Investigational intravenous bispecific antibody (anti-PSMA × CD28) T-cell co-stimulatory engager that binds PSMA on tumor cells and CD28 on T cells to deliver conditional CD28 agonist co-stimulation, enhancing T-cell activation and tumor cell killing in PSMA-positive lesions.
A bispecific antibody that binds PSMA on tumor cells and CD28 on T cells to provide conditional CD28 co-stimulation at PSMA-positive sites, enhancing T-cell activation, proliferation, cytokine release, and cytotoxic killing of PSMA-expressing tumor cells.
NO
INDIRECT
The antibody binds CD28 on T cells to provide co-stimulation only when also bound to PSMA on tumor cells, activating T cells to lyse PSMA-positive tumor cells (perforin/granzyme, cytokines). CD28-expressing cells are not targeted for killing.
Intravenous chimeric anti-CD20 IgG1 monoclonal antibody that targets CD20 on B cells, inducing B-cell depletion via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and direct apoptosis.
Chimeric anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells and mediates B‑cell depletion via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and direct induction of apoptosis.
YES
DIRECT
Anti-CD20 antibody binds CD20 on B cells, inducing complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC)/phagocytosis via Fcγ receptors, and direct apoptosis.
Autologous GPC3-targeted chimeric antigen receptor T-cell (CAR-T) therapy for advanced/recurrent hepatocellular carcinoma; patient T cells are collected via leukapheresis, engineered ex vivo to express a GPC3-specific CAR, and reinfused to mediate antigen-directed cytotoxicity.
Autologous T cells engineered with a GPC3-specific chimeric antigen receptor recognize glypican-3 on tumor cells, triggering T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxicity against GPC3-positive cells. The cells are armored with a dominant-negative TGF-beta receptor II to block TGF-beta signaling in the tumor microenvironment, increasing resistance to immunosuppression and enhancing antitumor activity.
YES
DIRECT
GPC3-specific CAR-T cells bind glypican-3 on target cells, triggering T-cell activation and perforin/granzyme-mediated apoptosis/lysis.
Autologous GPC3-targeted chimeric antigen receptor T-cell (CAR-T) therapy for advanced/recurrent hepatocellular carcinoma; patient T cells are collected via leukapheresis, engineered ex vivo to express a GPC3-specific CAR, and reinfused to mediate antigen-directed cytotoxicity.
Autologous T cells engineered with a GPC3-specific chimeric antigen receptor recognize glypican-3 on tumor cells, triggering T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxicity against GPC3-positive cells. The cells are armored with a dominant-negative TGF-beta receptor II to block TGF-beta signaling in the tumor microenvironment, increasing resistance to immunosuppression and enhancing antitumor activity.
NO
INDIRECT
AZD5851 CAR T cells kill only GPC3-positive cells via CAR-triggered perforin/granzyme cytotoxicity; the dnTGF-βRII armor blocks TGF-β1 signaling but does not target or kill TGF-β1-expressing cells.
Autologous GPC3-targeted chimeric antigen receptor T-cell (CAR-T) therapy for advanced/recurrent hepatocellular carcinoma; patient T cells are collected via leukapheresis, engineered ex vivo to express a GPC3-specific CAR, and reinfused to mediate antigen-directed cytotoxicity.
Autologous T cells engineered with a GPC3-specific chimeric antigen receptor recognize glypican-3 on tumor cells, triggering T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxicity against GPC3-positive cells. The cells are armored with a dominant-negative TGF-beta receptor II to block TGF-beta signaling in the tumor microenvironment, increasing resistance to immunosuppression and enhancing antitumor activity.
NO
INDIRECT
CAR T cells kill GPC3-positive cells via perforin/granzyme. The dominant-negative TGF-beta receptor blocks TGF-beta2 signaling in the CAR T cells and does not cause direct killing of TGF-beta2–expressing cells (unless they also express GPC3).