Anti-CD38 IgG1 monoclonal antibody (Sarclisa) that induces ADCC, CDC, ADCP, direct apoptosis, and inhibits CD38 ectoenzyme activity.
Isatuximab is an IgG1 monoclonal antibody targeting CD38 on plasma cells. It mediates antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and antibody-dependent cellular phagocytosis, can trigger direct apoptosis, and inhibits CD38 ectoenzyme (NADase) activity, leading to depletion/lysis of CD38-expressing tumor cells.
Anti-CD38 IgG1 mAb binds CD38 on target cells and induces ADCC, CDC, and ADCP, and can trigger direct apoptosis, leading to lysis of CD38-expressing cells.
Fully human anti-CD20 monoclonal antibody that depletes CD20+ B cells to reduce antigen presentation, cytokines, and autoantibody activity.
Fully human anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells and depletes CD20+ B cells primarily via complement-dependent cytotoxicity (CDC) and antibody-dependent cell-mediated cytotoxicity (ADCC), thereby reducing antigen presentation, pro-inflammatory cytokines, and autoantibody production.
Ofatumumab binds CD20 on B cells and induces complement-dependent cytotoxicity and Fc-mediated ADCC (and phagocytosis), causing lysis of CD20+ cells.
A humanized anti-CD2 monoclonal antibody (TCD601) that binds CD2 on T cells and NK cells, blocks CD2–LFA-3 (CD58) costimulatory signaling, induces lymphocyte depletion with preferential reduction of CD2high effector/memory T cells, and aims to shift T-cell phenotypes toward a more regulatory profile to preserve β-cell function in recent-onset type 1 diabetes.
Humanized IgG1 anti-CD2 monoclonal antibody that binds CD2 on T cells and NK cells, blocks CD2–CD58 (LFA-3) costimulatory signaling, and engages Fc-mediated effector functions (e.g., ADCC/CDC) to deplete CD2+ lymphocytes—preferentially CD2high effector/memory T cells—shifting the T-cell compartment toward a more regulatory phenotype and suppressing pathogenic T-cell activity.
Anti-CD2 IgG1 binds CD2+ lymphocytes and depletes them via Fc-mediated ADCC and complement-dependent cytotoxicity (CDC), causing lysis/apoptosis.
TROP‑2–directed antibody‑drug conjugate delivering SN‑38 (topoisomerase I inhibitor payload).
Humanized anti-TROP-2 monoclonal antibody (hRS7) conjugated to SN-38 (topoisomerase I inhibitor). After binding TROP-2 on tumor cells and internalization, linker cleavage releases SN-38, which stabilizes topoisomerase I–DNA complexes, causing DNA breaks, blocking replication, and inducing apoptosis; can also produce a bystander effect.
The ADC binds TROP-2, is internalized, and releases SN-38 (a topoisomerase I inhibitor) inside the cell, causing DNA damage, replication arrest, and apoptosis; can also produce a bystander effect.
Polyclonal antibody preparation that depletes T lymphocytes for induction immunosuppression.
Polyclonal anti–T-lymphocyte IgG that binds multiple T-cell surface antigens and depletes T cells via complement-dependent cytotoxicity and Fc-mediated ADCC, with additional T-cell apoptosis and functional inhibition, producing potent immunosuppression.
ATG contains antibodies that bind CD4 on T cells, triggering complement-dependent lysis and Fc-mediated ADCC by NK/macrophages, with additional apoptosis induction, depleting CD4+ cells.