Tag: 300-400

Aqueous metabolome of tissue-specific conditional Pten-knockout mouse prostate cancer and TRAMP neuroendocrine carcinoma was written by Kim, Sangyub;Li, Li;Zhang, Jinhui;Jiang, Cheng;Lue, Junxuan. And the article was included in Prostate (Hoboken, NJ, United States) in 2022.Computed Properties of C11H15N2O8P The following contents are mentioned in the article:

Metabolic reprograming is now a recognized hallmark of cancer. The prostate-specific phosphatase and tensin homolog deleted on chromosome 10 (Pten) gene-conditional knockout (KO) mouse carcinogenesis model is highly desirable for studying prostate cancer biol. and prevention due to its close resemblance of primary mol. defects and histopathol. features of human prostate cancer. We have recently published macromol. profiling of this model by proteomics and transcriptomics, denoting a preeminence of inflammation and myeloid suppressive immune cell features. Here, we performed metabolomic analyses of Pten-KO prostate vs. wild type (WT) counterpart for discernable changes in the aqueous metabolites and contrasted to those in the TRAMP neuroendocrine carcinoma (NECa). Three matched pairs of tissue-specific conditional Pten-KO mouse prostate and WT prostate of litter/cage-mates at 20-22 wk of age and three pairs of TRAMP NECa vs. WT (28-31 wk) were profiled for their global aqueous metabolite changes, using hydrophilic interaction liquid chromatog.-tandem mass spectrometry. The Pten-KO prostate increased purine nucleotide pools, cystathionine, and both reduced and oxidized glutathione (GSH, GSSG), and gluconate/glucuronate species in addition to cholesteryl sulfate and polyamine precursor ornithine. On the contrary, Pten-KO prostate contained diminished pools of glycolytic intermediates and phosphorylcholine derivatives, select amino acids, and their metabolites. Bioinformatic integration revealed a significant shunting of glucose away from glycolysis-citrate cycle and glycerol-lipid genesis to pentose phosphate cycle for NADPH/GSH/GSSG redox and pentose moieties for purine and pyrimidine nucleotides, and glycosylation/glucuronidation. Implicit arginine catabolism to ornithine was consistent with immunosuppression in Pten-KO model. While also increased in cystathionine-GSH/GSSG, purine, and pyrimidine nucleotide pools and glucuronidation at the expense of glycolysis-citrate cycle, the TRAMP NECa increased abundance of many amino acids, Me donor S-adenosyl-methionine, and intermediates for phospholipids without increasing cholesteryl sulfate or ornithine. The aqueous metabolomic patterns in Pten-KO prostate and TRAMP NECa shared similarities in the greater pools of cystathionine, GSH/GSSG redox pair, and nucleotides and shunting away from glycolysis-citrate cycle in both models. Remarkable metabolic distinctions between them included metabolisms of many amino acids (protein synthesis; arginine-ornithine/immune suppression) and cholesteryl sulfate and methylation donor for epigenetic regulations. 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: 1094-61-7Computed Properties of C11H15N2O8P).

((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. Amides are pervasive in nature and technology. Proteins and important plastics like Nylons, Aramid, Twaron, and Kevlar are polymers whose units are connected by amide groups (polyamides); these linkages are easily formed, confer structural rigidity, and resist hydrolysis. In simple aromatic amides, fragmentation occurs on both sides of the carbonyl group. If a hydrogen is available in N-substituted aromatic amides, it tends to migrate and form an aromatic amine and the loss of a ketene.Computed Properties of C11H15N2O8P

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

Aqueous metabolome of tissue-specific conditional Pten-knockout mouse prostate cancer and TRAMP neuroendocrine carcinoma was written by Kim, Sangyub;Li, Li;Zhang, Jinhui;Jiang, Cheng;Lue, Junxuan. And the article was included in Prostate (Hoboken, NJ, United States) in 2022.Recommanded Product: 1094-61-7 The following contents are mentioned in the article:

