Bispecific IgG1 monoclonal antibody targeting EGFR and MET; blocks EGFR/MET signaling, promotes receptor internalization/degradation, and mediates Fc-dependent cytotoxicity (ADCC/ADCP); administered IV.
Bispecific IgG1 monoclonal antibody targeting EGFR and MET; blocks EGFR/MET signaling, induces receptor internalization and degradation, and engages Fc receptors to mediate ADCC/ADCP against tumor cells.
YES
DIRECT
Amivantamab binds MET on target cells and engages Fcγ receptor–bearing effector cells via its Fc domain, inducing ADCC/ADCP to kill MET+ cells; receptor blockade/internalization may further promote apoptosis.
Investigational antibody–drug conjugate that targets TROP-2 on TNBC cells and, after internalization, releases a topoisomerase I inhibitor payload to induce DNA damage.
Targets TROP-2 on TNBC cells; after antibody-mediated binding and internalization, releases a topoisomerase I inhibitor payload that induces DNA damage and tumor cell death.
YES
DIRECT
ADC binds TROP-2, is internalized, and releases a topoisomerase I inhibitor payload that causes DNA damage, leading to apoptosis/tumor cell death.
Investigational antibody–drug conjugate that targets TROP-2 on TNBC cells and, after internalization, releases a topoisomerase I inhibitor payload to induce DNA damage.
Targets TROP-2 on TNBC cells; after antibody-mediated binding and internalization, releases a topoisomerase I inhibitor payload that induces DNA damage and tumor cell death.
NO
INDIRECT
The ADC binds TROP-2 on tumor cells and is internalized; its released topoisomerase I inhibitor poisons DNA topoisomerase I to cause DNA damage and cell death. DNA topoisomerase I is not the antibody’s binding target.
A fully human monoclonal antibody (VAY736) targeting the BAFF receptor (BAFF‑R; TNFRSF13C). Administered subcutaneously to block BAFF/BAFF‑R signaling and deplete B cells via ADCC, aiming to reduce autoreactive B cells and autoantibody production in SLE.
Fully human monoclonal antibody targeting the BAFF receptor (BAFF-R/TNFRSF13C); blocks BAFF–BAFF-R interaction and downstream NF-kB survival signaling, and depletes BAFF-R+ B cells via ADCC, reducing autoreactive B cells and autoantibody production.
YES
DIRECT
Anti-BAFF-R IgG binds BAFF-R+ cells and recruits FcγR-bearing effector cells to induce ADCC (± CDC); BAFF-R signaling blockade can also promote apoptosis.
Antibody–drug conjugate targeting TROP2; after binding, it is internalized and releases a camptothecin/topoisomerase I inhibitor payload that induces DNA damage and apoptosis.
Humanized anti-TROP2 monoclonal antibody linked via a cleavable linker to the camptothecin/topoisomerase I inhibitor tirumotecan. After binding TROP2 on tumor cells and internalization (and/or extracellular pH-sensitive cleavage), the payload is released to inhibit topoisomerase I, causing DNA damage, replication arrest, and apoptosis, with a bystander effect on neighboring tumor cells.
YES
DIRECT
The anti-TROP2 ADC binds TROP2, is internalized (and/or cleaved extracellularly), releasing the topoisomerase I inhibitor tirumotecan that causes DNA damage, replication arrest, and apoptosis; bystander killing can also occur.