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.
YES
DIRECT
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.
YES
DIRECT
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.
YES
DIRECT
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.
YES
DIRECT
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.
An intravenous anti-CD47 IgG4 monoclonal antibody that blocks the CD47–SIRPα checkpoint to enhance macrophage-mediated phagocytosis and potentially augment graft-versus-leukemia effects.
Humanized IgG4 monoclonal antibody against CD47 that blocks the CD47–SIRPα innate immune checkpoint, removing the 'don’t eat me' signal on tumor cells, enabling macrophage-mediated phagocytosis (via pro-phagocytic cues like calreticulin) and enhancing downstream anti-tumor T-cell responses; may augment graft-versus-leukemia.
YES
INDIRECT
Blocks CD47–SIRPα 'don’t eat me' signaling on CD47+ cells, enabling macrophage FcγR-mediated antibody-dependent phagocytosis (ADCP) and consequent cell death; may also enhance downstream T-cell responses.