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[155] [156] [157] [158] [159] [160] [161] [162] [163] [164] [165] [166]
Idiopathic pulmonary fibrosis (2014) NSCLC (Apr 2018) Advanced soft tissue sarcoma (Apr 27, 2012) Adult patients with chronic phase, accelerated phase, or blast phase CML or Ph+ ALL for whom no other TKI therapy is indicated (Dec 14, 2012) Gastric cancer, NSCLC, colorectal cancer, hepatocellular carcinoma (Apr 21, 2014) Hepatocellular carcinoma (Apr 27, 2017) Advanced gastrointestinal stromal tumour (Feb 25, 2013) Advanced colorectal cancer (Sep 27
β, and VEGFR 1-3. This results in blockage of the autophosphorylation
It binds to the intracellular ATP binding pockets of FGFR 1-3, PDGFRα/
of these receptors and the downstream signalling cascades
It inhibits VEGFR, PDGFR, c-KIT and FGFR It targets the mutated EGFR T790M within the cancer cells It inhibits Bcr-Abl, an abnormal tyrosine kinase that is the hallmark of CML and Ph+ ALL It is a direct VEGFR2 antagonist, that binds with high affinity to the extracellular domain of VEGFR2 and block the binding of natural VEGFR ligands (VEGF-A, VEGF-C and VEGF-D) Dual targeted VEGFR2 and Tie2 tyrosine kinase inhibition Protein kinase inhibitor
Ofev® and Vargatef® Tagrisso® Votrient® Iclusig® Cyramza® Stivarga® Nexavar® Sutent® Torisel® Thalomid® Caprelsa® Zaltrap®
Nintedanib Osimertinib Pazopanib Ponatinib Ramucirumab Regorafenib Sorafenib Sunitinib Temsirolimus Thalidomide Vandetanib Ziv- aflibercept
Sonoporation located ones.
16. 17. 18. 19. 20. 21. 22. 23. 24. 25. 26. 27.
