BCMA-targeting antibody-drug conjugate that delivers the microtubule inhibitor MMAF to induce apoptosis and engages immune effector functions (ADCC/ADCP).
Afucosylated anti-BCMA monoclonal antibody linked to the microtubule inhibitor MMAF. After binding BCMA on malignant plasma cells and internalization, MMAF inhibits tubulin polymerization causing G2/M arrest and apoptosis; Fc effector engagement drives ADCC/ADCP for additional tumor cell killing.
The anti-BCMA ADC binds BCMA, is internalized, and releases MMAF to inhibit tubulin, causing G2/M arrest and apoptosis; its afucosylated Fc also mediates ADCC/ADCP.
A chimeric IgG1 monoclonal antibody targeting EGFR that blocks ligand binding and downstream signaling and can induce antibody-dependent cellular cytotoxicity (ADCC).
Chimeric IgG1 monoclonal antibody against EGFR; binds the extracellular domain to block ligand binding, receptor activation and dimerization, inhibiting downstream RAS-RAF-MEK-ERK and PI3K-AKT signaling to suppress tumor cell proliferation; Fc region can engage immune effector cells to induce ADCC.
Cetuximab binds EGFR on target cells and its IgG1 Fc engages FcγR-expressing immune cells (e.g., NK cells) to mediate antibody‑dependent cellular cytotoxicity (and some complement activation), leading to lysis of EGFR-positive cells.
Anti-CD38 IgG1 monoclonal antibody that mediates ADCC, CDC, ADCP, and direct apoptosis, and depletes CD38+ immunosuppressive cells.
Human IgG1 monoclonal antibody targeting CD38 that induces tumor cell killing via ADCC, CDC, and ADCP and can trigger direct apoptosis; also depletes CD38+ immunosuppressive cells (e.g., Tregs, Bregs, MDSCs), enhancing antitumor immunity.
Daratumumab binds CD38 on target cells and induces killing via Fc-mediated ADCC (NK cells), complement-dependent cytotoxicity (CDC), antibody-dependent cellular phagocytosis (ADCP), and can trigger direct apoptosis upon binding/crosslinking.
Antibody fusion protein combining an anti-CD20 monoclonal antibody with the CD47-binding domain of SIRPα; blocks the CD47–SIRPα checkpoint to promote macrophage phagocytosis and engages Fcγ receptors to enhance ADCC against CD20+ B cells.
Bispecific antibody fusion that targets CD20 on B cells while presenting a SIRPα domain to bind CD47, locally blocking the CD47–SIRPα innate immune checkpoint. This removes the “don’t‑eat‑me” signal to promote macrophage-mediated phagocytosis (ADCP) and, via its IgG1 Fc, engages Fcγ receptors to enhance NK cell/macrophage ADCC against CD20+ B cells, with secondary activation of adaptive anti-tumor immunity.
The bispecific antibody binds CD20 on B cells and presents SIRPα to block CD47, removing the “don’t‑eat‑me” signal and promoting macrophage phagocytosis (ADCP). Its IgG1 Fc engages Fcγ receptors to recruit NK cells/macrophages for ADCC, leading to direct immune effector killing of CD20+ cells.
Type II glycoengineered anti-CD20 monoclonal antibody (Gazyva) that binds CD20 on mature/memory B cells, enhancing ADCC and direct cell death with reduced CDC versus rituximab, resulting in B-cell depletion and reduced antiplatelet autoantibody production.
Glycoengineered type II anti‑CD20 IgG1 that binds CD20 on mature/memory B cells with increased FcγRIII affinity, driving enhanced ADCC/ADCP and direct, caspase‑independent cell death (with reduced CDC), resulting in B‑cell depletion and decreased pathogenic autoantibody production.
Obinutuzumab binds CD20 on B cells, inducing type II direct (caspase‑independent) cell death and engaging FcγRIIIa on effector cells to drive ADCC/ADCP (with reduced CDC), leading to B‑cell killing.