Chimeric anti-CD20 monoclonal antibody administered intravenously (375 mg/m² ×2, 14 days apart) to deplete CD20+ B cells via complement-dependent cytotoxicity, ADCC, and apoptosis, aiming to reduce autoantibody production and immune-complex–mediated inflammation in rheumatic carditis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes them via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, thereby reducing autoantibody production and immune-complex–mediated inflammation.
YES
DIRECT
Binds CD20 on B cells and induces complement-dependent cytotoxicity (MAC lysis), antibody-dependent cellular cytotoxicity via FcγR-bearing effector cells (e.g., NK cells/macrophages), and apoptosis upon CD20 cross-linking.
A chimeric anti-CD20 IgG1 monoclonal antibody that depletes CD20-positive B cells via antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and apoptosis.
Rituximab is a chimeric anti-CD20 IgG1 monoclonal antibody that binds CD20 on B lymphocytes and depletes CD20-positive cells through antibody-dependent cellular cytotoxicity, complement-dependent cytotoxicity, and induction of apoptosis.
YES
DIRECT
Anti‑CD20 antibody binds CD20 on B cells and triggers Fc‑mediated ADCC (NK cells/macrophages) and complement‑dependent cytotoxicity; CD20 ligation can also induce apoptosis.
An antibody–drug conjugate (ADC) targeting CLDN18.2; after binding to CLDN18.2 on tumor cells it is internalized and releases a topoisomerase I–inhibiting cytotoxic payload, inducing DNA damage and cell death with a potential bystander effect.
Monoclonal antibody targeting CLDN18.2 linked to a topoisomerase I inhibitor; upon binding CLDN18.2 on tumor cells the ADC is internalized and releases the payload, inhibiting topoisomerase I to induce DNA damage and tumor cell death, with potential bystander effect.
YES
DIRECT
The anti-CLDN18.2 ADC binds CLDN18.2 on target cells, is internalized, and releases a topoisomerase I–inhibitor payload that induces DNA damage and apoptosis, with potential bystander killing.
An antibody–drug conjugate (ADC) targeting CLDN18.2; after binding to CLDN18.2 on tumor cells it is internalized and releases a topoisomerase I–inhibiting cytotoxic payload, inducing DNA damage and cell death with a potential bystander effect.
Monoclonal antibody targeting CLDN18.2 linked to a topoisomerase I inhibitor; upon binding CLDN18.2 on tumor cells the ADC is internalized and releases the payload, inhibiting topoisomerase I to induce DNA damage and tumor cell death, with potential bystander effect.
NO
INDIRECT
IBI343 targets CLDN18.2 on tumor cells; after internalization it releases a topoisomerase I–inhibiting payload that causes DNA damage and cell death (with possible bystander effect). DNA topoisomerase I is not the antigen bound by the ADC.
CD20×CD3 bispecific antibody that redirects T cells to kill CD20-positive B cells; administered subcutaneously.
Humanized CD20×CD3 bispecific antibody that binds CD20 on malignant B cells and CD3 on T cells, cross-linking them to redirect and activate T cells, inducing cytotoxic killing of CD20-positive B cells; administered subcutaneously.
NO
INDIRECT
CD3 epsilon is on T cells; mosunetuzumab binds CD3 to recruit/activate T cells, which then kill CD20-positive B cells via T-cell cytotoxicity (perforin/granzyme). CD3-positive cells are not targeted for killing.