TROP2-directed antibody–drug conjugate that delivers a topoisomerase I inhibitor payload via a cleavable linker to induce DNA damage and apoptosis (potential bystander effect).
TROP2-targeted monoclonal antibody linked via a cleavable linker to a topoisomerase I inhibitor. After binding TROP2 on tumor cells and internalization, the linker is cleaved to release the cytotoxic payload, causing DNA damage and apoptosis; membrane-permeable payload may enable a bystander effect on neighboring cells.
An anti-TROP2 ADC binds TROP2, is internalized, and its cleavable linker releases a topoisomerase I inhibitor that induces DNA damage and apoptosis; the membrane-permeable payload can also cause a bystander effect.
Autologous tumor-infiltrating lymphocyte (TIL) cell therapy expanded ex vivo and infused IV after lymphodepletion to mediate tumor cell killing via TCR recognition of neoantigens.
Autologous tumor-infiltrating lymphocytes expanded ex vivo are infused after lymphodepletion to recognize patient-specific tumor neoantigens via native TCR–MHC interactions and kill tumor cells through perforin/granzyme-mediated cytotoxicity and cytokine-driven immune activation and persistence.
Infused TILs recognize the neoantigen peptide–HLA class I complex via native TCRs and kill target cells through perforin/granzyme-mediated cytolysis and Fas–FasL apoptosis.
Intravenous type II glycoengineered anti-CD20 monoclonal antibody that induces direct B-cell death and enhances Fc-mediated ADCC/ADCP.
Glycoengineered humanized IgG1 type II anti-CD20 monoclonal antibody that binds CD20 on B cells and, via enhanced Fc gamma RIIIa interaction, induces potent ADCC/ADCP and direct cell death, resulting in depletion of malignant CD20-positive B cells.
Obinutuzumab binds CD20 on B cells and recruits immune effectors via Fc gamma RIIIa to mediate ADCC/ADCP, and as a type II anti-CD20 it also induces direct, caspase-independent cell death of CD20-positive cells.
Chimeric anti-CD20 monoclonal antibody that mediates complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity, leading to B-cell depletion.
Chimeric anti-CD20 monoclonal antibody that binds CD20 on B lymphocytes and induces B-cell depletion via complement-dependent cytotoxicity and antibody-dependent cellular cytotoxicity (and phagocytosis), with additional direct apoptotic signaling.
Rituximab binds CD20 on B cells and kills them via complement-dependent cytotoxicity and Fc-mediated ADCC/ADCP by NK cells and macrophages; it can also trigger direct apoptotic signaling.
Humanized, Fc-engineered anti-CD19 IgG1 monoclonal antibody that enhances ADCC/ADCP and induces apoptosis of B cells.
Humanized, Fc-engineered anti-CD19 IgG1 monoclonal antibody that binds CD19 on B cells and enhances Fcγ receptor engagement to promote antibody-dependent cellular cytotoxicity (ADCC) and antibody-dependent cellular phagocytosis (ADCP), leading to depletion and apoptosis of CD19-positive B cells.
The anti-CD19 IgG1 binds CD19 on B cells and its Fc engages Fcγ receptors on effector cells to trigger ADCC and ADCP, causing lysis/phagocytosis; it can also induce apoptosis of CD19+ cells.