Metabolic reprograming is now a recognized hallmark of cancer. The prostate-specific phosphatase and tensin homolog deleted on chromosome 10 (Pten) gene-conditional knockout (KO) mouse carcinogenesis model is highly desirable for studying prostate cancer biol. and prevention due to its close resemblance of primary mol. defects and histopathol. features of human prostate cancer. We have recently published macromol. profiling of this model by proteomics and transcriptomics, denoting a preeminence of inflammation and myeloid suppressive immune cell features. Here, we performed metabolomic analyses of Pten-KO prostate vs. wild type (WT) counterpart for discernable changes in the aqueous metabolites and contrasted to those in the TRAMP neuroendocrine carcinoma (NECa). Three matched pairs of tissue-specific conditional Pten-KO mouse prostate and WT prostate of litter/cage-mates at 20-22 wk of age and three pairs of TRAMP NECa vs. WT (28-31 wk) were profiled for their global aqueous metabolite changes, using hydrophilic interaction liquid chromatog.-tandem mass spectrometry. The Pten-KO prostate increased purine nucleotide pools, cystathionine, and both reduced and oxidized glutathione (GSH, GSSG), and gluconate/glucuronate species in addition to cholesteryl sulfate and polyamine precursor ornithine. On the contrary, Pten-KO prostate contained diminished pools of glycolytic intermediates and phosphorylcholine derivatives, select amino acids, and their metabolites. Bioinformatic integration revealed a significant shunting of glucose away from glycolysis-citrate cycle and glycerol-lipid genesis to pentose phosphate cycle for NADPH/GSH/GSSG redox and pentose moieties for purine and pyrimidine nucleotides, and glycosylation/glucuronidation. Implicit arginine catabolism to ornithine was consistent with immunosuppression in Pten-KO model. While also increased in cystathionine-GSH/GSSG, purine, and pyrimidine nucleotide pools and glucuronidation at the expense of glycolysis-citrate cycle, the TRAMP NECa increased abundance of many amino acids, Me donor S-adenosyl-methionine, and intermediates for phospholipids without increasing cholesteryl sulfate or ornithine. The aqueous metabolomic patterns in Pten-KO prostate and TRAMP NECa shared similarities in the greater pools of cystathionine, GSH/GSSG redox pair, and nucleotides and shunting away from glycolysis-citrate cycle in both models. Remarkable metabolic distinctions between them included metabolisms of many amino acids (protein synthesis; arginine-ornithine/immune suppression) and cholesteryl sulfate and methylation donor for epigenetic regulations. 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: 1094-61-7Recommanded Product: 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. The solubilities of amides and esters are roughly comparable. Typically amides are less soluble than comparable amines and carboxylic acids since these compounds can both donate and accept hydrogen bonds. Tertiary amides, with the important exception of N,N-dimethylformamide, exhibit low solubility in water. In simple aromatic amides, fragmentation occurs on both sides of the carbonyl group. If a hydrogen is available in N-substituted aromatic amides, it tends to migrate and form an aromatic amine and the loss of a ketene.Recommanded Product: 1094-61-7

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

Nicotinamide mononucleotide administration triggers macrophages reprogramming and alleviates inflammation during sepsis induced by experimental peritonitis was written by Cros, Cecile;Margier, Marielle;Cannelle, Helene;Charmetant, Julie;Hulo, Nicolas;Laganier, Laurent;Grozio, Alessia;Canault, Matthias. And the article was included in Frontiers in Molecular Biosciences in 2022.Application In Synthesis of ((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate The following contents are mentioned in the article:

Peritonitis and subsequent sepsis lead to high morbidity and mortality in response to uncontrolled systemic inflammation primarily mediated by macrophages. NAD (NAD+) is an important regulator of oxidative stress and immunoinflammatory responses. However, the effects of NAD+ replenishment during inflammatory activation are still poorly defined. Hence, we investigated whether the administration of β-NMN (β-NMN), a natural biosynthetic precursor of NAD+, could modulate the macrophage phenotype and thereby ameliorate the dysregulated inflammatory response during sepsis. For this purpose, C57BL6 mice were subjected to the cecal ligation and puncture (CLP) model to provoke sepsis or were injected with thioglycolate to induce sterile peritonitis with recruitment and differentiation of macrophages into the inflamed peritoneal cavity. βNMN was administered for 4 days after CLP and for 3 days post thioglycolate treatment where peritoneal macrophages were subsequently analyzed. In the CLP model, administration of β-NMN decreased bacterial load in blood and reduced clin. signs of distress and mortality during sepsis. These results were supported by transcriptomic anal. of hearts and lungs 24 h post CLP-induction, which revealed that β-NMN downregulated genes controlling the immuno-inflammatory response and upregulated genes involved in bioenergetic metabolism, mitochondria, and autophagy. In the thioglycolate model, a significant increase in the proportion of CD206 macrophages, marker of anti-inflammatory M2 phenotype, was detected on peritoneal exudate macrophages from β-NMN-administered mice. Transcriptomic signature of these macrophages after bacterial stimulation confirmed that β-NMN administration limited the pro-inflammatory M1 phenotype and induced the expression of specific markers of M2 type macrophages. Furthermore, our data show that β-NMN treatment significantly impacts NAD + metabolism This shift in the macrophage phenotype and metabolism was accompanied by a reduction in phagolysosome acidification and secretion of inflammatory mediators in macrophages from β-NMN-treated mice suggesting a reduced proinflammatory activation. In conclusion, administration of β-NMN prevented clin. deterioration and improved survival during sepsis. These effects relied on shifts in the metabolism of organs that face up an increased energy requirement caused by bacterial infection and in innate immunity response, including reprogramming of macrophages from a highly inflammatory phenotype to an anti-inflammatory/pro-resolving profile. 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: 1094-61-7Application In Synthesis of ((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate).

