Xu, Lin et al. published their research in Human & Experimental Toxicology 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. Ionic, or saltlike, amides are strongly alkaline compounds ordinarily made by treating ammonia, an amine, or a covalent amide with a reactive metal such as sodium.Category: amides-buliding-blocks

NAMPT-mediated NAD+ biosynthesis suppresses activation of hepatic stellate cells and protects against CCl4-induced liver fibrosis in mice was written by Xu, Lin;Yang, Chenyan;Ma, Jie;Zhang, Xinge;Wang, Qingzhi;Xiong, Xiwen. And the article was included in Human & Experimental Toxicology in 2021.Category: amides-buliding-blocks The following contents are mentioned in the article:

Nicotinamide phosphoribosyltransferase (NAMPT) catalyzes the rate-limiting step in the salvage pathway of mammalian NAD (NAD+) biosynthesis. Through its NAD+-biosynthetic activity, NAMPT is able to regulate the development of hepatic steatosis and inflammation induced by diet or alc. However, the roles NAMPT plays in the development of liver fibrosis remain obscure. To investigate the roles of NAMPT-mediated NAD+ biosynthesis in hepatic stellate cell (HSC) activation and liver fibrosis. Realtime RT-PCR and western blot analyses were performed to analyze the expression of profibrogenic genes. Sirius red staining was conducted to examine the fibrosis in liver. Mouse liver fibrosis was induced by i.p. injection of carbon tetrachloride (CCl4) 2 times a week for 6 wk. Adenovirus-mediated NAMPT overexpression or NMN (NMN) administration was carried out to study the effects of elevation of NAD+ levels on protecting CCl4-induced liver fibrosis in mice. The LX2 cells or primary HSCs were used to study the role of NAMPT overexpression or NMN treatment in reducing profibrogenic gene expression in vitro. The CCl4 administration suppresses NAMPT expression in liver and reduces hepatic NAD+ content. The Tgfβ1 treatment decreases intracellular NAD+ levels and NAMPT expression in LX2 cells. Adenovirus-mediated NAMPT overexpression augments liver NAD+ levels, inhibits HSC activation and alleviates CCl4-induced liver fibrosis in mice. Administration of NMN also suppresses HSC activation and protects against CCl4-induced liver fibrosis in mice. The NAMPT-mediated NAD+ biosynthesis inhibits HSC activation and protects against CCl4-induced liver fibrosis. 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: 1094-61-7Category: amides-buliding-blocks).

((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. Ionic, or saltlike, amides are strongly alkaline compounds ordinarily made by treating ammonia, an amine, or a covalent amide with a reactive metal such as sodium.Category: amides-buliding-blocks

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