Anti-CD38 IgG1 monoclonal antibody that induces ADCC, CDC, and apoptosis of CD38+ myeloma and immunosuppressive cells.
Human IgG1κ monoclonal antibody targeting CD38 on myeloma and immunosuppressive cells; binding triggers direct apoptosis and immune effector killing via ADCC, ADCP, and CDC, depleting CD38+ tumor cells as well as Tregs, B cells, and MDSCs to produce antitumor and immunomodulatory effects.
Anti-CD38 IgG1 binds CD38 on target cells and triggers killing via Fc-mediated ADCC (NK cells), ADCP (macrophages), CDC (complement), and can induce direct apoptosis upon binding/crosslinking.
Anti-CD38 monoclonal antibody that mediates ADCC/ADCP and direct proapoptotic signaling against CD38+ myeloma cells.
Humanized IgG1 anti‑CD38 monoclonal antibody that binds CD38 on myeloma cells, inducing antibody‑dependent cellular cytotoxicity and phagocytosis, complement‑dependent cytotoxicity, and direct pro‑apoptotic signaling; also inhibits CD38 ecto‑enzyme activity, depleting CD38+ malignant and immunosuppressive cells.
Isatuximab binds CD38 on target cells and triggers Fc-mediated ADCC and ADCP, complement-dependent cytotoxicity (CDC), and direct pro-apoptotic signaling, leading to killing of CD38+ cells.
Anti-SLAMF7 monoclonal antibody that activates NK cells and promotes ADCC against SLAMF7+ myeloma cells.
Humanized IgG1 monoclonal antibody targeting SLAMF7 (CS1). Binds SLAMF7 on myeloma and NK cells, activating NK cells and promoting Fcγ-mediated ADCC (and ADCP) against SLAMF7-positive myeloma cells, with minimal expression on normal tissues.
Elotuzumab binds SLAMF7 on myeloma cells and its Fc engages FcγRIIIa on NK cells, triggering ADCC (and ADCP by macrophages), with NK activation via SLAMF7 further enhancing killing.
Type II, glycoengineered anti‑CD20 monoclonal antibody that depletes CD20+ B cells via enhanced ADCC/ADCP and direct cell death.
Type II, glycoengineered anti‑CD20 IgG1 that binds CD20 on B cells and depletes CD20+ malignant cells via enhanced FcγRIIIa‑mediated ADCC/ADCP from afucosylation and by inducing direct, largely caspase‑independent cell death.
Obinutuzumab binds CD20 and directly kills CD20+ B cells by inducing caspase‑independent cell death and by engaging FcγRIIIa on NK cells/macrophages to drive ADCC and ADCP.
Autologous gene-modified T cells engineered to express a dual-target chimeric antigen receptor against CD19 and BCMA, intended to deplete CD19+ B cells and BCMA+ plasmablasts/plasma cells to suppress pathogenic autoantibody production in refractory immune thrombocytopenia.
Autologous T cells gene-modified to express dual chimeric antigen receptors targeting CD19 and BCMA. Upon binding CD19+ B cells and BCMA+ plasmablasts/plasma cells, CAR signaling activates T‑cell cytotoxicity and cytokine release, depleting B‑lineage cells and suppressing pathogenic autoantibody production; dual targeting reduces antigen escape.
CAR T cells bind CD19 via the CAR and directly kill target cells through perforin/granzyme-mediated lysis and death-receptor (Fas/FasL) apoptosis.