1073353-55-5Relevant articles and documents
Pyridoazepine derivative, pharmaceutical composition and applications thereof
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Paragraph 0148-0149; 0151; 0155-0157, (2019/05/16)
The present invention discloses a pyridoazepine derivative, a pharmaceutical composition and applications thereof, wherein the pyridoazepine derivative (I), the isomer, the prodrug, the stable isotopederivative or the pharmaceutically acceptable salt thereof have the following structure. According to the present invention, the pyridoazepine derivative has good regulatory effects on TLR family andrelated signaling pathways, particularly on TLR8, can effectively treat, alleviate and/or prevent various diseases mediated by signaling pathways related to TLR family and TLR, and particularly can effectively treat, alleviate and/or prevent various TLR8 mediated diseases such as cancers, autoimmune diseases, infections, inflammations, transplant rejections, graft versus host diseases and the like. The formula (I) is defined in the specification.
Identification of new γ-hydroxybutenolides that preferentially inhibit the activity of mPGES-1
De Simone, Rosa,Bruno, Ines,Riccio, Raffaele,Stadler, Katharina,Bauer, Julia,Schaible, Anja M.,Laufer, Stefan,Werz, Oliver
, p. 5012 - 5016 (2012/09/22)
Microsomal prostaglandin E2 synthase-1 (mPGES-1) has been recognized as novel, promising drug target for anti-inflammatory and anticancer drugs. mPGES-1 catalyzes the synthesis of the inducible prostaglandin E 2 in response to pro-inflammatory stimuli, rendering this enzyme extremely interesting in drug discovery process owing to the drastic reduction of the severe side effects typical for traditional non-steroidal anti-inflammatory drugs. In the course of our investigations focused on this topic, we identified two interesting molecules bearing the γ- hydroxybutenolide scaffold which potently inhibit the activity of mPGES-1. Notably, the lead compound 2c that inhibited mPGES-1 with IC50 = 0.9 μM, did not affect other related enzymes within the arachidonic acid cascade.