A glycoengineered type I anti-CD20 monoclonal antibody that depletes B cells via high-affinity Fc-mediated ADCC and complement-dependent cytotoxicity, with secondary induction of apoptosis; reduces B-cell antigen presentation, cytokine production, and T–B cell costimulation in multiple sclerosis.
Ublituximab is a glycoengineered type I anti‑CD20 IgG1 monoclonal antibody that binds CD20 on B cells and depletes them via enhanced Fc‑mediated antibody‑dependent cellular cytotoxicity (ADCC), complement‑dependent cytotoxicity (CDC), and induction of apoptosis, leading to reduced B‑cell antigen presentation, cytokine production, and T–B costimulation.
YES
DIRECT
Binds CD20 on B cells and triggers Fc-mediated ADCC by effector cells, activates complement for CDC, and can induce apoptosis via CD20 crosslinking.
Individualized, gene-modified autologous CAR T-cell therapy targeting GPRC5D, using a fully human VHH binder with 4-1BB costimulatory and CD3ζ activation domains; administered as a single infusion (1.0–3.0×10^6 CAR-T cells/kg) after lymphodepletion.
Autologous T cells are lentivirally engineered to express a chimeric antigen receptor with a fully human VHH binder targeting GPRC5D and 4-1BB costimulatory plus CD3zeta activation domains. After lymphodepletion and infusion, CAR engagement of GPRC5D on malignant plasma cells triggers T-cell activation, expansion, and cytotoxic killing of GPRC5D-expressing cells.
YES
DIRECT
CAR T cells bind GPRC5D on target cells and induce cytolysis via immune synapse formation with perforin/granzyme release (and Fas–FasL signaling), causing apoptosis of GPRC5D-expressing cells.
Chimeric anti-EGFR monoclonal antibody that inhibits EGFR signaling and can mediate antibody-dependent cellular cytotoxicity (ADCC).
Chimeric monoclonal antibody against EGFR that binds the receptor’s extracellular domain, blocking ligand binding and receptor dimerization/activation, thereby inhibiting downstream signaling (e.g., RAS–RAF–MEK–ERK, PI3K–AKT) to suppress tumor cell proliferation and survival; also engages immune effector functions to mediate ADCC.
YES
DIRECT
Binds EGFR on tumor cells and engages Fcγ receptors on immune effector cells to trigger ADCC (and potentially CDC), leading to lysis of EGFR-expressing cells.
Autologous, fourth-generation, dual-target chimeric antigen receptor T-cell therapy engineered to recognize CD19 and CD22 on malignant B cells, leading to T-cell activation and cytotoxic killing; administered with optional repeat doses after lymphodepletion.
Autologous, gene-modified T cells engineered with a dual-target chimeric antigen receptor that binds CD19 and CD22 on malignant B cells; CAR engagement triggers T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing. Lymphodepletion supports in vivo expansion and persistence.
YES
DIRECT
CD19-specific CAR T cells bind CD19 on target cells and directly kill them via T-cell cytotoxicity (perforin/granzyme release and death-receptor pathways).
Autologous, fourth-generation, dual-target chimeric antigen receptor T-cell therapy engineered to recognize CD19 and CD22 on malignant B cells, leading to T-cell activation and cytotoxic killing; administered with optional repeat doses after lymphodepletion.
Autologous, gene-modified T cells engineered with a dual-target chimeric antigen receptor that binds CD19 and CD22 on malignant B cells; CAR engagement triggers T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing. Lymphodepletion supports in vivo expansion and persistence.
YES
DIRECT
CD22 engagement by the CAR activates T cells to form an immune synapse and kill target cells via perforin/granzyme-mediated apoptosis (and death-receptor pathways).