((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. The solubilities of amides and esters are roughly comparable. Typically amides are less soluble than comparable amines and carboxylic acids since these compounds can both donate and accept hydrogen bonds. Tertiary amides, with the important exception of N,N-dimethylformamide, exhibit low solubility in water. 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.Application In Synthesis of ((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate

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

Effects of NAD+ precursor supplementation on glucose and lipid metabolism in humans: a meta-analysis was written by Zhong, Ou;Wang, Jinyuan;Tan, Yongpeng;Lei, Xiaocan;Tang, Zhihan. And the article was included in Nutrition & Metabolism in 2022.Application In Synthesis of ((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate The following contents are mentioned in the article:

This meta-anal. was performed to investigate the effects of NAD (NAD+) precursor supplementation on glucose and lipid metabolism in human body. PubMed, Embase, CENTRAL, Web of Science, Scopus databases were searched to collect clin. studies related to the supplement of NAD+ precursor from inception to Feb. 2021. Then the retrieved documents were screened, the content of the documents that met the requirements was extracted Meta-anal. and quality evaluation was performed detection were performed using RevMan5.4 software. Stata16 software was used to detect publication bias, Egger and Begg methods were mainly used. The main research terms of NAD+ precursors were Nicotinamide Riboside (NR), NMN (NMN), Nicotinic Acid (NA), Nicotinamide (NAM). The changes in the levels of triglyceride (TG), total cholesterol (TC), low-d. lipoprotein (LDL), high-d. lipoprotein (HDL), and fasting blood glucose were mainly concerned. A total of 40 articles were included in the meta-anal., with a sample of 14,750 cases, including 7406 cases in the drug group and 7344 cases in the control group. The results of meta-anal. showed that: NAD+ precursor can significantly reduce TG level (SMD = – 0.35, 95% CI (- 0.52, – 0.18), P < 0.0001), and TC (SMD = – 0.33, 95% CI (- 0.51, – 0.14), P = 0.0005), and LDL (SMD = – 0.38, 95% CI (- 0.50, – 0.27), P < 0.00001), increase HDL level (SMD = 0.66, 95% CI (0.56, 0.76), P < 0.00001), and plasma glucose level in the patients (SMD = 0.27, 95% CI (0.12, 0.42), P = 0.0004). Subgroup anal. showed that supplementation of NA had the most significant effect on the levels of TG, TC, LDL, HDL and plasma glucose. In this study, a meta-anal. based on currently published clin. trials with NAD+ precursors showed that supplementation with NAD+ precursors improved TG, TC, LDL, and HDL levels in humans, but resulted in hyperglycemia, compared with placebo or no treatment. Among them, NA has the most significant effect on improving lipid metabolism In addition, although NR and NAM supplementation had no significant effect on improving human lipid metabolism, the role of NR and NAM could not be directly denied due to the few relevant studies at present. Based on subgroup anal., we found that the supplement of NAD+ precursors seems to have little effect on healthy people, but it has a significant beneficial effect on patients with cardiovascular disease and dyslipidemia. Due to the limitation of the number and quality of included studies, the above conclusions need to be verified by more high-quality studies. 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: 1094-61-7Application In Synthesis of ((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate).

