117490-57-0Relevant articles and documents
Synthesis of the β2-Agonist Tulobuterol and Its Metabolite 4-Hydroxytulobuterol
Burdeinyi, M. L.,Glushkova, M. A.,Popkov, S. V.
, p. 390 - 394 (2020/04/27)
Abstract: Alternative methods have been developed for the synthesis of theβ2-agonist tulobuterol and its metabolite4-hydroxytulobuterol with a similar activity. The proposed procedures utilizeavailable reagents, and the key stage in the synthesis is the formation ofintermediate oxirane according to the Corey–Chaykovsky reaction, followed byopening of the oxirane ring by the action of excess tert-butylamine. In the synthesis of 4-hydroxytulobuterol, thehydroxy group was protected by benzylation, and the protecting group was removedin the final stage by hydrogenation over carbon-supported palladium.
Control of the intracellular levels of prostaglandin E2 through inhibition of the 15-hydroxyprostaglandin dehydrogenase for wound healing
Choi, Dubok,Piao, Yu Lan,Wu, Ying,Cho, Hoon
, p. 4477 - 4484 (2013/07/26)
Excessive scar formation is an aberrant form of wound healing and is an indication of an exaggerated function of fibroblasts and excess accumulation of extracellular matrix during wound healing. Much experimental data suggests that prostaglandin E2 (PGE2) plays a role in the prevention of excessive scarring. However, it has a very short half-live in blood, its oxidization to 15-ketoprostaglandins is catalyzed by 15-hydroxyprostaglandin dehydrogenase (15-PGDH). Previously, we reported that 15-PGDH inhibitors significantly increased PGE2 levels in A549 cells. In our continuing attempts to develop highly potent 15-PGDH inhibitors, we newly synthesized various thiazolidine-2,4-dione derivatives. Compound 27, 28, 29, and 30 demonstrated IC50 values of 0.048, 0.020, 0.038 and 0.048 μM, respectively. They also increased levels of PGE2 in A549 cells. Especially, compound 28 significantly increased level of PGE2 at 260 pg/mL, which was approximately fivefold higher than that of control. Scratch wounds were analyzed in confluent monolayers of HaCaT cells. Cells exposed to compound 28 showed significantly improved wound healing with respect to control.
SUBSTITUTED AZOLE DERIVATIVES, PHARMACEUTICAL COMPOSITION CONTAINING THE DERIVATIVES, AND METHOD FOR TREATING PARKINSON'S DISEASE USING THE SAME
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Paragraph 188-189, (2010/09/17)
Provided are a substituted azole derivative and pharmaceutically acceptable salts thereof, a pharmaceutical composition including an effective amount of the derivative, and a method for treating Parkinson's disease in a mammal including administering an e