Intravenous chimeric monoclonal antibody targeting CD20 on B cells; depletes B cells via ADCC/CDC and apoptosis to reduce autoreactive B-cell activity and autoantibody production.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on pre-B and mature B cells and depletes them via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis, thereby reducing autoreactive B-cell activity and autoantibody production.
Rituximab binds CD20 on B cells and triggers Fc-mediated ADCC (NK cells/macrophages) and complement-dependent cytotoxicity, and can also induce apoptosis of the target cells.
An intratumoral oncolytic biologic composed of recombinant, nonreplicating, noninfectious bacterial minicells; designed to directly lyse tumor cells upon injection, increasing local tumor antigen release and inflammation.
Recombinant, nonreplicating bacterial minicells engineered to target un-ligated a3b1/a5b1 integrins on tumor cells deliver the pore-forming toxin perfringolysin O, causing membrane disruption and rapid tumor cell lysis after intratumoral injection. The resulting oncolysis increases local tumor antigen release and inflammation, which can enhance antitumor immunity and synergize with PD-1 blockade.
Recombinant bacterial minicells bind unligated α3β1 integrin on tumor cells and deliver the pore-forming toxin perfringolysin O, causing membrane disruption and rapid lysis.
An intratumoral oncolytic biologic composed of recombinant, nonreplicating, noninfectious bacterial minicells; designed to directly lyse tumor cells upon injection, increasing local tumor antigen release and inflammation.
Recombinant, nonreplicating bacterial minicells engineered to target un-ligated a3b1/a5b1 integrins on tumor cells deliver the pore-forming toxin perfringolysin O, causing membrane disruption and rapid tumor cell lysis after intratumoral injection. The resulting oncolysis increases local tumor antigen release and inflammation, which can enhance antitumor immunity and synergize with PD-1 blockade.
VAX014 binds un-ligated alpha5beta1 integrin on tumor cells and delivers perfringolysin O, a pore-forming toxin that disrupts the membrane and causes rapid cell lysis.
Autologous gene-modified T-cell therapy engineered via Sleeping Beauty to express a ROR1-targeted CAR, membrane-bound IL-15, an EGFRt/HER1t safety switch, and intrinsic PD-1 downregulation to recognize and kill ROR1+ tumor cells with enhanced persistence and resistance to PD-1/PD-L1 suppression.
Autologous T cells engineered with a ROR1-targeted chimeric antigen receptor to recognize and kill ROR1-positive tumor cells; membrane-bound IL-15 enhances T-cell survival and expansion; intrinsic PD-1 downregulation resists PD-1/PD-L1–mediated inhibition; an EGFRt/HER1t safety switch allows conditional ablation of the cells.
ROR1-targeted CAR T cells recognize ROR1 on tumor cells and directly kill them via T-cell cytotoxicity (perforin/granzyme-mediated apoptosis and Fas/FasL).
Polyclonal antibody preparation that depletes T lymphocytes for induction immunosuppression.
Polyclonal anti–T-lymphocyte IgG that binds multiple T-cell surface antigens and depletes T cells via complement-dependent cytotoxicity and Fc-mediated ADCC, with additional T-cell apoptosis and functional inhibition, producing potent immunosuppression.
ATG antibodies bind CD3ε on T cells and trigger complement-dependent lysis and Fcγ receptor–mediated ADCC, with additional apoptosis, leading to T-cell depletion.