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.
YES
DIRECT
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.
YES
DIRECT
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.
YES
DIRECT
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.
YES
DIRECT
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 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.
NO
INDIRECT
3BNC117-LS binds HIV-1 Env on infected cells and engages CD16a on NK cells/monocytes via its Fc to trigger ADCC/phagocytosis, killing the Env-expressing infected cells; CD16a+ effector cells are not targeted for killing.