Afucosylated anti-IL-5Rα monoclonal antibody that induces NK cell–mediated ADCC, depleting eosinophils and basophils.
Afucosylated anti–IL-5Rα monoclonal antibody that binds IL-5Rα on eosinophils and basophils and induces potent NK cell–mediated ADCC, depleting these cells and reducing type 2 inflammation.
Benralizumab binds IL-5Rα on eosinophils/basophils and engages NK cells via its afucosylated Fc (FcγRIIIa), triggering potent antibody-dependent cellular cytotoxicity (ADCC) that kills the target cells.
An antibody–drug conjugate consisting of a pH-dependent anti-cMET monoclonal antibody linked to the antimicrotubule payload monomethyl auristatin E (MMAE). It binds c-MET on tumor cells, is internalized, and releases MMAE in acidic compartments to disrupt microtubules and induce G2/M arrest and apoptosis.
MYTX-011 is an anti-c-MET monoclonal antibody-drug conjugate linked via a cleavable valine-citrulline linker to the microtubule inhibitor MMAE. After binding c-MET on tumor cells, the complex is internalized and MMAE is released in acidic compartments, where it inhibits tubulin polymerization, leading to microtubule disruption, G2/M cell-cycle arrest, and apoptosis. The pH-dependent antibody design enhances tumor-selective uptake and may improve tolerability.
The anti‑c‑MET ADC binds c‑MET on target cells, is internalized, and the val‑cit linker is cleaved in acidic compartments to release MMAE, which inhibits tubulin polymerization, causing microtubule disruption, G2/M arrest, and apoptosis of c‑MET–expressing cells.
Fully human bispecific IgG1 monoclonal antibody targeting EGFR and MET; blocks ligand binding and signaling, induces receptor internalization/degradation, and mediates Fc-dependent ADCC/ADCP.
Fully human bispecific IgG1 that binds EGFR and MET to block ligand binding and receptor phosphorylation, promotes receptor internalization/degradation, suppresses downstream RAS/MAPK and PI3K/AKT signaling, and mediates Fc-dependent ADCC/ADCP against tumor cells.
Amivantamab binds EGFR on target cells and engages Fcγ receptor–bearing immune cells to mediate Fc-dependent ADCC and ADCP, leading to lysis/phagocytosis of EGFR-expressing cells.
Fully human IgG1 monoclonal antibody (VAY736) that binds and blocks the BAFF receptor (BAFF-R/TNFRSF13C) on B cells, inhibiting BAFF-mediated survival signaling and inducing B-cell depletion via ADCC (and potentially complement), thereby reducing pathogenic autoantibody production.
Fully human IgG1 monoclonal antibody against BAFF receptor (TNFRSF13C) that blocks BAFF–BAFF-R binding and downstream survival signaling in B cells, and engages Fc effector functions (ADCC ± complement) to deplete B cells, thereby reducing BAFF-dependent B-cell survival and pathogenic autoantibody production.
IgG1 anti-BAFF-R binds BAFF-R on B cells and recruits immune effectors via its Fc to induce ADCC (and possibly complement-dependent cytotoxicity), depleting BAFF-R–positive cells.
Antibody–drug conjugate targeting CD30; internalized upon binding and releases MMAE to disrupt microtubules and induce apoptosis; may also engage immune effector functions.
CD30-targeted monoclonal antibody linked via a protease-cleavable valine–citrulline linker to the microtubule toxin MMAE. After binding CD30 on tumor cells and internalization, MMAE is released intracellularly to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; the antibody Fc may also recruit immune effector functions (e.g., ADCC).
ADC binds CD30, is internalized, and releases MMAE intracellularly to inhibit tubulin polymerization, causing G2/M arrest and apoptosis; Fc-mediated ADCC may also contribute.