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@ARTICLE{Wydra:301539,
author = {V. R. Wydra and N. Plank and S. Zwirner and R. Selig and A.
Rasch and B. Masberg and M. Lämmerhofer and L. Zender$^*$
and P. Koch and W. Albrecht and S. Laufer$^*$},
title = {{A} '{L}igand {F}irst' {A}pproach toward {S}elective,
{C}ovalent {JNK}2/3 {I}nhibitors.},
journal = {Journal of medicinal chemistry},
volume = {68},
number = {11},
issn = {0095-9065},
address = {Washington, DC},
publisher = {ACS},
reportid = {DKFZ-2025-01060},
pages = {12004-12028},
year = {2025},
note = {2025 Jun 12;68(11):12004-12028},
abstract = {All JNK isoforms play a specific role in various diseases.
The role of the JNK2 isoform has so far received little
attention compared to its JNK1 and JNK3 counterparts with
JNK3 being a potential target for neurodegenerative diseases
and an inhibitor with JNK1 bias being currently investigated
in clinical trials. Using an iterative, structure-guided
optimization approach starting from a reported reversible
binding aminopyrazole-derived scaffold, novel highly potent
JNK2/3 selective inhibitors were generated ('ligand-first
approach'). These reversible inhibitors were further
transformed to covalent inhibitors by attaching an
electrophilic warhead moiety, able to address a conserved
cysteine side chain present in JNKs. Reversible and covalent
inhibitors presented in this study show high JNK2/3 isoform
selectivity and activity in cells. The covalently acting
lead compound 56d shows good kinetic data with a kinact/KI
(JNK2) = 38,200 M-1 s-1 as well as cellular isoform
selectivity and a clean kinome profile.},
cin = {TU01},
ddc = {610},
cid = {I:(DE-He78)TU01-20160331},
pnm = {899 - ohne Topic (POF4-899)},
pid = {G:(DE-HGF)POF4-899},
typ = {PUB:(DE-HGF)16},
pubmed = {pmid:40404564},
doi = {10.1021/acs.jmedchem.5c00884},
url = {https://inrepo02.dkfz.de/record/301539},
}