Wu, Keke et al. published their research in Life Sciences in 2021 | CAS: 1094-61-7

((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate (cas: 1094-61-7) belongs to amides. In primary and secondary amides, the presence of N–H dipoles allows amides to function as H-bond donors as well. Thus amides can participate in hydrogen bonding with water and other protic solvents; the oxygen atom can accept hydrogen bonds from water and the N–H hydrogen atoms can donate H-bonds. Amides can be freed from solvent or water by drying below their melting points. These purifications can also be used for sulfonamides and acid hydrazides.Reference of 1094-61-7

Nicotinamide mononucleotide attenuates isoproterenol-induced cardiac fibrosis by regulating oxidative stress and Smad3 acetylation was written by Wu, Keke;Li, Biao;Lin, Qiuzhen;Xu, Wanghan;Zuo, Wanyun;Li, Jiayi;Liu, Na;Tu, Tao;Zhang, Baojian;Xiao, Yichao;Liu, Qiming. And the article was included in Life Sciences in 2021.Reference of 1094-61-7 The following contents are mentioned in the article:

Cardiac fibrosis is a pathol. hallmark of progressive heart diseases currently lacking effective treatment. NMN (NMN), a member of the vitamin B3 family, is a defined biosynthetic precursor of NAD (NAD+). Its beneficial effects on cardiac diseases are known, but its effects on cardiac fibrosis and the underlying mechanism remain unclear. We aimed to elucidate the protective effect of NMN against cardiac fibrosis and its underlying mechanisms of action. Cardiac fibrosis was induced by isoproterenol (ISO) in mice. NMN was administered by i.p. injection. In vitro, cardiac fibroblasts (CFs) were stimulated by transforming growth factor-beta (TGF-β) with or without NMN and sirtinol, a SIRT1 inhibitor. Levels of cardiac fibrosis, NAD+/SIRT1 alteration, oxidative stress, and Smad3 acetylation were evaluated by real-time polymerase chain reaction, western blots, immunohistochem. staining, immunoprecipitation, and assay kits. ISO treatment induced cardiac dysfunction, fibrosis, and hypertrophy in vivo, whereas NMN alleviated these changes. Addnl., NMN suppressed CFs activation stimulated by TGF-β in vitro. Mechanistically, NMN restored the NAD+/SIRT1 axis and inhibited the oxidative stress and Smad3 acetylation induced by ISO or TGF-β. However, the protective effects of NMN were partly antagonized by sirtinol in vitro. NMN could attenuate cardiac fibrosis in vivo and fibroblast activation in vitro by suppressing oxidative stress and Smad3 acetylation in a NAD+/SIRT1-dependent manner. This study involved multiple reactions and reactants, such as ((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate (cas: 1094-61-7Reference of 1094-61-7).

((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate (cas: 1094-61-7) belongs to amides. In primary and secondary amides, the presence of N–H dipoles allows amides to function as H-bond donors as well. Thus amides can participate in hydrogen bonding with water and other protic solvents; the oxygen atom can accept hydrogen bonds from water and the N–H hydrogen atoms can donate H-bonds. Amides can be freed from solvent or water by drying below their melting points. These purifications can also be used for sulfonamides and acid hydrazides.Reference of 1094-61-7

Referemce:
Amide – Wikipedia,
Amide – an overview | ScienceDirect Topics