– 1. Yan H, Wu W, Hu Y, et al.Regorafenib inhibits EphA2 phosphorylation and leads to liver damage via the ERK/MDM2/p53 axis.Nature Communications.2023, 14(1): 2756.
2. Li P, Jia C, Fan Z, et al.Discovery of novel exceptionally potent and orally active c-MET PROTACs for the treatment of tumors with MET alterations.Acta Pharmaceutica Sinica B.2023
3. Zou X, Zeng M, Zheng Y, et al.Comparative Study of Hydroxytyrosol Acetate and Hydroxytyrosol in Activating Phase II Enzymes.Antioxidants.2023, 12(10): 1834.
4. Jiao D, Chen Y, Liu X, et al.Targeting MET endocytosis or degradation to overcome HGF-induced gefitinib resistance in EGFR-sensitive mutant lung adenocarcinoma.Biochemical and Biophysical Research Communications.2023
5. Yu J, Zhang L, Peng J, et al. Dictamnine, a novel c-Met inhibitor, suppresses the proliferation of lung cancer cells by downregulating the PI3K/AKT/mTOR and MAPK signaling pathways. Biochemical pharmacology. 2022, 195: 114864.
6. Arechederra M, Bazai S K, Abdouni A, et al. ADAMTSL5 is an epigenetically activated gene underlying tumorigenesis and drug resistance in hepatocellular carcinoma. Journal of Hepatology. 2021, 74(4): 893-906.
7. Yang Y, Huang J, Xie N, et al. lincROR influences the stemness and crizotinib resistance in eMl–alK+ non-small-cell lung cancer cells. OncoTargets and Therapy. 2018 Jun 22;11:3649-3657
8. Tao J, Tu Y, Liu P, et al. Detection of colorectal cancer using a small molecular fluorescent probe targeted against c-Met. Talanta. 2021: 122128.
9. Hu Y, Zhang X, Zhao Z, et al. Keratinocytes apoptosis contributes to crizotinib induced-erythroderma. Toxicology Letters. 2019
10. Zheng Y D, Zhong T, Wu H, et al. Crizotinib Shows Antibacterial Activity against Gram-Positive Bacteria by Reducing ATP Production and Targeting the CTP Synthase PyrG. Microbiology Spectrum. 2022: e00884-22
– Zou HY, et al. An orally available small-molecule inhibitor of c-Met, PF-2341066, exhibits cytoreductive antitumor efficacy through antiproliferative and antiangiogenic mechanisms. Cancer Res. 2007 May 1;67(9):4408-17.
– O([C@H](C)C1=C(Cl)C(F)=CC=C1Cl)C2=CC(C3=CN(N=C3)C4CCNCC4)=CN=C2N
– Aryl Hydrocarbon Receptor
– Angiogenesis|||Tyrosine Kinase/Adaptors|||Immunology/Inflammation|||Autophagy
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