((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. Amides can be viewed as a derivative of a carboxylic acid RC(=O)OH with the hydroxyl group –OH replaced by an amine group −NR′R″; or, equivalently, an acyl (alkanoyl) group RC(=O)− joined to an amine group. Amides are stable compounds. The lower-melting members (such as acetamide) can be readily purified by fractional distillation. Most amides are solids which have low solubilities in water.Application In Synthesis of ((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate

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

Effects of NAD+ precursor supplementation on glucose and lipid metabolism in humans: a meta-analysis was written by Zhong, Ou;Wang, Jinyuan;Tan, Yongpeng;Lei, Xiaocan;Tang, Zhihan. And the article was included in Nutrition & Metabolism in 2022.Synthetic Route of C11H15N2O8P The following contents are mentioned in the article:

This meta-anal. was performed to investigate the effects of NAD (NAD+) precursor supplementation on glucose and lipid metabolism in human body. PubMed, Embase, CENTRAL, Web of Science, Scopus databases were searched to collect clin. studies related to the supplement of NAD+ precursor from inception to Feb. 2021. Then the retrieved documents were screened, the content of the documents that met the requirements was extracted Meta-anal. and quality evaluation was performed detection were performed using RevMan5.4 software. Stata16 software was used to detect publication bias, Egger and Begg methods were mainly used. The main research terms of NAD+ precursors were Nicotinamide Riboside (NR), NMN (NMN), Nicotinic Acid (NA), Nicotinamide (NAM). The changes in the levels of triglyceride (TG), total cholesterol (TC), low-d. lipoprotein (LDL), high-d. lipoprotein (HDL), and fasting blood glucose were mainly concerned. A total of 40 articles were included in the meta-anal., with a sample of 14,750 cases, including 7406 cases in the drug group and 7344 cases in the control group. The results of meta-anal. showed that: NAD+ precursor can significantly reduce TG level (SMD = – 0.35, 95% CI (- 0.52, – 0.18), P < 0.0001), and TC (SMD = – 0.33, 95% CI (- 0.51, – 0.14), P = 0.0005), and LDL (SMD = – 0.38, 95% CI (- 0.50, – 0.27), P < 0.00001), increase HDL level (SMD = 0.66, 95% CI (0.56, 0.76), P < 0.00001), and plasma glucose level in the patients (SMD = 0.27, 95% CI (0.12, 0.42), P = 0.0004). Subgroup anal. showed that supplementation of NA had the most significant effect on the levels of TG, TC, LDL, HDL and plasma glucose. In this study, a meta-anal. based on currently published clin. trials with NAD+ precursors showed that supplementation with NAD+ precursors improved TG, TC, LDL, and HDL levels in humans, but resulted in hyperglycemia, compared with placebo or no treatment. Among them, NA has the most significant effect on improving lipid metabolism In addition, although NR and NAM supplementation had no significant effect on improving human lipid metabolism, the role of NR and NAM could not be directly denied due to the few relevant studies at present. Based on subgroup anal., we found that the supplement of NAD+ precursors seems to have little effect on healthy people, but it has a significant beneficial effect on patients with cardiovascular disease and dyslipidemia. Due to the limitation of the number and quality of included studies, the above conclusions need to be verified by more high-quality studies. 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: 1094-61-7Synthetic Route of C11H15N2O8P).

((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. Amides are pervasive in nature and technology. Proteins and important plastics like Nylons, Aramid, Twaron, and Kevlar are polymers whose units are connected by amide groups (polyamides); these linkages are easily formed, confer structural rigidity, and resist hydrolysis. Amides are not in general accessible by the direct condensation of amines with carboxylic acids for two reasons: first, both components are readily deactivated by a transfer of a proton from the acid to the amine and second, the hydroxy unit on the carbonyl of the acid is a relatively poor leaving group. Nevertheless, the formation of five- and six-membered rings is often surprisingly simple provided that other factors can be brought into play to assist in the condensation.Synthetic Route of C11H15N2O8P

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

Sulfonamides. I. “Marfanil” and its ο- and p-isomers was written by Angyal, S. J.;Jenkin, S. R.. And the article was included in Australian Journal of Scientific Research in 1950.Product Details of 857003-88-4 The following contents are mentioned in the article:

