59147-02-3Relevant articles and documents
[9,9]-Sigmatropic Shift in a Benzidine-Type Rearrangement
Park, Koon Ha,Kang, Jin Soo
, p. 3794 - 3795 (1997)
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Novel substituted benzoyl compound and its pharmaceutically acceptable salt and preparation method and application (by machine translation)
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Paragraph 0206-0207; 0211-0212, (2019/11/13)
The invention relates to the general formula I shown novel substituted benzoyl compound and its pharmaceutically acceptable salt and preparation method and application. The invention also provides pharmaceutical compositions containing them, in vitro and in vivo anti-tumor effect results and acute toxicity study, the obtained anti-tumor drug model substituted benzoyl compound, has more excellent anti-tumor activity and safety, can be in the treatment of leukemia, lung cancer, colon cancer, ovarian cancer and renal carcinoma tumor in the application, so that the therapeutic window, so in the medical field as antitumor agents in the very application value. (by machine translation)
Selective PPARδ Modulators Improve Mitochondrial Function: Potential Treatment for Duchenne Muscular Dystrophy (DMD)
Lagu, Bharat,Kluge, Arthur F.,Tozzo, Effie,Fredenburg, Ross,Bell, Eric L.,Goddeeris, Matthew M.,Dwyer, Peter,Basinski, Andrew,Senaiar, Ramesh S.,Jaleel, Mahaboobi,Tiwari, Nirbhay Kumar,Panigrahi, Sunil K.,Krishnamurthy, Narasimha Rao,Takahashi, Taisuke,Patane, Michael A.
supporting information, p. 935 - 940 (2018/09/06)
The X-ray structure of the previously reported PPARδ modulator 1 bound to the ligand binding domain (LBD) revealed that the amide moiety in 1 exists in the thermodynamically disfavored cis-amide orientation. Isosteric replacement of the cis-amide with five-membered heterocycles led to the identification of imidazole 17 (MA-0204), a potent, selective PPARδ modulator with good pharmacokinetic properties. MA-0204 was tested in vivo in mice and in vitro in patient-derived muscle myoblasts (from Duchenne Muscular Dystrophy (DMD) patients); 17 altered the expression of PPARδ target genes and improved fatty acid oxidation, which supports the therapeutic hypothesis for the study of MA-0204 in DMD patients.