Autologous anti-CD19 CAR T-cell therapy (Yescarta) used to treat relapsed/refractory DLBCL.
Autologous T cells are genetically modified with a retroviral vector to express an anti-CD19 chimeric antigen receptor that includes a CD28 costimulatory domain and a CD3 zeta signaling domain. On reinfusion, these CAR T cells recognize and bind CD19 on B-cell malignancies, become activated, proliferate, and kill CD19-positive cells via perforin/granzyme-mediated cytotoxicity and cytokine-driven immune responses.
Anti-CD19 CAR T cells bind CD19 on target cells and kill them via perforin/granzyme-mediated cytotoxicity and immune effector mechanisms after CAR activation.
TROP2-targeted antibody–drug conjugate (izalontamab brengitecan; BMS-986507) delivering a camptothecin-derived topoisomerase I inhibitor to TROP2-expressing tumor cells, causing TOP1 inhibition, DNA damage, and cell death.
TROP2-targeted antibody–drug conjugate that binds TROP2 on tumor cells, undergoes internalization, and releases a camptothecin-derived topoisomerase I inhibitor (brengitecan), leading to TOP1 inhibition, DNA damage, and tumor cell death (potential bystander effect).
An ADC binds TROP2 on tumor cells, is internalized, and releases a camptothecin-derived topoisomerase I inhibitor (brengitecan), causing TOP1 inhibition, DNA damage, and tumor cell death (with potential bystander effect).
Cetuximab is a chimeric IgG1 monoclonal antibody that binds the extracellular domain of EGFR, blocking ligand binding and receptor dimerization, thereby inhibiting downstream RAS/MAPK and PI3K/AKT signaling to reduce tumor cell proliferation and survival; its Fc region also engages Fcγ receptors on immune cells to mediate antibody-dependent cellular cytotoxicity (ADCC).
Cetuximab binds EGFR on target cells and its IgG1 Fc engages Fc-gamma receptors on NK cells and other effectors to trigger antibody-dependent cellular cytotoxicity (and some complement activation), resulting in killing of the bound cells.
Oral small-molecule EGFR tyrosine kinase inhibitor designed to selectively inhibit EGFR exon 20 insertion mutants, suppressing MAPK/ERK and PI3K–AKT signaling in tumor cells.
Oral, irreversible EGFR tyrosine kinase inhibitor that selectively targets mutant EGFR—especially exon 20 insertion variants (also T790M, Ex19del, L858R)—to block EGFR phosphorylation and downstream MAPK/ERK and PI3K–AKT signaling, leading to tumor cell growth inhibition and death.
Irreversible inhibition of mutant EGFR kinase blocks MAPK/ERK and PI3K–AKT signaling, leading to growth arrest and apoptosis of EGFR-mutant tumor cells.
Oral small-molecule EGFR tyrosine kinase inhibitor designed to selectively inhibit EGFR exon 20 insertion mutants, suppressing MAPK/ERK and PI3K–AKT signaling in tumor cells.
Oral, irreversible EGFR tyrosine kinase inhibitor that selectively targets mutant EGFR—especially exon 20 insertion variants (also T790M, Ex19del, L858R)—to block EGFR phosphorylation and downstream MAPK/ERK and PI3K–AKT signaling, leading to tumor cell growth inhibition and death.
Irreversible inhibition of mutant EGFR kinase blocks MAPK/ERK and PI3K–AKT signaling, leading to growth arrest and apoptosis of EGFR-mutant tumor cells.