Category: 54-47-7

Imaging active site chemistry and protonation states: NMR crystallography of the tryptophan synthase α-aminoacrylate intermediate was written by Holmes, Jacob B.;Liu, Viktoriia;Caulkins, Bethany G.;Hilario, Eduardo;Ghosh, Rittik K.;Drago, Victoria N.;Young, Robert P.;Romero, Jennifer A.;Gill, Adam D.;Bogie, Paul M.;Paulino, Joana;Wang, Xiaoling;Riviere, Gwladys;Bosken, Yuliana K.;Struppe, Jochem;Hassan, Alia;Guidoulianov, Jevgeni;Perrone, Barbara;Mentink-Vigier, Frederic;Chang, Chia-en A.;Long, Joanna R.;Hooley, Richard J.;Mueser, Timothy C.;Dunn, Michael F.;Mueller, Leonard J.. And the article was included in Proceedings of the National Academy of Sciences of the United States of America in 2022.Name: (4-Formyl-5-hydroxy-6-methylpyridin-3-yl)methyl dihydrogen phosphate The following contents are mentioned in the article:

NMR-assisted crystallog.-the integrated application of solid-state NMR, x-ray crystallog., and 1st-principles computational chem.-holds significant promise for mechanistic enzymol.: by providing at.-resolution characterization of stable intermediates in enzyme active sites, including H atom locations and tautomeric equilibrium, NMR crystallog. offers insight into both structure and chem. dynamics. This integrated approach is used to characterize the tryptophan synthase α-aminoacrylate intermediate, a defining species for pyridoxal-5′-phosphate-dependent enzymes that catalyze β-elimination and replacement reactions. For this intermediate, NMR-assisted crystallog. is able to identify the protonation states of the ionizable sites on the cofactor, substrate, and catalytic side chains as well as the location and orientation of crystallog. waters within the active site. Most notable is the H₂O mol. immediately adjacent to the substrate β-C, which serves as a H bond donor to the ε-amino group of the acid-base catalytic residue βLys87. From this anal., a detailed 3-dimensional picture of structure and reactivity emerges, highlighting the fate of the L-serine hydroxyl leaving group and the reaction pathway back to the preceding transition state. Reaction of the α-aminoacrylate intermediate with benzimidazole, an isostere of the natural substrate indole, shows benzimidazole bound in the active site and poised for, but unable to initiate, the subsequent bond formation step. When modeled into the benzimidazole position, indole is positioned with C3 in contact with the α-aminoacrylate Cβ and aligned for nucleophilic attack. The chem. detailed, 3-dimensional structure from NMR-assisted crystallog. is key to understanding why benzimidazole does not react, while indole does. This study involved multiple reactions and reactants, such as (4-Formyl-5-hydroxy-6-methylpyridin-3-yl)methyl dihydrogen phosphate (cas: 54-47-7Name: (4-Formyl-5-hydroxy-6-methylpyridin-3-yl)methyl dihydrogen phosphate).

(4-Formyl-5-hydroxy-6-methylpyridin-3-yl)methyl dihydrogen phosphate (cas: 54-47-7) belongs to pyridine derivatives. Pyridine has a dipole moment and a weaker resonant stabilization than benzene (resonance energy 117 kJ·mol−1 in pyridine vs. 150 kJ·mol−1 in benzene). Halopyridines are particularly attractive synthetic building blocks in a variety of cross-coupling methods, including the Suzuki-Miyaura cross-coupling reaction.Name: (4-Formyl-5-hydroxy-6-methylpyridin-3-yl)methyl dihydrogen phosphate

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Drosophila carrying epilepsy-associated variants in the vitamin B6 metabolism gene PNPO display allele- and diet-dependent phenotypes was written by Chi, Wanhao;Iyengar, Atulya S. R.;Fu, Wenqin;Liu, Wei;Berg, Abigayle E.;Wu, Chun-Fang;Zhuang, Xiaoxi. And the article was included in Proceedings of the National Academy of Sciences of the United States of America in 2022.Synthetic Route of C8H10NO6P The following contents are mentioned in the article:

