Allogeneic, banked Epstein–Barr virus–specific T lymphocytes engineered to express a CD30-directed chimeric antigen receptor (CAR); binds CD30 on tumor cells to trigger T-cell activation and cytotoxicity, while the native EBV-specific TCR enables recognition of EBV antigens in EBV+ tumors, supporting persistence/expansion and dual targeting.
Allogeneic EBV-specific T lymphocytes engineered to express a CD30-directed chimeric antigen receptor. CAR engagement of CD30 on tumor cells triggers T-cell activation and cytotoxic killing of CD30+ malignant cells, while the native EBV-specific TCR enables recognition of EBV antigens in EBV+ tumors, supporting persistence/expansion and dual targeting.
YES
DIRECT
Native EBV-specific TCRs on the infused T cells recognize EBV peptide–HLA class I complexes on target cells and trigger T‑cell cytotoxic killing (perforin/granzyme, Fas–FasL).
Chimeric anti-CD20 monoclonal antibody that depletes CD20+ B cells via complement-dependent cytotoxicity, antibody-dependent cell-mediated cytotoxicity, and apoptosis, reducing B-cell antigen presentation, autoantibody production, and pro-inflammatory cytokines (e.g., IL-6).
Chimeric anti-CD20 monoclonal antibody that binds CD20 on pre-B and mature B cells and depletes them via complement-dependent cytotoxicity, antibody-dependent cell-mediated cytotoxicity, and apoptosis, reducing B-cell antigen presentation, autoantibody production, and pro-inflammatory cytokines.
YES
DIRECT
Binds CD20 on B cells and eliminates them via complement-dependent cytotoxicity and Fc-mediated ADCC; crosslinking can also induce apoptosis.
Autologous peripheral blood T cells expanded and activated ex vivo to recognize MUC1 via TCR; infused intravenously as adoptive cellular immunotherapy to mediate tumor cell killing and cytokine release.
Autologous peripheral blood T cells are expanded ex vivo and enriched/activated for TCR-mediated recognition of MUC1 peptides presented on MHC. After infusion, these MUC1‑reactive T cells engage tumor cells, become activated, and mediate cytotoxicity via perforin/granzyme release and cytokine secretion (e.g., IFN-γ, TNF), leading to targeted tumor cell killing and immune amplification.
YES
DIRECT
MUC1-specific T cells recognize MUC1 peptide–MHC on target cells and induce apoptosis via perforin/granzyme release (with possible Fas–FasL and cytokine-mediated effects).
Anti-CD79b antibody-drug conjugate that delivers the microtubule inhibitor MMAE to B cells, causing microtubule disruption and cell death.
Anti-CD79b monoclonal antibody linked via a protease-cleavable linker to the microtubule inhibitor MMAE. After binding CD79b on B cells and internalization, MMAE is released to inhibit tubulin polymerization, leading to G2/M arrest and apoptotic death of malignant B cells.
YES
DIRECT
ADC binds CD79b on B cells, is internalized, and releases MMAE via a protease-cleavable linker; MMAE inhibits tubulin polymerization, causing G2/M arrest and apoptotic cell death.
Anti-CD79b antibody-drug conjugate that delivers the microtubule inhibitor MMAE to B cells, causing microtubule disruption and cell death.
Anti-CD79b monoclonal antibody linked via a protease-cleavable linker to the microtubule inhibitor MMAE. After binding CD79b on B cells and internalization, MMAE is released to inhibit tubulin polymerization, leading to G2/M arrest and apoptotic death of malignant B cells.
NO
INDIRECT
The ADC binds CD79b on B cells, is internalized, and releases MMAE, which binds beta‑tubulin (vinca site) to disrupt microtubules, causing G2/M arrest and apoptosis; tubulin expression alone is not targeted by the antibody.