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.
YES
DIRECT
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.
YES
DIRECT
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.
YES
DIRECT
Irreversible small-molecule inhibition of mutant EGFR kinase blocks phosphorylation and downstream MAPK/ERK and PI3K–AKT signaling, leading to growth arrest and apoptosis of EGFR-mutant tumor cells.
Adoptive γδ T‑cell therapy using Vγ9Vδ2 T cells expanded from healthy donors and administered intraventricularly/intracavitary via an Ommaya reservoir. These innate‑like cytotoxic lymphocytes recognize tumor phosphoantigens via BTN3A1/BTN2A1 independent of MHC, triggering perforin/granzyme‑mediated killing and cytokine release; they can also respond via NKG2D and mediate ADCC.
Allogeneic Vγ9Vδ2 T cells recognize tumor-derived phosphoantigens generated by dysregulated mevalonate metabolism via BTN3A1/BTN2A1 in an MHC-independent manner, triggering perforin/granzyme-mediated cytotoxicity and cytokine release. They also respond to stress ligands through NKG2D and can mediate ADCC.
YES
DIRECT
Vγ9Vδ2 T cells express NKG2D, which binds ULBP1 on target cells and triggers perforin/granzyme-mediated lysis.