A new synthesis of “Marfanil” (p-H₂NCH₂.C₆H₄SO₂NH₂) from p-MeC₆H₄SO₂Cl is described. The ο- and m-isomers were also prepared and found to have low bacteriostatic activity. p-ClCH₂C₆H₄SO₂Cl, prepared (23% yield)by chlorinating com. p-MeC₆H₄SO₂Cl at 160°, was added with stirring to alc. NH₃ and the product precipitated with H₂O to give 86% p-ClCH₂C₆H₄SO₂NH₂. With hexamine in cold EtOH, this formed p-sulphamylbenzylhexaminium chloride (96%; low Cl content), decomposing at 180°, which on refluxing 30 min. with concentrated HCl in EtOH furnished 85% marfanil, m. 148°, [sulfate, m. 254-5° (decomposition)]. The original synthesis from AcNHCH₂Ph (C.A. 38, 5805.6; 34, 6587.8) was also studied. PhCH₂NHAc (977 g.) was added to ClSO₃H (2.1 l.) below 20°, the mixture heated 1 hr. at 70°, cooled, added to 10 kg. ice, and the resulting oil decanted and added to concentrated NH₄OH (2 l.) and H₂O (one l.) below 40°, to give 47% acetylmarfanil and 9% ο-(acetamidomethyl)benzenesulfonamide-HCl (I), m. 137-8°. I refluxed 8 hrs. in EtOH with concentrated HCl gave 82% ο-(aminomethyl)benzenesulfonamide-HCl, m. 238-9° [free base (II), m. 83-4°]. Attempted crystallization of II from Me₂CO produced the isopropylene derivative, C₁₀H₁₄O₂SN₂ (83%), m. 136°. m-H₂NC₆H₄SO₂NH₂ (17.2 g.) was diazotized in 23 ml. concentrated HCl and 50 ml. H₂O with 7.6 g. NaNO₂ in H₂O and the mixture added below 20° to 12 g. CuCl₂ and 16 g. NaCN in 100 ml. water (the temperature finally raised to 70°) to give 9 g. (50%) m-NCC₆H₄SO₂NH₂ (III), m. 148-50°. III was reduced (H, Pd/C) in the presence of NH₃ to 60% m,m’-disulfamyldibenzylamine, m. 176.5-7° (HCl salt, m. 216-18°), while in aqueous HCl, 57% m-(aminomethyl)benzenesulfonamide-HCl, m. 232° (free base, an oil), resulted. There was no correlation between basic strength and antibacterial action of marfanil and its ο- and p-isomers, whose pK values were found to be resp. 8.52, 10.08 (literature, 8.18, 10.23); 8.53, 10.11; 8.55, 10.14. This study involved multiple reactions and reactants, such as 3,3′-(Azanediylbis(methylene))dibenzenesulfonamide (cas: 857003-88-4Product Details of 857003-88-4).

3,3′-(Azanediylbis(methylene))dibenzenesulfonamide (cas: 857003-88-4) belongs to amides. Amides can be viewed as a derivative of a carboxylic acid RC(=O)OH with the hydroxyl group –OH replaced by an amine group −NR′R″; or, equivalently, an acyl (alkanoyl) group RC(=O)− joined to an amine group. 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.Product Details of 857003-88-4

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

Nicotinic acid mononucleotide is an allosteric SARM1 inhibitor promoting axonal protection was written by Sasaki, Yo;Zhu, Jian;Shi, Yun;Gu, Weixi;Kobe, Bostjan;Ve, Thomas;DiAntonio, Aaron;Milbrandt, Jeffrey. And the article was included in Experimental Neurology in 2021.Category: amides-buliding-blocks The following contents are mentioned in the article:

