% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{GalvezBPedreira:300125,
      author       = {J. Galvez B Pedreira and P. Woelffing and M. Schwarz and S.
                      Ebner and R. Rudalska and B. Masberg and A. Esposito and A.
                      Rashidian and E. Schevchenko and L. Smutna and P. Pavek and
                      J. Kublbeck and T. Kronenberger and L. Zender$^*$ and M.
                      Lämmerhofer and D. Dauch and S. A. Laufer},
      title        = {{U}ncovering α-{S}electivity for {L}iver {X} {R}eceptor
                      {A}gonists for {L}ipotoxic {C}ancer {T}herapies.},
      journal      = {Journal of medicinal chemistry},
      volume       = {68},
      number       = {7},
      issn         = {0095-9065},
      address      = {Washington, DC},
      publisher    = {ACS},
      reportid     = {DKFZ-2025-00623},
      pages        = {7180-7196},
      year         = {2025},
      note         = {2025 Apr 10;68(7):7180-7196},
      abstract     = {Hepatocellular carcinoma (HCC) is one of the most frequent
                      causes of cancer-related deaths worldwide. We recently
                      showed that pharmacologically induced lipotoxicity
                      represents a promising therapeutic strategy for the
                      treatment of HCC. Synthetic LXRα agonists induce the
                      production of toxic saturated fatty acids in tumor cells.
                      When combined with DFG-out Raf inhibitors, which block fatty
                      acid desaturation by inducing proteasomal degradation of
                      stearoyl-CoA desaturase (SCD1), LXRα activation can trigger
                      lipotoxicity-induced cancer cell death. However, the
                      clinical translation of this therapeutic strategy is limited
                      by the lack of specific LXRα agonists for clinical use.
                      Here, we have developed a series of promising maleimide LXR
                      agonists with increased potency for LXRα and enhanced
                      specificity. Our agonist frontrunner 40 shows high
                      selectivity for LXRα and strong therapeutic efficacy in HCC
                      organoids, therefore illustrating a strong potential for
                      advancing this lipotoxic treatment strategy to clinical
                      application.},
      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:40127224},
      doi          = {10.1021/acs.jmedchem.4c02712},
      url          = {https://inrepo02.dkfz.de/record/300125},
}