Third-generation, irreversible EGFR tyrosine kinase inhibitor (also known as alflutinib) designed to target activating and T790M EGFR mutations.
Furmonertinib (alflutinib) is a third-generation, mutant-selective, irreversible EGFR tyrosine kinase inhibitor that covalently binds the ATP site (e.g., Cys797) of EGFR, potently inhibiting activating and T790M resistance mutations. This blocks EGFR phosphorylation and downstream MAPK and PI3K–AKT signaling, suppressing proliferation and inducing death of EGFR-mutant tumor cells, including those with T790M-mediated resistance.
Small-molecule TKI covalently inhibits EGFR kinase (Cys797), blocking EGFR phosphorylation and downstream MAPK/PI3K–AKT signaling, causing growth arrest and apoptosis of EGFR-mutant (incl. T790M) tumor cells.
HER2-directed antibody–drug conjugate that binds HER2 on tumor cells, is internalized, and delivers a cytotoxic payload.
Trastuzumab-based HER2-directed ADC (trastuzumab rezetecan) that binds HER2 on tumor cells, is internalized, and upon linker cleavage releases a camptothecin-derived topoisomerase I inhibitor, inducing DNA breaks, apoptosis, and growth inhibition in HER2-expressing tumors.
HER2-binding ADC is internalized into HER2+ cells; linker cleavage releases a camptothecin-derived topoisomerase I inhibitor that causes DNA breaks, leading to apoptosis and growth inhibition.
An intravenous, every-2-weeks bispecific monoclonal antibody immunotherapy that binds CLDN18.2 on tumor cells and blocks the CD47–SIRPα checkpoint to enhance macrophage-mediated phagocytosis and antigen presentation, aiming to focus CD47 blockade on CLDN18.2-positive tumors to reduce off-tumor hematologic toxicity.
Bispecific monoclonal antibody that binds CLDN18.2 on tumor cells while blocking the CD47–SIRPα checkpoint, concentrating CD47 inhibition on CLDN18.2-positive tumors to enhance macrophage-mediated phagocytosis and antigen presentation (with potential Fc effector functions), thereby promoting anti-tumor immunity and reducing off-tumor hematologic toxicity.
AK132 binds CLDN18.2 on tumor cells and locally blocks CD47–SIRPα, removing the “don’t eat me” signal and enabling Fc-dependent macrophage-mediated phagocytosis (ADCP) of CLDN18.2+ cells.
Autologous T lymphocytes genetically modified to express a chimeric antigen receptor that recognizes BCMA (TNFRSF17) on malignant plasma cells, activating T-cell cytotoxicity and cytokine release to kill myeloma cells.
Autologous T lymphocytes are genetically engineered to express a chimeric antigen receptor that recognizes BCMA (TNFRSF17) on malignant plasma cells. CAR engagement activates T-cell signaling, inducing targeted cytotoxicity (perforin/granzyme) and cytokine release to kill myeloma cells.
BCMA-directed CAR T cells bind BCMA on target cells, activate T-cell cytotoxicity, and kill them via perforin/granzyme release and Fas–FasL–mediated apoptosis.
Third-generation, irreversible EGFR tyrosine kinase inhibitor (also known as alflutinib) designed to target activating and T790M EGFR mutations.
Furmonertinib (alflutinib) is a third-generation, mutant-selective, irreversible EGFR tyrosine kinase inhibitor that covalently binds the ATP site (e.g., Cys797) of EGFR, potently inhibiting activating and T790M resistance mutations. This blocks EGFR phosphorylation and downstream MAPK and PI3K–AKT signaling, suppressing proliferation and inducing death of EGFR-mutant tumor cells, including those with T790M-mediated resistance.
Furmonertinib covalently inhibits mutant EGFR kinase (e.g., T790M/activating), blocking EGFR phosphorylation and downstream MAPK/PI3K–AKT signaling, leading to growth arrest and apoptosis of EGFR‑mutant tumor cells.