1 monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding and receptor dimerization/activation, thereby inhibiting downstream signaling and tumor cell proliferation; can also mediate antibody-dependent cellular cytotoxicity (ADCC).
Cetuximab’s IgG1 Fc engages Fcγ receptors on NK cells and other effectors to mediate ADCC against EGFR-expressing cells (with possible complement activation), causing target-cell lysis.
Autologous, genetically engineered CAR T-cell therapy targeting CLDN18.2; engineered T cells bind CLDN18.2 on tumor cells to activate T-cell proliferation, cytokine release, and cytotoxic killing.
Autologous T cells are genetically engineered to express a chimeric antigen receptor targeting CLDN18.2. Upon binding CLDN18.2 on tumor cells, the CAR activates T cells independently of native TCR/MHC, driving T‑cell expansion, cytokine release, and cytotoxic killing of CLDN18.2‑expressing tumor cells.
CLDN18.2-specific CAR T cells bind CLDN18.2 on target cells, become activated, and kill them via T-cell cytotoxic mechanisms (perforin/granzyme-mediated lysis and cytokine-driven apoptosis), independent of native TCR/MHC.
Subcutaneous BCMA/CD3 bispecific T-cell engager (BiTE) antibody that binds BCMA (TNFRSF17) on malignant plasma cells and CD3 on T cells to redirect T-cell cytotoxicity and cytokine release against BCMA-positive plasma cells; uses step-up priming followed by weekly/biweekly dosing to prevent progression of high-risk smoldering multiple myeloma.
Bispecific T-cell engager antibody that binds BCMA on malignant plasma cells and CD3 on T cells to form an immunologic synapse, activating T-cell cytotoxicity and cytokine release to kill BCMA-positive plasma cells.
BiTE antibody bridges BCMA on target cells and CD3 on T cells, forming an immunologic synapse that activates T-cell killing via perforin/granzyme-mediated cytotoxicity and cytokine release against BCMA+ cells.
Genetically engineered natural killer cells expressing an anti-CD19 chimeric antigen receptor to target and deplete CD19+ B cells via NK cytotoxicity.
Genetically engineered natural killer cells expressing an anti‑CD19 chimeric antigen receptor bind CD19 on B cells and trigger NK cell activation and cytotoxicity (perforin/granzyme), leading to targeted depletion of CD19+ B cells and reduction of pathogenic humoral responses.
Anti-CD19 CAR NK cells bind CD19 on target B cells, triggering NK activation and killing via degranulation (perforin/granzyme) and death-ligand pathways.
An autologous, dual-target CD19/BCMA chimeric antigen receptor T-cell (CAR-T) therapy engineered to deplete CD19+ B cells and BCMA+ plasmablasts/plasma cells to ablate autoreactive B-cell compartments in refractory SLE.
Autologous T cells engineered with dual CARs targeting CD19 and BCMA bind B cells and plasmablasts/plasma cells, triggering CAR signaling that activates T-cell proliferation and cytolytic activity (perforin/granzyme and cytokines) to deplete CD19+ and BCMA+ compartments, thereby abrogating autoreactive B-cell populations and autoantibody production in refractory SLE.
CD19-binding CAR-T cells engage target cells and, upon activation, induce cytolysis via perforin/granzyme release (and death-receptor/cytokine-mediated apoptosis).