Third-generation EGFR inhibitor active against T790M with CNS penetration.
Third‑generation, orally available, irreversible and mutant‑selective EGFR tyrosine kinase inhibitor that covalently binds EGFR at C797, potently inhibiting mutant forms including T790M, L858R, and exon 19 deletions, thereby blocking EGFR signaling, suppressing tumor growth, and inducing cancer cell death; demonstrates CNS penetration and relatively spares wild‑type EGFR.
Osimertinib covalently inhibits the T790M-mutant EGFR kinase (C797), blocking EGFR signaling (e.g., PI3K–AKT, MAPK) in addicted tumor cells, leading to growth arrest and apoptosis of the target-expressing cells.
Multikinase TKI targeting ROS1, NTRK, and ALK with CNS activity.
Oral multikinase tyrosine kinase inhibitor that targets TRKA/B/C (NTRK1/2/3), ROS1, and ALK. By binding the ATP site, it inhibits kinase signaling (e.g., MAPK and PI3K/AKT pathways), leading to tumor cell growth arrest and apoptosis in cancers driven by these fusions/rearrangements; demonstrates CNS penetration.
ATP-competitive inhibition of TRKA kinase blocks downstream MAPK and PI3K/AKT signaling, leading to growth arrest and apoptosis in TRKA-driven cells.
Multikinase TKI targeting ROS1, NTRK, and ALK with CNS activity.
Oral multikinase tyrosine kinase inhibitor that targets TRKA/B/C (NTRK1/2/3), ROS1, and ALK. By binding the ATP site, it inhibits kinase signaling (e.g., MAPK and PI3K/AKT pathways), leading to tumor cell growth arrest and apoptosis in cancers driven by these fusions/rearrangements; demonstrates CNS penetration.
Entrectinib directly inhibits TRKB (NTRK2) kinase activity at the ATP site, blocking downstream MAPK/PI3K-AKT signaling and triggering growth arrest and apoptosis in TRKB-driven tumor cells.
Multikinase TKI targeting ROS1, NTRK, and ALK with CNS activity.
Oral multikinase tyrosine kinase inhibitor that targets TRKA/B/C (NTRK1/2/3), ROS1, and ALK. By binding the ATP site, it inhibits kinase signaling (e.g., MAPK and PI3K/AKT pathways), leading to tumor cell growth arrest and apoptosis in cancers driven by these fusions/rearrangements; demonstrates CNS penetration.
Entrectinib directly inhibits TRKC (NTRK3) kinase activity by binding the ATP site, blocking MAPK and PI3K/AKT signaling in TRKC-driven tumor cells, leading to growth arrest and apoptosis.
Multikinase TKI targeting ROS1, NTRK, and ALK with CNS activity.
Oral multikinase tyrosine kinase inhibitor that targets TRKA/B/C (NTRK1/2/3), ROS1, and ALK. By binding the ATP site, it inhibits kinase signaling (e.g., MAPK and PI3K/AKT pathways), leading to tumor cell growth arrest and apoptosis in cancers driven by these fusions/rearrangements; demonstrates CNS penetration.
ATP-competitive inhibition of ROS1 kinase blocks downstream MAPK/PI3K-AKT signaling in ROS1-driven tumor cells, causing growth arrest and apoptosis.