Anti-TROP2 antibody–drug conjugate (ADC) that delivers a cytotoxic payload to TROP2-expressing tumor cells.
Anti-TROP2 IgG1 antibody–drug conjugate linked via a cleavable linker to an exatecan-derived topoisomerase I inhibitor (SHR9265). After binding TROP2 on tumor cells and internalization, the linker is cleaved to release the payload, which inhibits topoisomerase I, blocking DNA replication and inducing cell-cycle arrest and apoptosis in TROP2-expressing cells.
ADC binds TROP2, is internalized, linker is cleaved, and an exatecan-derived topoisomerase I inhibitor is released inside the cell, blocking DNA replication and inducing cell-cycle arrest and apoptosis.
Type II, glycoengineered, humanized anti-CD20 monoclonal antibody that binds CD20 on B cells to induce direct cell death and enhance antibody-dependent cellular cytotoxicity and phagocytosis, depleting malignant CD20+ B cells.
Type II, glycoengineered humanized anti-CD20 IgG1 that binds CD20 on B cells and depletes malignant CD20+ cells by inducing direct cell death and enhancing FcγRIIIa-mediated ADCC and antibody-dependent phagocytosis; Fc glycoengineering (reduced fucosylation) increases effector function.
Anti-CD20 mAb that induces type II CD20-mediated direct cell death and, via its afucosylated Fc, engages FcγRIIIa on effector cells to drive ADCC (NK cells) and antibody-dependent phagocytosis, depleting CD20+ cells.
Antigen-specific T cells expanded ex vivo and reinfused to recognize tumor peptides on MHC class I via the TCR, mediating cytotoxicity through perforin/granzyme release and IFN-gamma-mediated effects.
Autologous antigen-specific CTLs expanded ex vivo are reinfused to recognize tumor peptides presented on MHC class I via their endogenous TCR, inducing tumor-cell killing via perforin/granzyme release and death-receptor pathways (FasL/TRAIL), along with IFN-γ secretion to enhance antitumor immune responses.
Antigen-specific CTLs recognize the tumor peptide–HLA-C complex via their TCR and directly kill target cells through perforin/granzyme release and death-receptor (FasL/TRAIL) pathways.
Antibody–drug conjugate targeting integrin αvβ6; internalization releases the vedotin payload MMAE (monomethyl auristatin E), a microtubule-disrupting agent that causes G2/M arrest and apoptosis.
Monoclonal antibody targets integrin αvβ6 on tumor cells, is internalized, and releases the vedotin payload MMAE via a cleavable linker. MMAE disrupts microtubules by inhibiting tubulin polymerization, causing G2/M arrest and apoptosis, with potential bystander killing.
ADC binds integrin αvβ6 on target cells, is internalized, and releases MMAE via a cleavable linker; MMAE inhibits tubulin polymerization, causing G2/M arrest and apoptosis (with potential bystander killing).
An autologous anti-CD19 chimeric antigen receptor (CAR) T-cell therapy. Patient T cells are genetically engineered to express an anti-CD19 CAR; upon engagement of CD19 on B-lineage malignant cells, the CAR T cells activate and mediate cytotoxicity, leading to elimination of CD19+ tumor cells and on-target B-cell depletion. Administered as a single IV infusion (0.5–6×10^6 cells/kg).
Autologous patient T cells are engineered to express an anti-CD19 chimeric antigen receptor; upon binding CD19 on B-lineage malignant cells, the CAR T cells activate, proliferate, and mediate cytotoxic killing, eliminating CD19-positive tumor cells and causing on-target B-cell depletion.
Anti-CD19 CAR T cells recognize CD19, become activated, and kill CD19+ cells via perforin/granzyme-mediated cytolysis and apoptosis (e.g., Fas/FasL), causing on-target B-cell depletion.