Tranilast inhibits pulmonary fibrosis by suppressing TGFβ/SMAD2 pathway was written by Kato, Motoyasu;Takahashi, Fumiyuki;Sato, Tadashi;Mitsuishi, Yoichiro;Tajima, Ken;Ihara, Hiroaki;Nurwidya, Fariz;Baskoro, Hario;Murakami, Akiko;Kobayashi, Isao;Hidayat, Moulid;Shimada, Naoko;Sasaki, Shinichi;Mineki, Reiko;Fujimura, Tsutomu;Kumasaka, Toshio;Niwa, Shin-ichiro;Takahashi, Kazuhisa. And the article was included in Drug Design, Development and Therapy in 2020.Quality Control of 2-(3-(3,4-Dimethoxyphenyl)acrylamido)benzoic acid This article mentions the following:
Purpose: Idiopathic pulmonary fibrosis (IPF) is characterized by the accumulation of extracellular matrix (ECM) protein in the lungs. Transforming growth factor (TGF) β- induced ECM protein synthesis contributes to the development of IPF. Tranilast, an antiallergy drug, suppresses TGFβ expression and inhibits interstitial renal fibrosis in animal models. However, the beneficial effects of tranilast or its mechanism as a therapy for pulmonary fibrosis have not been clarified. Methods: We investigated the in vitro effect of tranilast on ECM production and TGFβ/SMAD2 pathway in TGFβ2-stimulated A549 human alveolar epithelial cells, using quant. polymerase chain reaction, Western blotting, and immunofluorescence. In vitro observations were validated in the lungs of a murine pulmonary fibrosis model, which we developed by i.v. injection of bleomycin. Results: Treatment with tranilast suppressed the expression of ECM proteins, such as fibronectin and type IV collagen, and attenuated SMAD2 phosphorylation in TGFβ2-stimulated A549 cells. In addition, based on a wound healing assay in these cells, tranilast significantly inhibited cell motility, with foci formation that comprised of ECM proteins. Histol. analyses revealed that the administration of tranilast significantly attenuated lung fibrosis in mice. Furthermore, tranilast treatment significantly reduced levels of TGFβ, collagen, fibronectin, and phosphorylated SMAD2 in pulmonary fibrotic tissues in mice. Conclusion: These findings suggest that tranilast inhibits pulmonary fibrosis by suppressing TGFβ/SMAD2-mediated ECM protein production, presenting tranilast as a promising and novel anti-fibrotic agent for the treatment of IPF. In the experiment, the researchers used many compounds, for example, 2-(3-(3,4-Dimethoxyphenyl)acrylamido)benzoic acid (cas: 53902-12-8Quality Control of 2-(3-(3,4-Dimethoxyphenyl)acrylamido)benzoic acid).
2-(3-(3,4-Dimethoxyphenyl)acrylamido)benzoic acid (cas: 53902-12-8) belongs to amides. Because of the greater electronegativity of oxygen, the carbonyl (C=O) is a stronger dipole than the N–C dipole. The presence of a C=O dipole and, to a lesser extent a N–C dipole, allows amides to act as H-bond acceptors. Amides can be recrystallised from large quantities of water, ethanol, ethanol/ether, aqueous ethanol, chloroform/toluene, chloroform or acetic acid. The likely impurities are the parent acids or the alkyl esters from which they have been made. The former can be removed by thorough washing with aqueous ammonia followed by recrystallisation, whereas elimination of the latter is by trituration or recrystallisation from an organic solvent.Quality Control of 2-(3-(3,4-Dimethoxyphenyl)acrylamido)benzoic acid
Referemce:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics