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@ARTICLE{Bhatia:907780,
author = {Bhatia, Sanil and Spanier, Lukas and Bickel, David and
Dienstbier, Niklas and Woloschin, Vitalij and Vogt, Melina
and Pols, Henrik and Lungerich, Beate and Reiners, Jens and
Aghaallaei, Narges and Diedrich, Daniela and Frieg, Benedikt
and Schliehe-Diecks, Julian and Bopp, Bertan and Lang,
Franziska and Gopalswamy, Mohanraj and Loschwitz, Jennifer
and Bajohgli, Baubak and Skokowa, Julia and Borkhardt, Arndt
and Hauer, Julia and Hansen, Finn K. and Smits, Sander H. J.
and Jose, Joachim and Gohlke, Holger and Kurz, Thomas},
title = {{D}evelopment of a {F}irst-in-{C}lass {S}mall-{M}olecule
{I}nhibitor of the {C}-{T}erminal {H}sp90 {D}imerization},
journal = {ACS central science},
volume = {8},
number = {5},
issn = {2374-7943},
address = {Washington, DC},
publisher = {ACS Publ.},
reportid = {FZJ-2022-02209},
pages = {636–655},
year = {2022},
abstract = {Heat shock proteins 90 (Hsp90) are promising therapeutic
targets due to their involvement in stabilizing several
aberrantly expressed oncoproteins. In cancerous cells, Hsp90
expression is elevated, thereby exerting antiapoptotic
effects, which is essential for the malignant transformation
and tumor progression. Most of the Hsp90 inhibitors (Hsp90i)
under investigation target the ATP binding site in the
N-terminal domain of Hsp90. However, adverse effects,
including induction of the prosurvival resistance mechanism
(heat shock response or HSR) and associated dose-limiting
toxicity, have so far precluded their clinical approval. In
contrast, modulators that interfere with the C-terminal
domain (CTD) of Hsp90 do not inflict HSR. Since the CTD
dimerization of Hsp90 is essential for its chaperone
activity, interfering with the dimerization process by
small-molecule protein–protein interaction inhibitors is a
promising strategy for anticancer drug research. We have
developed a first-in-class small-molecule inhibitor (5b)
targeting the Hsp90 CTD dimerization interface, based on a
tripyrimidonamide scaffold through structure-based molecular
design, chemical synthesis, binding mode model prediction,
assessment of the biochemical affinity, and efficacy against
therapy-resistant leukemia cells. 5b reduces
xenotransplantation of leukemia cells in zebrafish models
and induces apoptosis in BCR-ABL1+ (T315I) tyrosine kinase
inhibitor-resistant leukemia cells, without inducing HSR.},
cin = {IBG-4 / JSC / NIC / IBI-7},
ddc = {540},
cid = {I:(DE-Juel1)IBG-4-20200403 / I:(DE-Juel1)JSC-20090406 /
I:(DE-Juel1)NIC-20090406 / I:(DE-Juel1)IBI-7-20200312},
pnm = {5111 - Domain-Specific Simulation $\&$ Data Life Cycle Labs
(SDLs) and Research Groups (POF4-511) / 2171 - Biological
and environmental resources for sustainable use (POF4-217) /
Forschergruppe Gohlke $(hkf7_20200501)$ / 5241 - Molecular
Information Processing in Cellular Systems (POF4-524)},
pid = {G:(DE-HGF)POF4-5111 / G:(DE-HGF)POF4-2171 /
$G:(DE-Juel1)hkf7_20200501$ / G:(DE-HGF)POF4-5241},
typ = {PUB:(DE-HGF)16},
pubmed = {35647282},
UT = {WOS:000806002600015},
doi = {10.1021/acscentsci.2c00013},
url = {https://juser.fz-juelich.de/record/907780},
}