SARM1 is an inducible NAD⁺ hydrolase that is the central executioner of pathol. axon loss. Recently, we elucidated the mol. mechanism of SARM1 activation, demonstrating that SARM1 is a metabolic sensor regulated by the levels of NAD⁺ and its precursor, NMN (NMN), via their competitive binding to an allosteric site within the SARM1 N-terminal ARM domain. In healthy neurons with abundant NAD⁺, binding of NAD⁺ blocks access of NMN to this allosteric site. However, with injury or disease the levels of the NAD⁺ biosynthetic enzyme NMNAT2 drop, increasing the NMN/ NAD⁺ ratio and thereby promoting NMN binding to the SARM1 allosteric site, which in turn induces a conformational change activating the SARM1 NAD⁺ hydrolase. Hence, NAD⁺ metabolites both regulate the activation of SARM1 and, in turn, are regulated by the SARM1 NAD⁺ hydrolase. This dual upstream and downstream role for NAD⁺ metabolites in SARM1 function has hindered mechanistic understanding of axoprotective mechanisms that manipulate the NAD⁺ metabolome. Here we reevaluate two methods that potently block axon degeneration via modulation of NAD⁺ related metabolites, 1) the administration of the NMN biosynthesis inhibitor FK866 in conjunction with the NAD⁺ precursor nicotinic acid riboside (NaR) and 2) the neuronal expression of the bacterial enzyme NMN deamidase. We find that these approaches not only lead to a decrease in the levels of the SARM1 activator NMN, but also an increase in the levels of the NAD⁺ precursor nicotinic acid mononucleotide (NaMN). We show that NaMN inhibits SARM1 activation, and demonstrate that this NaMN-mediated inhibition is important for the long-term axon protection induced by these treatments. Anal. of the NaMN-ARM domain co-crystal structure shows that NaMN competes with NMN for binding to the SARM1 allosteric site and promotes the open, autoinhibited configuration of SARM1 ARM domain. Together, these results demonstrate that the SARM1 allosteric pocket can bind a diverse set of metabolites including NMN, NAD⁺, and NaMN to monitor cellular NAD⁺ homeostasis and regulate SARM1 NAD⁺ hydrolase activity. The relative promiscuity of the allosteric site may enable the development of potent pharmacol. inhibitors of SARM1 activation for the treatment of neurodegenerative disorders. 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. 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 are stable compounds. The lower-melting members (such as acetamide) can be readily purified by fractional distillation. Most amides are solids which have low solubilities in water.Category: amides-buliding-blocks

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

Nicotinic acid mononucleotide is an allosteric SARM1 inhibitor promoting axonal protection was written by Sasaki, Yo;Zhu, Jian;Shi, Yun;Gu, Weixi;Kobe, Bostjan;Ve, Thomas;DiAntonio, Aaron;Milbrandt, Jeffrey. And the article was included in Experimental Neurology in 2021.Quality Control of ((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate The following contents are mentioned in the article:

SARM1 is an inducible NAD⁺ hydrolase that is the central executioner of pathol. axon loss. Recently, we elucidated the mol. mechanism of SARM1 activation, demonstrating that SARM1 is a metabolic sensor regulated by the levels of NAD⁺ and its precursor, NMN (NMN), via their competitive binding to an allosteric site within the SARM1 N-terminal ARM domain. In healthy neurons with abundant NAD⁺, binding of NAD⁺ blocks access of NMN to this allosteric site. However, with injury or disease the levels of the NAD⁺ biosynthetic enzyme NMNAT2 drop, increasing the NMN/ NAD⁺ ratio and thereby promoting NMN binding to the SARM1 allosteric site, which in turn induces a conformational change activating the SARM1 NAD⁺ hydrolase. Hence, NAD⁺ metabolites both regulate the activation of SARM1 and, in turn, are regulated by the SARM1 NAD⁺ hydrolase. This dual upstream and downstream role for NAD⁺ metabolites in SARM1 function has hindered mechanistic understanding of axoprotective mechanisms that manipulate the NAD⁺ metabolome. Here we reevaluate two methods that potently block axon degeneration via modulation of NAD⁺ related metabolites, 1) the administration of the NMN biosynthesis inhibitor FK866 in conjunction with the NAD⁺ precursor nicotinic acid riboside (NaR) and 2) the neuronal expression of the bacterial enzyme NMN deamidase. We find that these approaches not only lead to a decrease in the levels of the SARM1 activator NMN, but also an increase in the levels of the NAD⁺ precursor nicotinic acid mononucleotide (NaMN). We show that NaMN inhibits SARM1 activation, and demonstrate that this NaMN-mediated inhibition is important for the long-term axon protection induced by these treatments. Anal. of the NaMN-ARM domain co-crystal structure shows that NaMN competes with NMN for binding to the SARM1 allosteric site and promotes the open, autoinhibited configuration of SARM1 ARM domain. Together, these results demonstrate that the SARM1 allosteric pocket can bind a diverse set of metabolites including NMN, NAD⁺, and NaMN to monitor cellular NAD⁺ homeostasis and regulate SARM1 NAD⁺ hydrolase activity. The relative promiscuity of the allosteric site may enable the development of potent pharmacol. inhibitors of SARM1 activation for the treatment of neurodegenerative disorders. 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: 1094-61-7Quality Control of ((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate).

