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.
YES
DIRECT
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.
YES
DIRECT
Anti-CD22 ADC binds CD22, is internalized, and releases calicheamicin that induces DNA double‑strand breaks, leading to apoptosis of CD22+ cells.
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.
NO
INDIRECT
The ADC targets CD22 on B cells, is internalized, and releases calicheamicin, which then binds the DNA minor groove to cause double‑strand breaks and apoptosis. The DNA minor groove is the payload binding site, not the targeting antigen, so its presence alone does not lead to killing.
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.
YES
DIRECT
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.
YES
DIRECT
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.