Fully humanized IgG1 antibody-drug conjugate targeting B7-H3 (CD276); binds B7-H3 on tumor cells, is internalized, and releases a cytotoxic payload to induce tumor-cell death, with potential Fc effector activity.
Fully human IgG1 ADC targeting B7-H3 (CD276); after binding to B7-H3 on tumor cells and internalization, it releases a topoisomerase inhibitor payload that inhibits DNA topoisomerase activity, blocking DNA replication and inducing cell-cycle arrest and apoptosis; the IgG1 Fc may also elicit effector functions such as ADCC/CDC.
ADC binds B7-H3 on target cells, is internalized, and releases a topoisomerase inhibitor that blocks DNA replication leading to cell-cycle arrest and apoptosis; the IgG1 Fc can also trigger ADCC/CDC against B7-H3–expressing cells.
An antibody–drug conjugate consisting of a humanized anti-B7-H3 (CD276) IgG1 monoclonal antibody linked via a cleavable linker to a deruxtecan (DXd) topoisomerase I inhibitor payload. After binding B7-H3 on tumor cells and internalization, the linker is cleaved to release DXd, inducing DNA damage and apoptosis with potential bystander effect; the antibody may also mediate Fc-dependent ADCC/ADCP.
Ifinatamab deruxtecan is a B7-H3–targeted antibody–drug conjugate. After binding B7-H3 on tumor cells and internalization, a cleavable linker releases the deruxtecan (DXd) topoisomerase I inhibitor payload, causing DNA damage and apoptosis. The membrane-permeable payload can produce a bystander effect, and the IgG1 antibody may also mediate Fc-dependent ADCC/ADCP.
The ADC binds B7-H3 on target cells, is internalized, and releases a DXd topoisomerase I inhibitor that induces DNA damage and apoptosis; the IgG1 Fc can also mediate ADCC/ADCP, with possible bystander killing from the membrane‑permeable payload.
Anti-EGFR IgG1 monoclonal antibody that inhibits EGFR signaling and mediates ADCC against EGFR-expressing tumor cells.
Cetuximab is an IgG1 monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding, receptor activation and dimerization, thereby inhibiting downstream signaling (e.g., RAS/RAF/MEK/ERK and PI3K/AKT) and tumor cell proliferation; its Fc domain can also engage Fcγ receptors to mediate antibody-dependent cellular cytotoxicity (ADCC) against EGFR-expressing tumor cells.
Cetuximab binds EGFR on target cells; its IgG1 Fc engages Fcγ receptors on immune effectors (e.g., NK cells) to trigger ADCC (and some CDC), causing lysis of EGFR-expressing cells. Signaling blockade is primarily antiproliferative.
Anti–PD-L1 monoclonal antibody that inhibits PD-L1/PD-1 signaling and can mediate antibody-dependent cellular cytotoxicity.
Avelumab is a human IgG1 anti–PD-L1 monoclonal antibody that blocks PD-L1 from engaging PD-1 (and CD80), preventing PD-1 inhibitory signaling and restoring T-cell activation and antitumor immunity; its Fc region can also mediate antibody-dependent cellular cytotoxicity against PD-L1–expressing tumor cells.
Avelumab’s IgG1 Fc engages Fc receptors on NK cells to mediate antibody-dependent cellular cytotoxicity (ADCC) against PD-L1–expressing cells; it also indirectly enhances T-cell killing by blocking PD-1/PD-L1 signaling.
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.
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.