Intravenous bispecific T‑cell–engaging monoclonal antibody that binds FcRH5 on malignant plasma cells and CD3 on T cells to redirect T‑cell cytotoxicity.
Bispecific antibody that binds FcRH5 on malignant plasma cells and CD3 on T cells, crosslinking and activating cytotoxic T cells to mediate targeted lysis of FCRH5-expressing myeloma cells.
Cevostamab bridges CD3 on T cells to FCRH5 on target cells, activating T cells to kill FCRH5-expressing cells via perforin/granzyme-mediated cytotoxicity.
Biosimilar chimeric IgG1 anti–TNF-α monoclonal antibody. Binds soluble and transmembrane TNF-α, blocks TNFR1/TNFR2 signaling, induces apoptosis and immune clearance of TNF-expressing cells via ADCC/CDC, and suppresses NF-κB–mediated inflammation and associated cytokines.
Chimeric IgG1 anti-TNF-alpha monoclonal antibody (biosimilar infliximab) that binds soluble and transmembrane TNF-alpha, neutralizing it and blocking TNFR1/TNFR2 signaling; also mediates ADCC and CDC to deplete TNF-expressing cells, leading to suppression of NF-kB-driven inflammation and proinflammatory cytokines.
Infliximab binds transmembrane TNF-alpha on target cells and engages Fc-mediated effector functions, causing ADCC by NK/macrophages and CDC via complement; crosslinking tmTNF can also induce apoptosis (reverse signaling).
A HER2-targeted antibody–drug conjugate (RC48-ADC) that delivers the microtubule inhibitor MMAE to HER2-expressing tumor cells, leading to microtubule disruption, apoptosis, and potential ADCC.
HER2-targeted IgG1 antibody–drug conjugate that delivers the microtubule inhibitor MMAE to HER2-expressing tumor cells. After HER2 binding and internalization, MMAE is released to inhibit tubulin polymerization, leading to microtubule disruption, G2/M arrest, and apoptosis; the IgG1 Fc may also mediate ADCC.
Binds HER2, is internalized, and releases MMAE to inhibit tubulin, causing microtubule disruption, G2/M arrest, and apoptosis; IgG1 Fc can also mediate ADCC.
Anti-CD20 monoclonal antibody that depletes B cells to limit donor-specific antibodies.
Anti-CD20 monoclonal antibody that binds CD20 on pre-B and mature B cells and depletes them via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis, thereby reducing donor-specific antibody production.
Rituximab binds CD20 on B cells and eliminates them via Fc-mediated ADCC (engaging NK cells/macrophages), complement-dependent cytotoxicity, and can directly induce apoptosis.
Anti-CD2 monoclonal antibody that depletes or blocks T and NK cells.
Humanized IgG1 monoclonal antibody targeting CD2 on T and NK cells; blocks CD2-mediated activation/adhesion and induces Fc-dependent depletion (ADCC/complement), reducing CD2+ lymphocytes and suppressing immune responses.
Anti-CD2 IgG1 binds CD2 on T/NK cells and triggers Fc-dependent ADCC and complement-mediated lysis (CDC), depleting CD2+ cells.