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6vh4

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(New page: '''Unreleased structure''' The entry 6vh4 is ON HOLD Authors: Description: Category: Unreleased Structures)
Current revision (09:14, 9 October 2024) (edit) (undo)
 
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'''Unreleased structure'''
 
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The entry 6vh4 is ON HOLD
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==Wild type EGFR in complex with LN2380==
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<StructureSection load='6vh4' size='340' side='right'caption='[[6vh4]], [[Resolution|resolution]] 2.80&Aring;' scene=''>
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== Structural highlights ==
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<table><tr><td colspan='2'>Full crystallographic information is available from [http://oca.weizmann.ac.il/oca-bin/ocashort?id=6VH4 OCA]. For a <b>guided tour on the structure components</b> use [https://proteopedia.org/fgij/fg.htm?mol=6VH4 FirstGlance]. <br>
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</td></tr><tr id='method'><td class="sblockLbl"><b>[[Empirical_models|Method:]]</b></td><td class="sblockDat" id="methodDat">X-ray diffraction, [[Resolution|Resolution]] 2.8&#8491;</td></tr>
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<tr id='ligand'><td class="sblockLbl"><b>[[Ligand|Ligands:]]</b></td><td class="sblockDat" id="ligandDat"><scene name='pdbligand=QQM:N-[3-({4-[4-(4-fluorophenyl)-2-(3-hydroxypropyl)-1H-imidazol-5-yl]pyridin-2-yl}amino)-4-methoxyphenyl]propanamide'>QQM</scene></td></tr>
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<tr id='resources'><td class="sblockLbl"><b>Resources:</b></td><td class="sblockDat"><span class='plainlinks'>[https://proteopedia.org/fgij/fg.htm?mol=6vh4 FirstGlance], [http://oca.weizmann.ac.il/oca-bin/ocaids?id=6vh4 OCA], [https://pdbe.org/6vh4 PDBe], [https://www.rcsb.org/pdb/explore.do?structureId=6vh4 RCSB], [https://www.ebi.ac.uk/pdbsum/6vh4 PDBsum], [https://prosat.h-its.org/prosat/prosatexe?pdbcode=6vh4 ProSAT]</span></td></tr>
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</table>
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<div style="background-color:#fffaf0;">
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== Publication Abstract from PubMed ==
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Acquired drug resistance in epidermal growth factor receptor (EGFR) mutant non-small-cell lung cancer is a persistent challenge in cancer therapy. Previous studies of trisubstituted imidazole inhibitors led to the serendipitous discovery of inhibitors that target the drug resistant EGFR(L858R/T790M/C797S) mutant with nanomolar potencies in a reversible binding mechanism. To dissect the molecular basis for their activity, we determined the binding modes of several trisubstituted imidazole inhibitors in complex with the EGFR kinase domain with X-ray crystallography. These structures reveal that the imidazole core acts as an H-bond acceptor for the catalytic lysine (K745) in the "alphaC-helix out" inactive state. Selective N-methylation of the H-bond accepting nitrogen ablates inhibitor potency, confirming the role of the K745 H-bond in potent, noncovalent inhibition of the C797S variant. Insights from these studies offer new strategies for developing next generation inhibitors targeting EGFR in non-small-cell lung cancer.
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Authors:
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Structural Basis for EGFR Mutant Inhibition by Trisubstituted Imidazole Inhibitors.,Heppner DE, Gunther M, Wittlinger F, Laufer SA, Eck MJ J Med Chem. 2020 Apr 14. doi: 10.1021/acs.jmedchem.0c00200. PMID:32243152<ref>PMID:32243152</ref>
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Description:
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From MEDLINE&reg;/PubMed&reg;, a database of the U.S. National Library of Medicine.<br>
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[[Category: Unreleased Structures]]
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</div>
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<div class="pdbe-citations 6vh4" style="background-color:#fffaf0;"></div>
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==See Also==
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*[[Epidermal growth factor receptor 3D structures|Epidermal growth factor receptor 3D structures]]
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== References ==
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<references/>
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__TOC__
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</StructureSection>
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[[Category: Large Structures]]
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[[Category: Eck MJ]]
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[[Category: Heppner DE]]

Current revision

Wild type EGFR in complex with LN2380

PDB ID 6vh4

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