Intravenous type II anti-CD20 monoclonal antibody that targets CD20 on B cells to induce direct cell death and immune effector killing (ADCC/ADCP, some CDC).
Glycoengineered type II humanized IgG1 anti‑CD20 monoclonal antibody that binds CD20 on B cells and depletes them via enhanced FcγRIIIa‑mediated ADCC/ADCP and induction of direct, caspase‑independent cell death, with limited complement activation.
Obinutuzumab binds CD20 on B cells, triggering type II, caspase‑independent direct cell death and engaging FcγRIIIa on NK cells/macrophages to mediate ADCC/ADCP (with limited CDC).
Intravenous CD20×CD3 bispecific antibody that binds CD20 on lymphoma cells and CD3 on T cells, redirecting and activating T cells to kill B cells.
Glofitamab is a bispecific monoclonal antibody that simultaneously binds CD20 on B‑cell lymphoma cells and CD3 on T cells, crosslinking the two to redirect and activate T cells. This induces T‑cell activation and cytotoxicity against CD20‑expressing B cells, leading to targeted tumor cell lysis.
By binding CD20 on target cells and CD3 on T cells, glofitamab redirects and activates T cells to form immune synapses and kill CD20+ cells via perforin/granzyme-mediated cytolysis and apoptosis.
Autologous patient T cells genetically engineered to express a CD19-directed chimeric antigen receptor (CAR) incorporating CD3ζ with CD28 or 4-1BB co-stimulatory domains, enabling HLA-independent recognition and cytotoxic elimination of CD19-positive malignant B cells.
Autologous T cells are genetically engineered to express a CD19-specific chimeric antigen receptor containing CD3ζ and CD28 or 4-1BB co-stimulatory domains. The CAR enables HLA-independent binding to CD19 on B cells, triggering T-cell activation, proliferation, cytokine release, and cytotoxic killing of CD19-positive malignant B cells.
CAR T cells recognize CD19 on target cells, activate, and induce cytotoxicity via perforin/granzyme release and Fas–FasL apoptosis.
Autologous patient T cells genetically engineered to express a BCMA-directed chimeric antigen receptor (CAR) incorporating CD3ζ with CD28 or 4-1BB co-stimulatory domains, enabling HLA-independent recognition and cytotoxic elimination of BCMA-positive malignant plasma cells.
Autologous T cells are genetically engineered to express a BCMA-directed chimeric antigen receptor containing CD3ζ signaling plus CD28 or 4-1BB co-stimulation. The CAR enables HLA-independent recognition of BCMA on malignant plasma cells, triggering T-cell activation, proliferation, cytokine release, and perforin/granzyme-mediated cytotoxic killing of BCMA-positive cells.
BCMA-targeted CAR T cells bind BCMA on tumor cells, triggering activation and degranulation with perforin/granzyme-mediated lysis (and Fas/FasL apoptosis) of BCMA-positive cells.
Type II, glycoengineered anti-CD20 monoclonal antibody that depletes CD20+ B cells via enhanced ADCC/ADCP and direct cell death (with some CDC).
Type II, glycoengineered humanized IgG1 anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes them via enhanced Fc gamma RIII (CD16)-mediated ADCC and ADCP and by inducing direct cell death/apoptosis, with some complement-dependent cytotoxicity (CDC). Afucosylated Fc glycosylation increases Fc receptor affinity and cytotoxic effector function.
Binds CD20 on B cells and kills via enhanced FcγRIIIa-mediated ADCC by NK cells, ADCP by macrophages, direct type II cell death/apoptosis, and some complement-dependent cytotoxicity (CDC).