HER2-targeted antibody–drug conjugate (RC48) comprising a humanized anti-HER2 IgG1 linked to the microtubule-disrupting payload MMAE; internalized upon HER2 binding and can mediate ADCC.
HER2-targeted IgG1 antibody–drug conjugate (RC48) that binds HER2 on tumor cells, is internalized, and via a cleavable linker releases the microtubule inhibitor MMAE, which disrupts tubulin polymerization to induce G2/M arrest and apoptosis; the IgG1 Fc can also mediate ADCC.
ADC binds HER2, is internalized, and releases MMAE to disrupt microtubules causing G2/M arrest and apoptosis; Fc can also trigger ADCC against HER2+ cells.
HER2-targeted antibody–drug conjugate composed of trastuzumab linked to the microtubule inhibitor DM1, delivering cytotoxic payload to HER2-overexpressing tumor cells.
HER2-targeted trastuzumab linked to the microtubule inhibitor DM1. Binds HER2 to inhibit signaling and mediate ADCC, is internalized into HER2-overexpressing tumor cells, then releases DM1 to disrupt microtubules, causing mitotic arrest and apoptosis.
The ADC binds HER2, is internalized, and releases the DM1 payload that disrupts microtubules, causing mitotic arrest and apoptosis; Fc-mediated ADCC can also contribute.
Chimeric anti-CD20 monoclonal antibody administered intravenously that depletes CD20+ B cells, reducing anti-PLA2R autoantibodies and immune complex formation.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on pre-B and mature B cells and depletes them via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, reducing anti-PLA2R autoantibodies and immune complex formation.
Rituximab binds CD20 on B cells and eliminates them via complement-dependent cytotoxicity and Fc-mediated ADCC; it can also induce apoptosis.
Autologous anti-CD19 chimeric antigen receptor (CAR) T-cell therapy; genetically engineered T cells administered IV to deplete CD19+ B-cell compartments.
Autologous T cells are engineered ex vivo to express an anti‑CD19 chimeric antigen receptor and, after IV infusion, bind CD19 on B‑lineage cells (naive and memory B cells and plasmablasts). CAR engagement activates the T cells to kill targets via perforin/granzyme and cytokine‑mediated cytotoxicity, depleting CD19+ B cells and reducing autoantibody production and B cell–mediated antigen presentation/co‑stimulation.
Anti-CD19 CAR T cells bind CD19 on B cells and directly kill them via T‑cell cytotoxicity, primarily perforin/granzyme-mediated apoptosis (with cytokine/Fas–FasL contributions).
An antibody-drug conjugate targeting Trop-2; a humanized anti–Trop-2 IgG linked to SN-38 (active metabolite of irinotecan), a topoisomerase I inhibitor that is released upon internalization to induce DNA damage and apoptosis.
Humanized anti–TROP2 IgG linked to SN-38. Binds TROP2 on tumor cells, is internalized, and releases SN-38 after linker cleavage. SN-38 inhibits topoisomerase I by stabilizing Topo I–DNA complexes, causing DNA strand breaks, impaired replication, and apoptosis; may exert a bystander effect due to membrane-permeable payload.
The ADC binds TROP-2 on target cells, is internalized, and releases SN-38 after linker cleavage; SN-38 inhibits topoisomerase I, causing DNA strand breaks and apoptosis (with possible bystander killing due to payload permeability).