First-in-human, intravenous investigational immunotherapy; precise target/mechanism not disclosed in the registry. PK/PD and preliminary antitumor activity are being characterized.
Humanized IgG1 bispecific checkpoint antibody targeting TIGIT and PVRIG (CD112R). Blocks TIGIT–CD155/CD112 and PVRIG–CD112 interactions, shifting signaling toward CD226 co-stimulation to activate CD8+ T cells and NK cells. Also leverages Fc effector function to deplete TIGIT+ regulatory T cells, enhancing antitumor immunity.
YES
DIRECT
IgG1 Fc-mediated effector function (ADCC/ADCP) can deplete PVRIG-expressing (TIGIT+) regulatory T cells bound by the antibody; effector T/NK cells are activated rather than depleted.
Autologous T cells genetically engineered to express a chimeric antigen receptor targeting CD19 on B-lineage malignant cells; used for CD19-positive lymphoproliferative disorders. CAR engagement triggers T-cell activation and cytotoxicity.
Autologous T cells are genetically engineered to express a chimeric antigen receptor that recognizes CD19 on B-lineage malignant cells; CAR engagement triggers CD3ζ and costimulatory signaling (e.g., CD28 or 4-1BB), leading to T-cell activation, proliferation, cytokine release, and targeted cytotoxic killing of CD19-positive cancer cells.
YES
DIRECT
CAR binding to CD19 activates engineered T cells (via CD3ζ and costimulatory domains), leading to targeted killing of CD19+ cells through perforin/granzyme release and Fas–FasL–mediated apoptosis.
Autologous T cells genetically engineered to express a chimeric antigen receptor targeting B-cell maturation antigen (BCMA) on plasma cells; used for multiple myeloma. CAR engagement triggers T-cell activation and cytotoxicity.
Autologous T cells are engineered to express a chimeric antigen receptor that binds BCMA on malignant plasma cells; CAR engagement triggers CD3ζ and costimulatory signaling, leading to T-cell activation, expansion, cytokine release, and perforin/granzyme-mediated cytotoxic killing of BCMA-expressing myeloma cells.
YES
DIRECT
CAR recognition of BCMA activates engineered T cells, which kill BCMA-expressing cells via perforin/granzyme-mediated cytotoxicity (and Fas–FasL pathways).
A bispecific T‑cell engager (BiTE) antibody construct linking CD3 on T cells to CD19 on B‑cell ALL blasts to drive T‑cell–mediated cytotoxicity and MRD clearance.
A bispecific T‑cell engager that binds CD19 on B‑cell blasts and CD3 on T cells, forming an immunologic synapse that activates and redirects T cells to kill CD19+ cells via perforin/granzyme‑mediated cytotoxicity, leading to clearance of minimal residual disease.
YES
DIRECT
Blinatumomab links CD3 on T cells to CD19 on target cells, forming an immunologic synapse that triggers perforin/granzyme-mediated killing of CD19+ cells.
A bispecific T‑cell engager (BiTE) antibody construct linking CD3 on T cells to CD19 on B‑cell ALL blasts to drive T‑cell–mediated cytotoxicity and MRD clearance.
A bispecific T‑cell engager that binds CD19 on B‑cell blasts and CD3 on T cells, forming an immunologic synapse that activates and redirects T cells to kill CD19+ cells via perforin/granzyme‑mediated cytotoxicity, leading to clearance of minimal residual disease.
NO
INDIRECT
Blinatumomab links CD3 on T cells to CD19 on target cells, activating T cells to kill CD19+ cells via perforin/granzyme; CD3-expressing cells are not targeted or killed.