Please use this identifier to cite or link to this item:
|Title:||Current strategies for inhibiting FGFR activities in clinical applications: Opportunities, challenges and toxicological considerations||Authors:||Ho, H.K.
|Issue Date:||Jan-2014||Citation:||Ho, H.K., Yeo, A.H.L., Kang, T.S., Chua, B.T. (2014-01). Current strategies for inhibiting FGFR activities in clinical applications: Opportunities, challenges and toxicological considerations. Drug Discovery Today 19 (1) : 51-62. ScholarBank@NUS Repository. https://doi.org/10.1016/j.drudis.2013.07.021||Abstract:||Aberrations in fibroblast growth factor receptor (FGFR) signaling are instrumental to the pathophysiology of several malignancies and disorders. Hence, FGFR inhibitors are explored in therapeutics with early candidates developed as competitors for the ATP-binding pocket in the kinase domain. More recent programs yielded compounds of diverse scaffolds with alternative binding modes. Concurrently, monoclonal antibodies and peptide-based agents provide independent options for clinical development. Notwithstanding this rapid progress, we contemplate the toxicological impact of FGFR inhibition based on the defined role of FGFR family members in physiology and homeostasis. The high homology among FGFR1-4 and also with other kinase subfamilies creates an additional challenge in developing selective inhibitors. It orchestrates an ongoing conundrum of moderating a balance between synergism through multitargeting kinase inhibition and minimizing off-target toxicities. © 2013 Elsevier Ltd. All rights reserved.||Source Title:||Drug Discovery Today||URI:||http://scholarbank.nus.edu.sg/handle/10635/106639||ISSN:||13596446||DOI:||10.1016/j.drudis.2013.07.021|
|Appears in Collections:||Staff Publications|
Show full item record
Files in This Item:
There are no files associated with this item.
checked on May 16, 2022
WEB OF SCIENCETM
checked on May 9, 2022
checked on May 12, 2022
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.