Autologous/allogeneic T cells engineered with a lentiviral vector to express a CAR targeting Epstein-Barr virus GP350; IV dose-escalated infusion; designed for MHC-independent killing of GP350-expressing EBV-associated malignant cells.
Autologous/allogeneic T cells are lentivirally engineered to express a CAR that binds EBV GP350 on EBV-associated malignant cells, enabling MHC-independent recognition and activation of T-cell cytotoxicity (perforin/granzyme release) and cytokine-mediated tumor cell killing.
CAR T cells bind GP350 on target cells in an MHC-independent manner, become activated, and kill the bound cells via perforin/granzyme-mediated cytolysis (and Fas/FasL apoptosis).
Anti-CD22 antibody–drug conjugate that delivers calicheamicin to induce DNA double-strand breaks in CD22+ cells.
Humanized anti-CD22 IgG4 antibody-drug conjugate; after binding CD22 on B cells it is internalized and releases a calicheamicin derivative that binds the DNA minor groove, causing double-strand breaks and apoptosis.
The ADC binds CD22, is internalized, and releases calicheamicin that induces DNA double-strand breaks, triggering apoptosis in CD22+ cells.
An autologous, gene-modified CAR T-cell therapy engineered via lentiviral transduction with a KIR-based CAR targeting mesothelin (MSLN) on tumor cells to activate T-cell effector functions and cytotoxic killing.
Autologous T cells are lentivirally transduced to express a KIR-based CAR comprising an anti-mesothelin scFv fused to KIR2DS2 signaling with DAP12. Upon binding mesothelin on tumor cells, the KIR-CAR activates T-cell effector functions via ITAM signaling, promoting cytotoxic killing of mesothelin-expressing cancer cells, with the KIR architecture designed to enhance persistence and reduce exhaustion.
KIR-based anti-mesothelin CAR T cells bind mesothelin and, via DAP12 ITAM signaling, kill target cells through T-cell cytotoxic mechanisms (perforin/granzyme and apoptosis pathways).