An autologous CLDN18.2-targeted chimeric antigen receptor T-cell (CAR-T) therapy engineered with an NKG2D receptor–based modification to enhance T-cell activation and recognition; mediates cytotoxicity and cytokine release against CLDN18.2-positive tumor cells with added co-stimulation via NKG2D ligands (MICA/B, ULBPs).
Autologous T cells engineered with a chimeric antigen receptor targeting CLDN18.2, augmented with an NKG2D receptor–based module that provides additional co-stimulation via recognition of NKG2D ligands (MICA/B, ULBPs). CAR engagement activates T-cell signaling and, together with NKG2D co-stimulation, drives T-cell activation, cytokine release, and cytolytic killing of CLDN18.2-positive tumor cells.
NO
INDIRECT
ULBP6 engages the NKG2D-based costimulatory module to enhance T-cell activation, but killing is triggered by CAR recognition of CLDN18.2; cytotoxicity occurs via T-cell degranulation (perforin/granzymes) against CLDN18.2-positive cells, not by ULBP6 alone.
Autologous T cells genetically modified via lentiviral transduction to express a B7-H3–targeting chimeric antigen receptor with CD28/CD3ζ signaling domains and membrane 4-1BB ligand to enhance costimulation and persistence; administered locoregionally via CNS reservoir to treat B7-H3 (CD276)-positive pediatric CNS tumors.
Autologous T cells are lentivirally engineered to express a B7-H3-specific chimeric antigen receptor with CD28/CD3zeta signaling. Binding to B7-H3 (CD276) on tumor cells triggers T-cell activation, cytokine release, and cytotoxic killing. Coexpressed membrane 4-1BB ligand provides costimulation to enhance expansion and persistence. Administered locoregionally into the CNS for B7-H3-positive pediatric brain tumors.
YES
DIRECT
B7-H3–specific CAR T cells recognize B7-H3 on target cells and directly kill them via T-cell cytotoxic mechanisms (perforin/granzyme release and death receptor pathways such as Fas/FasL).
Autologous T cells genetically modified via lentiviral transduction to express a B7-H3–targeting chimeric antigen receptor with CD28/CD3ζ signaling domains and membrane 4-1BB ligand to enhance costimulation and persistence; administered locoregionally via CNS reservoir to treat B7-H3 (CD276)-positive pediatric CNS tumors.
Autologous T cells are lentivirally engineered to express a B7-H3-specific chimeric antigen receptor with CD28/CD3zeta signaling. Binding to B7-H3 (CD276) on tumor cells triggers T-cell activation, cytokine release, and cytotoxic killing. Coexpressed membrane 4-1BB ligand provides costimulation to enhance expansion and persistence. Administered locoregionally into the CNS for B7-H3-positive pediatric brain tumors.
NO
INDIRECT
4-1BB (CD137) on T cells is costimulated by the CAR T cell–expressed 4-1BB ligand; it is not a killing target. Cytotoxicity is directed at B7-H3–positive tumor cells via CAR-triggered T-cell perforin/granzyme-mediated lysis.
Anti-CD38 IgG1 monoclonal antibody that binds CD38 on leukemic T cells to mediate ADCC, CDC, and ADCP and induce direct apoptosis; also inhibits CD38 ectoenzyme (NADase/cyclase) activity to reduce adenosine-mediated immunosuppression.
Isatuximab is an IgG1 monoclonal antibody against CD38. It binds CD38 on malignant T cells to induce Fc-mediated cytotoxicity (ADCC, CDC) and phagocytosis (ADCP) and can trigger direct apoptosis. It also inhibits CD38 ectoenzyme (NADase/cyclase) activity, lowering adenosine production and reducing adenosine-mediated immunosuppression.
YES
DIRECT
Isatuximab binds CD38 on target cells and induces Fc-mediated killing (ADCC, CDC, ADCP) and can trigger direct apoptosis of CD38+ cells.
An anti-CD19 antibody–drug conjugate (Zynlonta) that delivers a pyrrolobenzodiazepine dimer to CD19+ B cells, causing DNA crosslinking and apoptosis.
Anti-CD19 antibody–drug conjugate that binds CD19 on B cells, is internalized, and releases a pyrrolobenzodiazepine (PBD) dimer payload via a cleavable linker; the PBD binds the DNA minor groove to form interstrand crosslinks, blocking DNA replication and inducing apoptosis in CD19-expressing tumor cells.
YES
DIRECT
The anti-CD19 ADC binds CD19, is internalized, and releases a PBD dimer that crosslinks DNA, blocking replication and inducing apoptosis in CD19+ cells.