A bispecific IgG1 monoclonal antibody targeting EGFR and MET; blocks ligand binding and signaling, promotes receptor internalization/degradation, and mediates immune effector killing (ADCC/trogocytosis).
Bispecific IgG1 monoclonal antibody against EGFR and MET (c-Met) that blocks ligand binding and receptor phosphorylation, suppressing downstream signaling (e.g., MAPK/ERK, PI3K/AKT); promotes receptor internalization and degradation; and mediates Fc-dependent immune effector killing (ADCC/trogocytosis) of tumor cells.
Binds MET on tumor cells and engages Fc receptors on immune effectors (e.g., NK cells, macrophages) to induce ADCC and trogocytosis/phagocytosis; also drives receptor internalization/degradation and signaling blockade.
Autologous, gene-edited tumor-infiltrating lymphocyte (TIL) therapy engineered to inactivate SOCS1 and Regnase-1 (ZC3H12A) to enhance T-cell activation, cytokine production, proliferation, persistence, and tumor killing.
Autologous tumor-infiltrating lymphocytes edited with CRISPR-Cas9 to inactivate SOCS1 and Regnase-1 (ZC3H12A), removing intrinsic brakes on cytokine/JAK-STAT signaling and mRNA stability. This enhances T-cell activation, cytokine production, proliferation, persistence, and cytotoxic killing of tumor cells after infusion.
CRISPR-edited autologous TILs recognize HLA-presented tumor neoantigen peptides via their TCRs and directly lyse target-expressing cells through perforin/granzyme release and death receptor pathways (e.g., Fas–FasL), enhanced by SOCS1/Regnase-1 knockout.
Proposed biosimilar of daratumumab; an anti-CD38 human IgG1κ monoclonal antibody (IV) that binds CD38 on malignant plasma cells, inducing ADCC, CDC, antibody-dependent phagocytosis, and direct apoptosis; inhibits CD38 ectoenzyme activity and reduces CD38+ immunosuppressive cells, potentially enhancing T-cell–mediated antitumor activity.
Anti-CD38 human IgG1κ monoclonal antibody that binds CD38 on malignant plasma cells, triggering ADCC, CDC, and antibody-dependent phagocytosis and inducing direct apoptosis; also inhibits CD38 ectoenzyme activity and depletes CD38+ immunosuppressive cells, enhancing T-cell–mediated antitumor responses.
Binding to CD38 on target cells triggers Fc-mediated ADCC by NK cells, complement-dependent cytotoxicity (CDC), antibody-dependent phagocytosis (ADCP), and can induce direct apoptosis.
Anti-CD38 human IgG1κ monoclonal antibody (IV) that binds CD38 on malignant plasma cells, inducing ADCC, CDC, antibody-dependent phagocytosis, and direct apoptosis; inhibits CD38 ectoenzyme activity and reduces CD38+ immunosuppressive cells, potentially enhancing T-cell–mediated antitumor activity.
Human IgG1κ anti-CD38 monoclonal antibody that binds CD38 on malignant plasma cells, triggering ADCC, CDC, and antibody‑dependent phagocytosis, and inducing direct apoptosis; also inhibits CD38 ectoenzyme activity and depletes CD38+ immunosuppressive cells, enhancing T‑cell–mediated antitumor activity.
Daratumumab binds CD38 on target cells and mediates Fc-dependent killing (ADCC, CDC, ADCP) and can trigger direct apoptosis upon cross-linking, leading to depletion of CD38+ cells.
Genetically engineered autologous T cells expressing a chimeric antigen receptor targeting CD19, administered once to deplete CD19+ B-lineage cells and reset humoral immunity in refractory SLE/lupus nephritis.
Autologous T cells are genetically engineered to express a chimeric antigen receptor targeting CD19. When the CAR binds CD19 on B-lineage cells, it triggers T-cell activation (CD3zeta with costimulatory signaling), proliferation, cytokine release, and perforin/granzyme-mediated cytotoxicity, leading to depletion of CD19+ B cells and plasmablasts, reduction of autoantibody production, and reset of humoral immunity.
CAR T cells bind CD19 via the CAR and directly kill CD19+ cells through T‑cell activation with perforin/granzyme-mediated apoptosis (and death-receptor signaling).