Antibody–drug conjugate targeting EGFR and c-MET that delivers a topoisomerase I inhibitor payload to induce DNA damage and tumor cell kill.
Bispecific anti-EGFR/anti-c-MET antibody-drug conjugate that binds EGFR and c-MET on tumor cells, is internalized, and releases a topoisomerase I inhibitor payload which stabilizes TOP1-DNA cleavage complexes, preventing religation and inducing DNA strand breaks, cell-cycle arrest, and apoptosis in EGFR/c-MET–expressing tumors.
Bispecific ADC binds EGFR (and c-MET) on tumor cells, is internalized, and releases a topoisomerase I inhibitor that stabilizes TOP1–DNA cleavable complexes, causing DNA breaks, cell-cycle arrest, and apoptosis.
Antibody–drug conjugate targeting EGFR and c-MET that delivers a topoisomerase I inhibitor payload to induce DNA damage and tumor cell kill.
Bispecific anti-EGFR/anti-c-MET antibody-drug conjugate that binds EGFR and c-MET on tumor cells, is internalized, and releases a topoisomerase I inhibitor payload which stabilizes TOP1-DNA cleavage complexes, preventing religation and inducing DNA strand breaks, cell-cycle arrest, and apoptosis in EGFR/c-MET–expressing tumors.
ADC binds c-MET on tumor cells, is internalized, and releases a topoisomerase I inhibitor payload that induces DNA damage and apoptosis.
Chimeric monoclonal antibody targeting CD20 on B cells; depletes B cells to suppress humoral immunity and reduce anti-pegloticase antibodies.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on pre-B and mature B cells, inducing B-cell depletion via complement-dependent cytotoxicity, antibody-dependent cellular cytotoxicity, and apoptosis, thereby suppressing humoral immunity and reducing anti-drug antibody formation.
Binds CD20 on B cells and induces complement-dependent cytotoxicity and Fc-mediated ADCC by immune effector cells; can also trigger apoptosis.
Adoptive cellular gene therapy using a patient’s T cells engineered with a piggyBac transposon to express an anti-CD19 chimeric antigen receptor; upon infusion, the cells target CD19+ B-lineage cells to deplete autoreactive clones and reduce autoantibodies in SLE.
Autologous T cells are gene-modified with a piggyBac transposon to express an anti-CD19 chimeric antigen receptor; upon infusion they recognize CD19 on B-lineage cells and induce CAR-mediated activation and cytotoxicity, depleting CD19+ B cells (including autoreactive clones) and reducing autoantibodies in SLE.
Anti-CD19 CAR T cells bind CD19 and directly lyse target cells via immune synapse–mediated perforin/granzyme release and Fas–FasL apoptosis.
Autologous T cells engineered with the non-viral Sleeping Beauty transposon system to express an anti-CD19 chimeric antigen receptor incorporating 4-1BB costimulatory and CD3ζ activation domains, plus huEGFRt as a safety/selection tag; designed to mediate targeted cytotoxicity against CD19+ B-cell malignancies.
Autologous T cells are gene-modified using the Sleeping Beauty transposon to express an anti-CD19 chimeric antigen receptor with 4-1BB costimulatory and CD3zeta activation domains. Binding to CD19 on malignant B cells triggers T-cell activation, expansion, and targeted cytotoxic killing of CD19-positive cells; the huEGFRt tag enables selection, tracking, and potential antibody-mediated depletion for safety.
Anti-CD19 CAR T cells bind CD19 on target cells, become activated via CD3ζ/4-1BB signaling, and kill CD19+ cells through T-cell cytolysis (perforin/granzyme release and Fas–FasL-mediated apoptosis).