Anti-CD20 chimeric monoclonal antibody that tags B cells and mediates antibody-dependent cellular cytotoxicity (ADCC).
Chimeric anti‑CD20 monoclonal antibody that binds CD20 on B lymphocytes and depletes CD20+ cells primarily via antibody‑dependent cellular cytotoxicity (through FcγRIII/CD16 on NK cells), complement‑dependent cytotoxicity, and apoptosis signaling.
Anti-CD20 antibody binds CD20 on B cells and induces killing via Fc-engaged NK-cell ADCC, complement-dependent cytotoxicity, and apoptosis signaling.
Anti-CD22 antibody-drug conjugate that binds CD22 on B-cell precursor lymphoblasts, internalizes, and releases calicheamicin to cause DNA double-strand breaks and apoptosis.
Humanized anti-CD22 antibody-drug conjugate that binds CD22 on B-cell precursor lymphoblasts, is internalized, and releases calicheamicin, which binds the DNA minor groove to induce double-strand breaks and apoptosis.
Anti-CD22 ADC binds CD22, is internalized, and releases calicheamicin that induces DNA double‑strand breaks, leading to apoptosis of CD22+ cells.
Gene-modified natural killer (NK) cells engineered to express an NKG2D-based chimeric antigen receptor (CAR) that recognizes NKG2D ligands (MICA, MICB, ULBP family) on tumor cells, activating NK cytotoxicity for treatment of relapsed/refractory multiple myeloma.
Gene‑modified NK cells expressing an NKG2D‑based CAR recognize stress‑induced NKG2D ligands (MICA, MICB, ULBP family) on tumor cells. CAR signaling activates NK cytotoxic functions, inducing degranulation (perforin/granzyme), cytokine‑mediated killing, and apoptosis of malignant cells, targeting relapsed/refractory multiple myeloma.
NKG2D-CAR NK cells bind MICA on target cells, activating NK cytotoxicity and killing via perforin/granzyme-mediated lysis and apoptosis.
Fully human monoclonal antibody immunotherapy targeting CD47; blocks the CD47–SIRPα innate immune checkpoint to enhance macrophage-mediated phagocytosis of malignant myeloid cells.
Fully human anti-CD47 monoclonal antibody that blocks the CD47–SIRPα innate immune checkpoint, removing the "don't eat me" signal. This restores macrophage-mediated phagocytosis of tumor cells (via pro-phagocytic signals such as calreticulin-LRP) and can enhance downstream T-cell-mediated anti-tumor immunity; engineered to minimize binding to red blood cells.
Blocks CD47–SIRPα to remove the “don’t eat me” signal and, via Fc engagement of Fcγ receptors, enables macrophage antibody-dependent cellular phagocytosis of CD47+ cells; can secondarily enhance T cell–mediated killing.
Autologous, second-generation CD19-directed CAR T-cell therapy; patient T cells are engineered to express a CD19-specific chimeric antigen receptor with costimulation to kill CD19+ leukemic B cells. Expected on-target effect includes B-cell aplasia.
Autologous T cells engineered with a CD19-specific chimeric antigen receptor containing 4-1BB costimulatory and CD3zeta signaling domains. Upon binding CD19 on B-lineage cells, the CAR T cells activate, proliferate, release cytotoxic mediators, and kill CD19+ leukemic cells, with expected on-target B-cell aplasia.
CD19-directed CAR T cells bind CD19 on target cells, activate, and kill via perforin/granzyme-mediated cytolysis and apoptosis (e.g., Fas–FasL).