A small molecule–kinase interaction map for clinical kinase inhibitors

By M. A. Fabian, W. Biggs, D. K. Treiber, Corey E Atteridge, Mihai Dumitru Azimioara, Michael G. Benedetti, T. A. Carter, P. Ciceri, Philip T Edeen, Mark Floyd and 16 more. Nature Biotechnology, 2005

1,905 citations recorded by the source corpus.

Subfields: Genetics, Hematology, Organic Chemistry

View Paper: https://www.semanticscholar.org/paper/55c682095a6e181d2a8c8474ea7cd75055a25bcc

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Citations in the corpus

Molecular mechanisms of cardiotoxicity of tyrosine kinase inhibition (2007, background): “None of the small-molecule inhibitors are truly selective, and some (for example, sunitinib) seem to be relatively non-selectiv”
Epidermal growth factor receptor mutations in lung cancer (2007, methodology): “Another study, in which the phage-display method was used to examine the interaction of a large panel of kinases with selective inhibitors, concluded that EGFR mutations, including ΔE746-A750, do not themselves affect the affinity for gefitinib and erlotini”
How many drug targets are there? (2006, background): “(and which target association led to its first approval for chronic myeloid leukaemia), has subsequently been discovered to be have significant activity against several other clinically relevant kinases, such as c-KI”
Regorafenib (BAY 73‐4506): A new oral multikinase inhibitor of angiogenic, stromal and oncogenic receptor tyrosine kinases with potent preclinical antitumor activity (2011, background): “The structure of regorafenib differs from that of sorafenib by the addition of a fluorine atom in the center phenyl ring (Table 1) and leads to a similar but distinct biochemical profile compared with sorafenib.(22,29,30) In addition, regorafenib appears to be pharmacologically more potent.”
CDK8/9 drive Smad transcriptional action, turnover and YAP interactions in BMP and TGFβ pathways (2009, positive): “Elucidating the links between the Hippo pathway and other signaling cascades is an important open question ( Edgar, 2006; Pan, 2007; Zeng and Hong, 2008).”
Molecular determinants of the response of glioblastomas to EGFR kinase inhibitors. (2005, neutral): “EGFRvIII expression 7/8 (88) 11/25 (44) 0.”
Lessons in PROTAC design from selective degradation with a promiscuous warhead (2017, methodology): “…we found that 10 mM foretinib binds to 133 different kinases with a percent of control (a value with inverse relationship to affinity) value of 35 or less—the recommended cutoff to avoid false positives for kinase-inhibitor pairs (Figure 1A and Table S1) (Fabian et al., 2005; Karaman et al., 2008).”
Leveraging molecular structure and bioactivity with chemical language models for de novo drug design (2023, methodology): “Competition of the test compound with the immobilized ligand was measured via quantitativePCR (qPCR) of the DNA tag of DNA-tagged kinase 70 .”
Advances in immunotherapy for hepatocellular carcinoma (2021, background): “I.M. receives funding from MINECO SAF2014-52361-R and SAF 2017- 83267-C2-1R; Worldwide Cancer Research Grant (15-1146); the Asociacion Española Contra el Cancer (AECC) Foundation under grant GCB15152947MELE; and the European Union’s Horizon 2020 Program (grant agreement no. 635122 PROCROP).”
Quantitative chemical proteomics reveals mechanisms of action of clinical ABL kinase inhibitors (2007, background): “Conventional drug discovery mostly relies on panels of recombinant enzymes and cellular model systems to address compound potency, selectivity and potential off-target liabilities rather than attempting to determine the bona fide targets of a drug directly in an unbiased manne”
A dual PI3 kinase/mTOR inhibitor reveals emergent efficacy in glioma. (2006, positive): “Control siRNA directed against luciferase GL3 ( Elbashir et al., 2001 ) and p110a”