Entrectinib is an orally active, blood brain barrier(BBB)-penetrated and centrally active inhibitor of TrkA/B/C, ROS1 and ALK, with IC50 values of 1, 3, 5, 12 and 7nM, respectively[1]. TrkA/B/C are neurotrophin receptors, ROS1 is an orphan receptor tyrosine kinase, and ALK is an anaplastic lymphoma kinase; all three drive tumorigenesis through fusion or mutation[2]. Entrectinib is commonly used in the study of ROS1-rearranged non-small cell lung cancer (NSCLC) and NTRK fusion-positive solid tumors[3].
In vitro, Entrectinib (2.3-4.3μM; 48h) dose-dependently reduced viability, suppressed colony formation and EdU incorporation, and elevated apoptosis in PC12, HT22 and SK-N-SH nerve cells, with cellular IC50 values of 2.3, 4.2 and 4.3μM, respectively[4]. Entrectinib (100-400nM; 24h) dose-dependently inhibited TGF-β1-driven proliferation, migration, and myofibroblast activation of Mlg and HFL1 lung fibroblasts and blocked TGF-β1-induced epithelial-mesenchymal transition (EMT) in MLE12 epithelial cells[5].
In vivo, Entrectinib (60mg/kg; BID for 7 weeks; p.o.) markedly suppressed SY5Y-TrkB xenograft growth, prolonged mouse event-free survival, and blocked TrkB, Akt and Erk phosphorylation in athymic nu/nu mice[6]. Entrectinib (10mg/kg; i.p.) reduced LPS-induced serum IL-1β and hepatic AST/ALT levels, and improved 24h survival in C57BL/6J mice[7].
References:
[1] Ardini E, Menichincheri M, Banfi P, et al. Entrectinib, a Pan-TRK, ROS1, and ALK Inhibitor with Activity in Multiple Molecularly Defined Cancer Indications. Mol Cancer Ther. 2016;15(4):628-639.
[2] Drilon A, Siena S, Ou SI, et al. Safety and Antitumor Activity of the Multitargeted Pan-TRK, ROS1, and ALK Inhibitor Entrectinib: Combined Results from Two Phase I Trials (ALKA-372-001 and STARTRK-1). Cancer Discov. 2017;7(4):400-409.
[3] Osman HM, Tuncbilek M. Entrectinib: A New Selective Tyrosine Kinase Inhibitor Approved for the Treatment of Pediatric and Adult Patients with NTRK Fusionpositive, Recurrent or Advanced Solid Tumors. Curr Med Chem. 2022;29(15):2602-2616.
[4] Tang Q, Dong J, Zhang F, et al. Entrectinib can induce nerve cell damage by inhibiting PI3K-AKT and TGF-β signaling pathways. Front Pharmacol. 2025;16:1489210.
[5] Miao Y, Li X, Yang Y, et al. Entrectinib ameliorates bleomycin-induced pulmonary fibrosis in mice by inhibiting TGF-β1 signaling pathway. Int Immunopharmacol. 2022;113(Pt B):109427.
[6] Iyer R, Wehrmann L, Golden RL, et al. Entrectinib is a potent inhibitor of Trk-driven neuroblastomas in a xenograft mouse model. Cancer Lett. 2016;372(2):179-186.
[7] Jin X, Liu D, Zhou X, Luo X, Huang Q, Huang Y. Entrectinib inhibits NLRP3 inflammasome and inflammatory diseases by directly targeting NEK7. Cell Rep Med. 2023;4(12):101310.
















