Anti–CTLA-4 monoclonal antibody (IgG1) that blocks CTLA-4 to enhance CD28-mediated costimulation and T-cell priming; its IgG1 Fc may deplete intratumoral regulatory T cells (Tregs).
Anti–CTLA-4 IgG1 monoclonal antibody that blocks CTLA-4 checkpoint signaling on T cells, enhancing CD28-mediated costimulation and T-cell priming/activation; its IgG1 Fc can mediate depletion of intratumoral regulatory T cells, collectively boosting cytotoxic antitumor T-cell responses.
YES
DIRECT
IgG1 anti-CTLA-4 engages Fcγ receptors on NK cells/macrophages to deplete CTLA-4–high Tregs via ADCC/ADCP, killing CTLA-4–expressing cells.
An anti-HER2 antibody–drug conjugate (ADC) consisting of trastuzumab linked to a cleavable topoisomerase I inhibitor payload (DXd). It binds ERBB2/HER2 on tumor cells, is internalized, and releases the cytotoxic payload in lysosomes to induce tumor cell death.
Trastuzumab deruxtecan is a HER2-targeted monoclonal antibody linked via a cleavable linker to a topoisomerase I inhibitor payload (deruxtecan, DXd). After binding ERBB2/HER2 on tumor cells, the complex is internalized and the payload is released in lysosomes, inhibiting Top1 to cause DNA damage, replication arrest, and apoptosis. It also mediates ADCC and produces a bystander killing effect due to a membrane-permeable payload.
YES
DIRECT
The ADC binds HER2, is internalized, and releases a topoisomerase I inhibitor (deruxtecan) that causes DNA damage and apoptosis in HER2+ cells; Fc engagement can also trigger ADCC.
An anti-HER2 antibody–drug conjugate (ADC) consisting of trastuzumab linked to a cleavable topoisomerase I inhibitor payload (DXd). It binds ERBB2/HER2 on tumor cells, is internalized, and releases the cytotoxic payload in lysosomes to induce tumor cell death.
Trastuzumab deruxtecan is a HER2-targeted monoclonal antibody linked via a cleavable linker to a topoisomerase I inhibitor payload (deruxtecan, DXd). After binding ERBB2/HER2 on tumor cells, the complex is internalized and the payload is released in lysosomes, inhibiting Top1 to cause DNA damage, replication arrest, and apoptosis. It also mediates ADCC and produces a bystander killing effect due to a membrane-permeable payload.
NO
INDIRECT
Trastuzumab deruxtecan targets HER2 for uptake; once internalized it releases a Top1‑inhibiting payload that causes DNA damage and apoptosis, with additional ADCC and bystander effects.
Recombinant humanized bispecific IgG antibody that binds EGFR on tumor cells and agonizes 4-1BB (CD137) on activated T cells/NK cells to provide costimulatory signaling and enhance antitumor immunity.
HLX35 is a bispecific IgG that binds EGFR on tumor cells and 4-1BB (CD137) on activated T/NK cells, crosslinking them to deliver tumor-localized 4-1BB costimulatory signaling while concurrently blocking EGFR signaling. This conditional 4-1BB agonism enhances T-cell proliferation, survival, and cytotoxicity, and can activate NK and dendritic cells, promoting antitumor immunity.
YES
DIRECT
HLX35 binds EGFR on tumor cells and 4-1BB on activated T/NK cells, providing localized 4-1BB costimulation that enhances effector function and leads to T/NK cell–mediated lysis (perforin/granzyme) of EGFR+ cells; concurrent EGFR blockade adds antiproliferative effects.
Recombinant humanized bispecific IgG antibody that binds EGFR on tumor cells and agonizes 4-1BB (CD137) on activated T cells/NK cells to provide costimulatory signaling and enhance antitumor immunity.
HLX35 is a bispecific IgG that binds EGFR on tumor cells and 4-1BB (CD137) on activated T/NK cells, crosslinking them to deliver tumor-localized 4-1BB costimulatory signaling while concurrently blocking EGFR signaling. This conditional 4-1BB agonism enhances T-cell proliferation, survival, and cytotoxicity, and can activate NK and dendritic cells, promoting antitumor immunity.
NO
INDIRECT
HLX35 agonizes 4-1BB on activated T/NK cells to costimulate them; the activated immune cells then kill EGFR-positive tumor cells. 4-1BB–expressing cells are not directly lysed by the drug.