Anti-CD19 antibody–drug conjugate that delivers the PBD dimer tesirine to CD19+ B cells, causing DNA cross-links and cytotoxicity after internalization.
Humanized anti‑CD19 monoclonal antibody linked via a cleavable linker to the pyrrolobenzodiazepine (PBD) dimer tesirine. After binding CD19 on B cells and internalization, the linker is cleaved to release the PBD payload, which binds the DNA minor groove and forms interstrand crosslinks at N2‑guanine, inhibiting DNA replication and inducing cytotoxicity in CD19+ tumor cells.
The anti-CD19 ADC binds CD19, is internalized, and releases the PBD dimer tesirine via a cleavable linker; the payload forms DNA interstrand crosslinks (N2-guanine), inhibiting replication and killing CD19+ cells.
Chimeric anti-CD20 monoclonal antibody that depletes B cells via ADCC, complement activation, and apoptosis.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B cells and depletes CD20-positive malignant and normal B cells via antibody-dependent cellular cytotoxicity (ADCC), complement-dependent cytotoxicity (CDC), and direct induction of apoptosis.
Rituximab binds CD20 on B cells and eliminates them via Fc-mediated ADCC by NK/macrophages, complement-dependent cytotoxicity (CDC), and can directly induce apoptosis upon CD20 crosslinking.
IgG-based bispecific antibody–drug conjugate targeting HER3 (ERBB3) and TROP2; binds tumor cells, induces receptor-mediated internalization, and releases an intracellular cytotoxic payload to kill cancer cells, potentially dampening HER3 signaling and addressing antigen heterogeneity.
IgG-based bispecific antibody–drug conjugate that binds HER3 (ERBB3) and TROP2 on tumor cells, induces receptor-mediated internalization, and releases an intracellular cytotoxic payload to kill cancer cells; dual targeting may also dampen HER3 signaling and address antigen heterogeneity.
The bispecific ADC binds HER3 on tumor cells, undergoes receptor-mediated internalization, and releases an intracellular cytotoxic payload that kills the cell (e.g., via DNA damage or microtubule disruption).
IgG-based bispecific antibody–drug conjugate targeting HER3 (ERBB3) and TROP2; binds tumor cells, induces receptor-mediated internalization, and releases an intracellular cytotoxic payload to kill cancer cells, potentially dampening HER3 signaling and addressing antigen heterogeneity.
IgG-based bispecific antibody–drug conjugate that binds HER3 (ERBB3) and TROP2 on tumor cells, induces receptor-mediated internalization, and releases an intracellular cytotoxic payload to kill cancer cells; dual targeting may also dampen HER3 signaling and address antigen heterogeneity.
ADC binds TROP2 on tumor cells, is internalized, and releases an intracellular cytotoxic payload that kills the cell.
Autologous, gene-modified CAR T-cell therapy expressing two CARs targeting the EGFR 806 epitope and IL13Rα2; delivered intrathecally to induce T-cell activation, cytokine release, and cytotoxic killing of glioblastoma cells while aiming to reduce antigen escape through dual targeting.
Autologous T cells genetically engineered (lentiviral) to co-express two chimeric antigen receptors targeting the EGFR 806 epitope and IL13Ra2. Engagement of either antigen on glioblastoma cells triggers CAR signaling to activate T cells, leading to cytokine release, clonal expansion, and perforin/granzyme-mediated cytotoxic killing. Dual targeting is intended to reduce antigen escape; administered intrathecally for CNS tumor access.
CAR T cells recognize the EGFR 806 epitope, form an immune synapse, and kill target cells via perforin/granzyme-mediated cytolysis (and Fas–FasL apoptosis).