Biologic antibodies intended to bind glioblastoma-specific cell-surface antigens to block oncogenic/survival receptor signaling and recruit immune effector functions such as ADCC and CDC.
Unconjugated monoclonal antibodies that bind glioblastoma-restricted cell-surface antigens to block oncogenic/survival receptor signaling and trigger Fc-mediated immune effector functions (ADCC and CDC) to eliminate tumor cells.
Unconjugated mAbs bind glioblastoma-specific surface antigens and, via their Fc regions, recruit immune effectors to kill target cells through NK cell–mediated ADCC and complement-dependent cytotoxicity (CDC).
Humanized IgG1 anti-CD38 monoclonal antibody that binds CD38 on malignant plasma cells, mediates ADCC, CDC, and ADCP, directly induces apoptosis, and inhibits CD38 ectoenzyme (NADase) activity, leading to lysis and depletion of CD38-expressing tumor cells.
Binds CD38 on target cells and elicits Fc-mediated immune effector killing (ADCC by NK cells, CDC, ADCP) and can directly induce apoptosis, leading to lysis of CD38+ cells.
Subcutaneous bispecific T‑cell–redirecting antibody that binds BCMA on myeloma cells and CD3 on T cells to induce cytotoxic killing.
Bispecific antibody that binds BCMA on malignant plasma cells and CD3 on T cells, crosslinking them to activate T cells and drive perforin/granzyme-mediated cytotoxic killing of BCMA-expressing myeloma cells.
Bispecific T-cell engager binds BCMA on target cells and CD3 on T cells, forming an immune synapse and triggering perforin/granzyme-mediated cytotoxic killing of BCMA-expressing cells.
Autologous ROR1-directed CAR T-cell therapy; patient T cells are engineered to express a chimeric antigen receptor targeting ROR1 on malignant B cells, triggering T-cell activation, proliferation, cytokine release, and cytolytic killing of ROR1-positive tumor cells.
Autologous T cells are engineered to express a chimeric antigen receptor targeting ROR1 on malignant B cells; antigen engagement activates the T cells, driving proliferation, cytokine release, and perforin/granzyme-mediated cytolytic killing of ROR1-positive tumor cells.
Anti-ROR1 CAR T cells bind ROR1 on target cells, triggering T-cell activation and perforin/granzyme-mediated cytolytic killing.
Allogeneic, off-the-shelf CD123-directed CAR-NK cell therapy; NK cells engineered with a chimeric antigen receptor targeting IL-3Rα on AML cells, given after lymphodepleting chemotherapy.
Allogeneic, off-the-shelf NK cells engineered with a CD123-specific chimeric antigen receptor bind IL-3Rα on AML cells, triggering NK activation and targeted killing via perforin/granzyme release and death-receptor pathways, leading to selective lysis of CD123-positive leukemic blasts and stem cells with low GVHD risk.
CD123-directed CAR-NK cells bind IL-3Rα on target cells, activating NK effector functions and killing via perforin/granzyme release and death-receptor (FasL/TRAIL)–mediated apoptosis.