A recombinant humanized anti-CD52 monoclonal antibody (biologic immunosuppressant) administered subcutaneously as part of conditioning for allogeneic hematopoietic cell transplantation. It binds CD52 on mature lymphocytes and other immune cells, depleting them via complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity to reduce donor–recipient alloreactivity and graft-versus-host disease risk.
Humanized anti-CD52 monoclonal antibody that binds CD52 on mature lymphocytes and other CD52+ immune cells, depleting them via complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity to suppress alloimmune activation and reduce graft-versus-host disease risk during allogeneic transplantation conditioning.
Alemtuzumab binds CD52 on target cells and recruits immune effectors, causing complement-dependent cytotoxicity and Fc-mediated ADCC/ADCP, leading to depletion of CD52+ cells.
IgG1 monoclonal antibody targeting CD38 on myeloma plasma cells; induces ADCC, CDC, and ADCP, can trigger direct apoptosis, and depletes CD38+ immunosuppressive cells to enhance T/NK-cell activity.
Human IgG1k monoclonal antibody targeting CD38; binds CD38 on myeloma/plasma cells to induce antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and antibody-dependent cellular phagocytosis (ADCP), can trigger direct apoptosis, and depletes CD38+ immunosuppressive cells (Tregs, Bregs, MDSCs) to enhance T/NK-cell activity.
Anti-CD38 IgG1 binds CD38 on target cells and triggers Fc-mediated ADCC by NK cells, complement-dependent cytotoxicity (CDC), antibody-dependent cellular phagocytosis (ADCP), and can induce direct apoptosis.
IgG1 monoclonal antibody against CD38; mediates ADCC, CDC, and ADCP, can induce direct apoptosis, and reduces CD38+ immunosuppressive cells to augment T/NK-cell function.
Humanized IgG1 monoclonal antibody against CD38 that binds CD38 on tumor cells and induces ADCC, CDC, and ADCP, can trigger direct apoptosis, and depletes CD38+ immunosuppressive cells to enhance T/NK-cell function.
Isatuximab binds CD38 on target cells and induces NK cell–mediated ADCC, complement-dependent cytotoxicity (CDC), macrophage ADCP, and can trigger direct apoptosis.
Bispecific IgG1 monoclonal antibody targeting EGFR and MET; blocks ligand-mediated activation, inhibits downstream MAPK/PI3K-AKT/JAK-STAT signaling, promotes receptor internalization/degradation, and engages immune effector cells via Fc to mediate ADCC.
Bispecific IgG1 monoclonal antibody against EGFR and MET that blocks ligand-mediated receptor activation and phosphorylation, suppressing downstream MAPK, PI3K/AKT, and JAK/STAT signaling; induces receptor internalization/degradation and engages Fc-dependent immune effector functions to mediate ADCC.
Amivantamab binds EGFR on target cells and engages Fcγ receptor–bearing immune cells to mediate ADCC (and ADCP/CDC), resulting in killing of EGFR-expressing cells; it also promotes receptor internalization and signaling blockade.
Bispecific IgG1 monoclonal antibody targeting EGFR and MET; blocks ligand-mediated activation, inhibits downstream MAPK/PI3K-AKT/JAK-STAT signaling, promotes receptor internalization/degradation, and engages immune effector cells via Fc to mediate ADCC.
Bispecific IgG1 monoclonal antibody against EGFR and MET that blocks ligand-mediated receptor activation and phosphorylation, suppressing downstream MAPK, PI3K/AKT, and JAK/STAT signaling; induces receptor internalization/degradation and engages Fc-dependent immune effector functions to mediate ADCC.
Amivantamab binds MET on target cells and, via its IgG1 Fc, recruits Fc receptor–bearing immune effectors (e.g., NK cells) to mediate ADCC, killing MET-expressing cells.