Glycoengineered type II anti-CD20 monoclonal antibody that induces direct cell death and antibody-dependent/complement-dependent cytotoxicity of CD20+ B cells.
Glycoengineered humanized IgG1 type II anti-CD20 monoclonal antibody that binds CD20 on B cells; Fc afucosylation increases affinity for Fc-gamma RIII, enhancing antibody-dependent cellular cytotoxicity and phagocytosis; also triggers direct caspase-independent cell death and complement-dependent cytotoxicity, depleting CD20+ malignant B cells.
Obinutuzumab binds CD20 on B cells and kills them via direct type II, caspase‑independent cell death, and by recruiting immune effectors—enhanced FcγRIIIa-mediated ADCC/ADCP and complement-dependent cytotoxicity (CDC).
Humanized, Fc-engineered anti-CD19 IgG1 monoclonal antibody (Minjuvi) that binds CD19 on B cells, enhances ADCC/ADCP, and induces apoptosis.
Fc‑engineered humanized anti‑CD19 IgG1 monoclonal antibody that binds CD19 on B cells and enhances Fcγ receptor engagement, driving antibody‑dependent cellular cytotoxicity (ADCC) and antibody‑dependent cell‑mediated phagocytosis (ADCP), leading to depletion of CD19+ B cells and induction of apoptosis.
Binds CD19 and engages Fcγ receptors on NK cells/macrophages to induce ADCC and ADCP, with additional direct apoptosis of CD19+ B cells.
Chimeric anti-CD20 IgG1 monoclonal antibody that depletes B cells via complement-dependent cytotoxicity (CDC), ADCC, and apoptosis.
Chimeric anti-CD20 IgG1 monoclonal antibody that binds CD20 on B cells and induces cell killing via complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC), and apoptosis, resulting in depletion of CD20-positive B cells.
Anti-CD20 IgG1 binds CD20 on B cells and triggers complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC) via Fcγ receptor–bearing effector cells, and can induce apoptosis, killing CD20+ cells.
Autologous, genetically modified CAR T-cell therapy targeting CLEC12A (CD371/CLL-1) on AML cells; incorporates CD3ζ-based CAR signaling with costimulation and is "armored" to secrete IL-18 to enhance expansion/persistence, Th1 polarization, and recruitment/activation of innate immune cells, thereby broadening anti-leukemia activity. Administered after lymphodepleting chemotherapy in relapsed/refractory AML.
Autologous T cells engineered with a CAR that binds CLEC12A (CD371/CLL-1) on AML cells. CAR signaling via CD3zeta with costimulation triggers T-cell cytotoxicity against leukemic blasts and stem cells. The construct is armored to secrete IL-18, which enhances CAR T expansion and persistence, promotes Th1 polarization and IFN-gamma–driven immunity, and recruits/activates innate immune cells (e.g., NK cells, macrophages), broadening anti-leukemia activity after lymphodepletion.
CAR T cells recognize CLEC12A on AML cells and induce T-cell cytotoxicity, primarily via perforin/granzyme-mediated apoptosis and Fas/FasL signaling; IL-18 enhances CAR T activity and can recruit innate effectors.
Anti-CD38 IgG1 monoclonal antibody that depletes CD38+ plasmablasts and plasma cells to reduce anti-FVIII alloantibody production.
Human IgG1 anti‑CD38 monoclonal antibody that binds CD38 on plasmablasts, plasma cells, and other CD38+ immune cells and depletes them via Fc‑mediated effector functions (ADCC, ADCP) and complement‑dependent cytotoxicity (CDC), thereby reducing anti‑FVIII alloantibody production and modulating immune responses.
Daratumumab binds CD38 on target cells and triggers Fc-mediated ADCC (NK cells), ADCP (macrophages), and complement-dependent cytotoxicity (CDC), with possible direct apoptotic signaling upon cross-linking.