Off-the-shelf, allogeneic cord blood–derived natural killer (NK) cell therapy that provides cytotoxic NK cells mediating CD16 (FcγRIIIa)–dependent ADCC against anti-CD20–opsonized B cells.
Off-the-shelf allogeneic cord blood–derived NK cells that, via CD16 (FcγRIIIa), mediate antibody-dependent cellular cytotoxicity against anti-CD20–opsonized B cells (with rituximab/obinutuzumab), with additional innate NK cytotoxicity and cytokine effects.
NO
INDIRECT
AB-101 NK cells bind the IgG1 Fc of anti-CD20 antibodies via CD16 to engage CD20-opsonized B cells and mediate ADCC; the killed cells are CD20+ B cells, not cells expressing IgG Fc.
An antibody–drug conjugate targeting Trop-2 that delivers the topoisomerase I inhibitor SN-38 to tumor cells, causing DNA strand breaks, S-phase arrest, and apoptosis.
Humanized anti–Trop-2 monoclonal antibody (hRS7) delivers the topoisomerase I inhibitor SN-38 to Trop-2–expressing tumor cells. After binding and internalization, linker cleavage releases SN-38, which stabilizes Topo I–DNA cleavage complexes, causing DNA strand breaks, S-phase arrest, and apoptosis (with potential bystander effect).
YES
DIRECT
The ADC binds Trop-2 on target cells, is internalized, and releases SN-38 (a topoisomerase I inhibitor) that stabilizes Topo I-DNA cleavage complexes, causing DNA strand breaks, S-phase arrest, and apoptosis; a bystander effect may also occur.
An antibody–drug conjugate targeting Trop-2 that delivers the topoisomerase I inhibitor SN-38 to tumor cells, causing DNA strand breaks, S-phase arrest, and apoptosis.
Humanized anti–Trop-2 monoclonal antibody (hRS7) delivers the topoisomerase I inhibitor SN-38 to Trop-2–expressing tumor cells. After binding and internalization, linker cleavage releases SN-38, which stabilizes Topo I–DNA cleavage complexes, causing DNA strand breaks, S-phase arrest, and apoptosis (with potential bystander effect).
NO
INDIRECT
The ADC binds Trop-2 (not topoisomerase I) on tumor cells, is internalized, and releases SN-38, which inhibits topoisomerase I to cause DNA damage and apoptosis. Topoisomerase I is the payload’s enzymatic target, not the antigen that directs cell killing.
Anti-CD20 monoclonal antibody that depletes CD20-positive B cells via antibody-dependent cellular cytotoxicity, complement activation, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20-positive B lymphocytes via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
YES
DIRECT
Rituximab binds CD20 on B cells and triggers Fc-mediated ADCC by effector cells, complement-dependent cytotoxicity, and can induce apoptosis via CD20 crosslinking.
Fully human anti-CD20 IgG1 monoclonal antibody (brand: Kesimpta) administered subcutaneously; binds a membrane-proximal CD20 epitope and depletes CD20+ B cells via complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC), and apoptosis; spares stem cells and plasma cells and reduces antigen presentation and pro-inflammatory cytokines (e.g., IL-6, GM-CSF).
Fully human IgG1 anti‑CD20 monoclonal antibody that binds a membrane‑proximal CD20 epitope on B cells and depletes CD20+ B cells via complement‑dependent cytotoxicity, antibody‑dependent cellular cytotoxicity, and apoptosis; spares stem cells and plasma cells, reducing antigen presentation and pro‑inflammatory cytokines.
YES
DIRECT
Binds CD20 on B cells and triggers complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity (via Fc-engaged effector cells), with additional induction of apoptosis.