An allogeneic B7‑H3 (CD276) chimeric antigen receptor gamma‑delta T‑cell therapy; donor γδ T cells engineered with a CAR targeting B7‑H3 to induce MHC‑independent cytotoxicity and cytokine release, administered intrathecally/Ommaya for CNS delivery in recurrent/progressive high‑grade glioma/GBM.
Allogeneic gamma-delta T cells engineered with a CAR targeting B7‑H3 (CD276) bind B7‑H3 on tumor cells and induce MHC‑independent activation, cytotoxic killing (perforin/granzyme) and cytokine release. Administered intrathecally/Ommaya for CNS delivery to treat high‑grade glioma/GBM, with off‑the‑shelf potential and low GVHD risk.
Allogeneic gamma-delta CAR T cells bind B7-H3 on tumor cells and directly kill them via MHC-independent immune synapse with perforin/granzyme release (with cytokine-mediated effects).
Chimeric anti-CD20 monoclonal antibody that mediates B-cell depletion via ADCC, complement-dependent cytotoxicity, and direct apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on pre‑B and mature B cells and depletes CD20+ cells via Fc-mediated ADCC, complement-dependent cytotoxicity, and direct induction of apoptosis.
Rituximab binds CD20 on B cells and induces killing via Fc-mediated ADCC (NK cells/macrophages), complement-dependent cytotoxicity (C1q/MAC), and can directly trigger apoptosis upon CD20 crosslinking.
Glycoengineered humanized type II anti-CD20 IgG1 monoclonal antibody that depletes CD20+ B cells via enhanced Fcγ receptor–mediated ADCC and phagocytosis and by inducing direct type II cell death; relatively less complement-dependent cytotoxicity. Administered IV for maintenance every 60 days.
Glycoengineered type II anti‑CD20 IgG1 monoclonal antibody that binds CD20 on B cells and depletes them primarily via enhanced FcγRIIIa‑mediated ADCC and antibody‑dependent phagocytosis, plus direct type II cell death; exhibits relatively reduced complement‑dependent cytotoxicity.
B cells expressing CD20 are killed via anti-CD20 antibody binding that triggers Fc gamma RIIIa–mediated ADCC by NK cells, antibody-dependent phagocytosis, and direct type II cell death (with relatively reduced complement-mediated cytotoxicity).
Long-acting broadly neutralizing anti–HIV-1 human IgG1 monoclonal antibody with LS Fc mutations for extended half-life; targets the gp120 CD4-binding site to neutralize virus and block entry, and engages Fcγ receptor–mediated effector functions (ADCC, phagocytosis) to eliminate Env-expressing infected cells and reduce the intact proviral reservoir.
Long-acting human IgG1 broadly neutralizing antibody (LS Fc half-life mutations) that binds the HIV-1 gp120 CD4-binding site to neutralize virions and block entry into CD4+ T cells; engages Fcγ receptors to mediate ADCC and phagocytosis of Env-expressing infected cells, aiming to reduce the intact proviral reservoir.
The IgG1 bnAb binds gp120 on Env-expressing infected cells and recruits FcγR-bearing effector cells (e.g., NK cells, macrophages) to mediate ADCC and antibody-dependent phagocytosis, with possible complement-mediated lysis, thereby killing the target cells.
Long-acting broadly neutralizing anti–HIV-1 human IgG1 monoclonal antibody with LS Fc mutations for extended half-life; targets the gp120 V3 glycan (N332) supersite to neutralize virus and block entry, and engages Fcγ receptor–mediated effector functions (ADCC, phagocytosis) to eliminate Env-expressing infected cells and reduce the intact proviral reservoir.
A long-acting broadly neutralizing human IgG1 monoclonal antibody with LS Fc mutations that extend half-life; it binds the HIV-1 Env gp120 V3 glycan (N332) supersite to neutralize virions and block viral entry, and engages Fcγ receptors to mediate ADCC and phagocytosis of Env-expressing infected cells, aiming to reduce the intact proviral reservoir.
The antibody binds the gp120 V3 N332 supersite on Env displayed by infected cells and engages Fcγ receptors on NK cells/macrophages to trigger ADCC and antibody-dependent phagocytosis, leading to killing/removal of the target cells.