Bispecific IgG monoclonal antibody that binds CLDN18.2 on tumor cells and CD47 to localize CD47 blockade to CLDN18.2-positive tumors, enhancing macrophage phagocytosis and antigen presentation.
Bispecific IgG monoclonal antibody that binds CLDN18.2 on tumor cells and CD47 to localize CD47 blockade to CLDN18.2-positive tumors, disrupting the CD47–SIRPα 'don't-eat-me' signal and enhancing macrophage phagocytosis and antigen presentation to drive anti-tumor immunity.
YES
DIRECT
Binding to CLDN18.2 localizes CD47 blockade on tumor cells, enabling Fcγ receptor–mediated engagement of macrophages and release of the CD47–SIRPα checkpoint, leading to antibody-dependent cellular phagocytosis (ADCP) of CLDN18.2-positive cells.
Bispecific IgG monoclonal antibody that binds CLDN18.2 on tumor cells and CD47 to localize CD47 blockade to CLDN18.2-positive tumors, enhancing macrophage phagocytosis and antigen presentation.
Bispecific IgG monoclonal antibody that binds CLDN18.2 on tumor cells and CD47 to localize CD47 blockade to CLDN18.2-positive tumors, disrupting the CD47–SIRPα 'don't-eat-me' signal and enhancing macrophage phagocytosis and antigen presentation to drive anti-tumor immunity.
NO
INDIRECT
The antibody localizes CD47 blockade to CLDN18.2+ tumor cells, removing the CD47–SIRPα “don’t‑eat‑me” signal and enabling macrophage phagocytosis of CLDN18.2+ tumor cells; CD47 expression alone is not sufficient for killing.
A fully humanized IgG1 antibody–drug conjugate targeting B7‑H3 (CD276). Upon binding to B7‑H3 on tumor cells, it is internalized and releases a cytotoxic payload; as an IgG1 it may also mediate Fc‑effector functions. Evaluated as IV 8 mg/kg Q3W monotherapy in mCRPC and other advanced solid tumors.
Fully human IgG1 ADC targeting B7-H3 (CD276). Upon binding to B7-H3 on tumor cells, the complex is internalized and releases a topoisomerase inhibitor payload that inhibits DNA topoisomerase activity, blocking DNA replication and causing cell-cycle arrest and apoptosis of B7-H3–expressing cells; the IgG1 may also mediate Fc-effector functions (e.g., ADCC/ADCP).
YES
DIRECT
ADC binds B7-H3, is internalized, and releases a topoisomerase inhibitor that blocks DNA replication causing cell-cycle arrest and apoptosis; IgG1 Fc can also trigger ADCC/ADCP against B7-H3–expressing cells.
A fully humanized IgG1 antibody–drug conjugate targeting B7‑H3 (CD276). Upon binding to B7‑H3 on tumor cells, it is internalized and releases a cytotoxic payload; as an IgG1 it may also mediate Fc‑effector functions. Evaluated as IV 8 mg/kg Q3W monotherapy in mCRPC and other advanced solid tumors.
Fully human IgG1 ADC targeting B7-H3 (CD276). Upon binding to B7-H3 on tumor cells, the complex is internalized and releases a topoisomerase inhibitor payload that inhibits DNA topoisomerase activity, blocking DNA replication and causing cell-cycle arrest and apoptosis of B7-H3–expressing cells; the IgG1 may also mediate Fc-effector functions (e.g., ADCC/ADCP).
NO
INDIRECT
The ADC targets B7-H3 on the cell surface, is internalized, and releases a topoisomerase-inhibiting payload that blocks DNA replication and induces apoptosis; Fc-mediated ADCC/ADCP may contribute. DNA topoisomerase expression itself is not the targeting determinant.
Allogeneic CD19-directed CAR-γδ T cell therapy; γδ T cells engineered with an FMC63-based CD19 CAR to mediate largely MHC-independent cytotoxicity and cytokine release against CD19+ B-ALL.
Allogeneic γδ T cells engineered to express a CD19-specific CAR (FMC63 scFv) bind CD19 on malignant B cells and, upon CAR signaling, execute largely MHC-independent cytotoxicity via perforin/granzyme release and cytokine secretion, leading to targeted lysis of CD19+ leukemia cells.
YES
DIRECT
CD19-specific CAR-γδ T cells bind CD19 on target cells and, upon CAR signaling, induce MHC-independent killing via perforin/granzyme-mediated cytolysis and cytokine release.