Autologous gamma delta T cells engineered with a chimeric antigen receptor targeting Prostate Stem Cell Antigen (PSCA), redirecting γδ T-cell activation and cytotoxicity against PSCA-positive tumor cells.
Autologous gamma delta T cells engineered with a PSCA-specific chimeric antigen receptor bind PSCA on tumor cells, triggering MHC-independent activation, cytokine release, and perforin/granzyme-mediated cytotoxicity against PSCA-positive cancer cells.
PSCA-specific CAR-engineered gamma delta T cells bind PSCA on tumor cells and directly lyse them via immunologic synapse formation and perforin/granzyme-mediated cytotoxicity (MHC-independent).
Humanized IgG1 monoclonal antibody against the HER2 extracellular domain; blocks HER2 signaling/dimerization and triggers Fc-mediated ADCC.
Humanized IgG1 monoclonal antibody that binds the HER2 extracellular domain, blocking HER2 signaling and receptor dimerization, promoting receptor downregulation, and engaging Fcγ receptors to trigger antibody-dependent cellular cytotoxicity (ADCC), thereby suppressing PI3K/AKT and MAPK pathways in HER2-overexpressing tumor cells.
Trastuzumab binds HER2 on target cells and engages Fcγ receptor–bearing effector cells (e.g., NK cells) to mediate antibody-dependent cellular cytotoxicity; signaling blockade may also promote apoptosis.
Human IgG1k anti-CD38 monoclonal antibody that binds CD38 on malignant plasma cells and other CD38-positive cells, inducing direct apoptosis and immune effector-mediated killing (CDC, ADCC, and ADCP); also inhibits CD38 ectoenzyme activity and depletes CD38-expressing immunosuppressive cells (Tregs, Bregs, MDSCs).
Binds CD38 on target cells and triggers direct apoptosis plus Fc-mediated effector killing: complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC), and antibody-dependent cellular phagocytosis (ADCP).
Genetically engineered autologous T lymphocytes expressing a CD19-specific chimeric antigen receptor that activates T-cell cytotoxicity against CD19+ B-ALL cells, inducing B-cell aplasia and MRD eradication.
Autologous T lymphocytes are genetically engineered to express a CD19-specific chimeric antigen receptor (scFv fused to costimulatory domain(s) and CD3z), enabling MHC-independent recognition of CD19 on B cells and B-ALL blasts; CAR signaling triggers T-cell activation, proliferation, cytokine release, and cytotoxic killing, leading to depletion of CD19+ cells, B-cell aplasia, and eradication of residual disease.
CD19 CAR T cells bind CD19 on target cells, become activated, and kill via T‑cell effector mechanisms (perforin/granzyme-mediated cytolysis and death receptor signaling), depleting CD19+ cells.
An autologous CD19-directed chimeric antigen receptor (CAR) T-cell therapy. Patient T cells are engineered to express a CAR that binds CD19; upon engagement they activate and kill CD19-expressing B-lineage cells (naive and memory B cells and CD19+ plasmablasts), inducing deep B-cell depletion and an immune reset to reduce autoantibody production and inflammation in SLE. Tested in dose escalation (~25–150×10^6 CAR+ T cells).
Autologous patient T cells are engineered to express a CD19-specific chimeric antigen receptor; upon recognizing CD19 on B-lineage cells (naive and memory B cells and CD19+ plasmablasts), the CAR T cells become activated and kill these targets, producing deep B-cell depletion and an immune reset that reduces autoantibody production and inflammation.
CD19-directed CAR T cells bind CD19 on target cells and induce killing via T-cell cytotoxic pathways (perforin/granzyme release and Fas–FasL-mediated apoptosis).