Anti-CD38 IgG1 monoclonal antibody that binds CD38 on plasmablasts/plasma cells and depletes them via ADCC, CDC, ADCP, and apoptosis to reduce factor VIII–neutralizing autoantibodies.
Human IgG1-kappa anti-CD38 monoclonal antibody that binds CD38 on plasmablasts/plasma cells and other CD38+ cells and depletes them via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), antibody-dependent cellular phagocytosis (ADCP), and apoptosis, thereby reducing pathogenic autoantibody production (e.g., factor VIII inhibitors).
Daratumumab binds CD38 on target cells and induces killing via Fc-mediated ADCC (NK cells), complement-dependent cytotoxicity (CDC), antibody-dependent cellular phagocytosis (ADCP), and direct apoptosis.
Autologous, genetically modified anti-CD19 chimeric antigen receptor (CAR) T-cell therapy made from a patient’s T cells; engineered to express an anti-CD19 CAR that, upon binding CD19 on B cells, induces antigen-dependent T-cell activation, proliferation, and cytotoxic killing, with expected on-target B-cell aplasia and risk of cytokine release.
Autologous patient T cells engineered to express an anti‑CD19 chimeric antigen receptor. Binding CD19 on malignant and normal B cells triggers CAR signaling, activating and expanding the T cells and inducing cytokine release and perforin/granzyme‑mediated cytotoxic killing, resulting in depletion of CD19+ cells (on‑target B‑cell aplasia).
Anti-CD19 CAR T cells bind CD19 on B cells and directly kill them via T-cell cytotoxicity (perforin/granzyme-mediated apoptosis, with possible Fas/FasL involvement), causing depletion of CD19+ cells.
Gene-modified autologous T cells engineered to express a chimeric antigen receptor that recognizes VEGFR1 and PD-L1; upon antigen engagement, the CAR T cells exert cytotoxic activity against VEGFR1+ and/or PD-L1+ cells, aiming to disrupt VEGF/VEGFR1-driven angiogenesis and overcome PD-L1–mediated immune suppression. Administered regionally into the pleural or peritoneal cavity.
Autologous T cells genetically engineered to express a chimeric antigen receptor recognizing VEGFR1 and PD-L1. Binding to either antigen triggers T‑cell activation, cytotoxicity, and cytokine release to kill VEGFR1+ vascular/endothelial cells and PD‑L1+ tumor and immunosuppressive stromal/immune cells, disrupting VEGF/VEGFR1‑driven angiogenesis and overcoming PD‑L1–mediated immune evasion. Administered regionally into the pleural or peritoneal cavity.
VEGFR1-specific CAR-T cells bind VEGFR1 on target cells, activate, and kill via T-cell cytotoxic pathways (perforin/granzyme and Fas–FasL), with supportive cytokine-mediated effects.
Gene-modified autologous T cells engineered to express a chimeric antigen receptor that recognizes VEGFR1 and PD-L1; upon antigen engagement, the CAR T cells exert cytotoxic activity against VEGFR1+ and/or PD-L1+ cells, aiming to disrupt VEGF/VEGFR1-driven angiogenesis and overcome PD-L1–mediated immune suppression. Administered regionally into the pleural or peritoneal cavity.
Autologous T cells genetically engineered to express a chimeric antigen receptor recognizing VEGFR1 and PD-L1. Binding to either antigen triggers T‑cell activation, cytotoxicity, and cytokine release to kill VEGFR1+ vascular/endothelial cells and PD‑L1+ tumor and immunosuppressive stromal/immune cells, disrupting VEGF/VEGFR1‑driven angiogenesis and overcoming PD‑L1–mediated immune evasion. Administered regionally into the pleural or peritoneal cavity.
CAR-T cells bind PD-L1 and are activated to kill PD-L1+ cells via perforin/granzyme-mediated cytolysis and apoptotic death ligand pathways, with cytokine release.
Recombinant humanized monoclonal antibody targeting Claudin 18.2 (CLDN18.2); promotes antitumor activity via direct tumor cell targeting and immune effector mechanisms such as ADCC and CDC.
Humanized monoclonal antibody targeting Claudin 18.2 on tumor cells; induces immune-mediated tumor cell killing via antibody-dependent cellular cytotoxicity (ADCC) and complement-dependent cytotoxicity (CDC) after binding to CLDN18.2-expressing cells.
Binds CLDN18.2 on tumor cells and recruits immune effector functions—Fc-mediated ADCC (e.g., NK cells) and complement-dependent cytotoxicity (CDC)—to lyse target-expressing cells.