((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. The solubilities of amides and esters are roughly comparable. Typically amides are less soluble than comparable amines and carboxylic acids since these compounds can both donate and accept hydrogen bonds. Tertiary amides, with the important exception of N,N-dimethylformamide, exhibit low solubility in water. 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.Quality Control of ((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate

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

Novel Strategy for Untargeted Chiral Metabolomics using Liquid Chromatography-High Resolution Tandem Mass Spectrometry was written by Pandey, Renu;Collins, Meghan;Lu, Xiyuan;Sweeney, Shannon R.;Chiou, Jennifer;Lodi, Alessia;Tiziani, Stefano. And the article was included in Analytical Chemistry (Washington, DC, United States) in 2021.Safety of ((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate The following contents are mentioned in the article:

Stereospecific recognition of metabolites plays a significant role in the detection of potential disease biomarkers thereby providing new insights in diagnosis and prognosis. D-Hdroxy/amino acids are recognized as potential biomarkers in several metabolic disorders. Despite continuous advances in metabolomics technologies, the simultaneous measurement of different classes of enantiomeric metabolites in a single anal. run remains challenging. Here, we develop a novel strategy for untargeted chiral metabolomics of hydroxy/amine groups (-OH/-NH₂) containing metabolites, including all hydroxy acids (HAs) and amino acids (AAs), by chiral derivatization coupled with liquid chromatog.-high resolution tandem mass spectrometry (LC-HR-MS/MS). Diacetyl-tartaric anhydride (DATAN) was used for the simultaneous derivatization of-OH/-NH₂ containing metabolites as well as the resulting diastereomers, and all the derivatized metabolites were resolved in a single anal. run. Data independent MS/MS acquisition (DIA) was applied to pos. identify DATAN-labeled metabolites based on reagent specific diagnostic fragment ions. We discriminated chiral from achiral metabolites based on the reversal of elution order of D and L isomers derivatized with the enantiomeric pair (±) of DATAN in an untargeted manner. Using the developed strategy, a library of 301 standards that consisted of 214 chiral and 87 achiral metabolites were separated and detected in a single anal. run. This approach was then applied to investigate the enantioselective metabolic profile of the bone marrow (BM) and peripheral blood (PB) plasma samples from patients with acute myeloid leukemia (AML) at diagnosis and following completion of the induction phase of chemotherapeutic treatment. The sensitivity and selectivity of the developed method enabled the detection of trace levels of the D-enantiomer of HAs and AAs in primary plasma patient samples. Several of these metabolites were significantly altered in response to chemotherapy. The developed LC-HR-MS method entails a valuable step forward in chiral metabolomics. 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: 1094-61-7Safety of ((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate).

((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. The amide group is called a peptide bond when it is part of the main chain of a protein, and an isopeptide bond when it occurs in a side chain, such as in the amino acids asparagine and glutamine. 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.Safety of ((2R,3S,4R,5R)-5-(3-Carbamoylpyridin-1-ium-1-yl)-3,4-dihydroxytetrahydrofuran-2-yl)methyl hydrogen phosphate

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

On December 21, 2000, Wagner, Alain; Mioskowski, Charles; Mohar, Barbara; Desmurs, Jean-roger; Le Guyader, Frederic; Schlama, Thierry published a patent.Application of 167316-28-1 The title of the patent was Sulfonamides and carboxamides and their use in asymmetrical catalysis. And the patent contained the following:

Optically active diamines were converted to their monosulfonamides with fluorinated alkane- or arenesulfonyl halides. The resulting sulfona,ides were used as ligands in the stereoselective reduction of ketones or in the stereoselective oxidation of racemic alcs. Thus, (1S,2S)-1,2-cyclohexanediamine was treated with F3CSO2Cl to give (1S,2S)-N-trifluoromethylsulfonyl-1,2-cyclohexanediamine (I). I was used together with [RuCl2(p-cymene)]2 to reduce PhCOMe to (S)-HOCHPhMe and to preferentially oxidize (S)-HOCHPhMe to PhCOMe, leaving enriched (R)-HOCHPhMe. The experimental process involved the reaction of N-[(1S,2S)-2-Amino-1,2-diphenylethyl]-1,1,1-trifluoromethanesulfonamide(cas: 167316-28-1).Application of 167316-28-1

The Article related to diamine monosulfonamide preparation ligand asym reduction oxidation, General Organic Chemistry: Synthetic Methods and other aspects.Application of 167316-28-1

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