R
Rolf W. Hartmann
Researcher at Saarland University
Publications - 371
Citations - 8686
Rolf W. Hartmann is an academic researcher from Saarland University. The author has contributed to research in topics: Aromatase & Enzyme. The author has an hindex of 47, co-authored 365 publications receiving 7834 citations. Previous affiliations of Rolf W. Hartmann include University of Regensburg & Free University of Berlin.
Papers
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Journal ArticleDOI
Targeting Steroidogenic Cytochromes P450 (CYPs) with 6‐Substituted 1‐Imidazolylmethylxanthones
Silvia Gobbi,Qingzhong Hu,Qingzhong Hu,Christina Zimmer,Federica Belluti,Angela Rampa,Rolf W. Hartmann,Alessandra Bisi +7 more
TL;DR: A small library of imidazolylmethylxanthones was designed based on the results of a previously described compound series, showing selectivity toward the related steroidogenic enzymes CYP19 and CYP17, even if the problem of selectivity between the two CYP11B isoforms remains unsolved.
Journal ArticleDOI
Evaluation of Cell Permeation of a Potent 5α-Reductase Inhibitor Using MALDI-TOF MS
Sonal Mathur,Franck Picard,Ulrich Dossou,Catherine Barassin,Stefanie B. Seidel,Min Jung Kang,Rolf W. Hartmann +6 more
TL;DR: Results suggest that the in vivo activity of 1 might be increased by the use of its methyl ester prodrug 1a, which showed a stronger inhibition of 5αR in intact DU145 cells than 1.
Journal ArticleDOI
Targeted Endocrine Therapy: Design, Synthesis, and Proof-of-Principle of 17β-Hydroxysteroid Dehydrogenase Type 2 Inhibitors in Bone Fracture Healing
Ahmed S. Abdelsamie,Steven C. Herath,Yannik Biskupek,Carsten Börger,Lorenz Siebenbürger,Mohamed Salah,Claudia Scheuer,Sandrine Marchais-Oberwinkler,Martin Frotscher,Tim Pohlemann,Michael D. Menger,Rolf W. Hartmann,Matthias W. Laschke,Chris J. van Koppen +13 more
TL;DR: Administration of compound 15 in the mouse fracture model strongly increases the mechanical stability of the healing fractured bone because of a larger periosteal callus with newly formed bone without changing the plasma E2 and T concentrations, and enables targeted intracrine therapy.
Book ChapterDOI
Synthetic Quorum Sensing Inhibitors (QSIs) Blocking Receptor Signaling or Signal Molecule Biosynthesis in Pseudomonas aeruginosa
TL;DR: The interruption of these pathways by blocking the receptors or inhibiting the signal synthesis via small molecules is an attractive therapeutic strategy to attenuate the bacterial pathogenicity, thereby overcoming intractable P. aeruginosa infections.