Pyridox(am)ine 5′-phosphate oxidase (PNPO) catalyzes the rate-limiting step in the synthesis of pyridoxal 5′-phosphate (PLP), the active form of vitamin B6 required for the synthesis of neurotransmitters gamma-aminobutyric acid (GABA) and the monoamines. Pathogenic variants in PNPO have been increasingly identified in patients with neonatal epileptic encephalopathy and early-onset epilepsy. These patients often exhibit different types of seizures and variable comorbidities. Recently, the PNPO gene has also been implicated in epilepsy in adults. It is unclear how these phenotypic variations are linked to specific PNPO alleles and to what degree diet can modify their expression. Using CRISPR-Cas9, we generated four knock-in Drosophila alleles, hWT, hR116Q, hD33V, and hR95H, in which the endogenous Drosophila PNPO was replaced by wild-type human PNPO complementary DNA (cDNA) and three epilepsy-associated variants. We found that these knock-in flies exhibited a wide range of phenotypes, including developmental impairments, abnormal locomotor activities, spontaneous seizures, and shortened life span. These phenotypes are allele dependent, varying with the known biochem. severity of these mutations and our characterized mol. defects. We also showed that diet treatments further diversified the phenotypes among alleles, and PLP supplementation at larval and adult stages prevented developmental impairments and seizures in adult flies, resp. Furthermore, we found that hR95H had a significant dominant-neg. effect, rendering heterozygous flies susceptible to seizures and premature death. Together, these results provide biol. bases for the various phenotypes resulting from multifunction of PNPO, specific mol. and/or genetic properties of each PNPO variant, and differential allele-diet interactions. This study involved multiple reactions and reactants, such as (4-Formyl-5-hydroxy-6-methylpyridin-3-yl)methyl dihydrogen phosphate (cas: 54-47-7Synthetic Route of C8H10NO6P).

(4-Formyl-5-hydroxy-6-methylpyridin-3-yl)methyl dihydrogen phosphate (cas: 54-47-7) belongs to pyridine derivatives. Pyridines are an important class of heterocycles and occur in polysubstituted forms in many naturally occurring biologically active compounds, drug molecules and chiral ligands. Pyridine groups exist in countless molecules, and their applications include catalysis, drug design, molecular recognition, and natural product synthesis.Synthetic Route of C8H10NO6P

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Drosophila carrying epilepsy-associated variants in the vitamin B6 metabolism gene PNPO display allele- and diet-dependent phenotypes was written by Chi, Wanhao;Iyengar, Atulya S. R.;Fu, Wenqin;Liu, Wei;Berg, Abigayle E.;Wu, Chun-Fang;Zhuang, Xiaoxi. And the article was included in Proceedings of the National Academy of Sciences of the United States of America in 2022.SDS of cas: 54-47-7 The following contents are mentioned in the article:

Pyridox(am)ine 5′-phosphate oxidase (PNPO) catalyzes the rate-limiting step in the synthesis of pyridoxal 5′-phosphate (PLP), the active form of vitamin B6 required for the synthesis of neurotransmitters gamma-aminobutyric acid (GABA) and the monoamines. Pathogenic variants in PNPO have been increasingly identified in patients with neonatal epileptic encephalopathy and early-onset epilepsy. These patients often exhibit different types of seizures and variable comorbidities. Recently, the PNPO gene has also been implicated in epilepsy in adults. It is unclear how these phenotypic variations are linked to specific PNPO alleles and to what degree diet can modify their expression. Using CRISPR-Cas9, we generated four knock-in Drosophila alleles, hWT, hR116Q, hD33V, and hR95H, in which the endogenous Drosophila PNPO was replaced by wild-type human PNPO complementary DNA (cDNA) and three epilepsy-associated variants. We found that these knock-in flies exhibited a wide range of phenotypes, including developmental impairments, abnormal locomotor activities, spontaneous seizures, and shortened life span. These phenotypes are allele dependent, varying with the known biochem. severity of these mutations and our characterized mol. defects. We also showed that diet treatments further diversified the phenotypes among alleles, and PLP supplementation at larval and adult stages prevented developmental impairments and seizures in adult flies, resp. Furthermore, we found that hR95H had a significant dominant-neg. effect, rendering heterozygous flies susceptible to seizures and premature death. Together, these results provide biol. bases for the various phenotypes resulting from multifunction of PNPO, specific mol. and/or genetic properties of each PNPO variant, and differential allele-diet interactions. This study involved multiple reactions and reactants, such as (4-Formyl-5-hydroxy-6-methylpyridin-3-yl)methyl dihydrogen phosphate (cas: 54-47-7SDS of cas: 54-47-7).

(4-Formyl-5-hydroxy-6-methylpyridin-3-yl)methyl dihydrogen phosphate (cas: 54-47-7) belongs to pyridine derivatives. The ring atoms in the pyridine molecule are sp2-hybridized. The nitrogen is involved in the π-bonding aromatic system using its unhybridized p orbital. The lone pair is in an sp2 orbital, projecting outward from the ring in the same plane as the σ bonds. Many analogues of pyridine are known where N is replaced by other heteroatoms . Substitution of one C–H in pyridine with a second N gives rise to the diazine heterocycles (C4H4N2), with the names pyridazine, pyrimidine, and pyrazine.SDS of cas: 54-47-7

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Clinical, biochemical and genetic findings in adult patients with chronic hypophosphatasemia was written by Guarnieri, V.;Sileri, F.;Indirli, R.;Guabello, G.;Longhi, M.;Dito, G.;Verdelli, C.;Corbetta, S.. And the article was included in Journal of Endocrinological Investigation in 2022.Name: (4-Formyl-5-hydroxy-6-methylpyridin-3-yl)methyl dihydrogen phosphate The following contents are mentioned in the article:

The study aimed to define the clin., biochem. and genetic features of adult patients with osteopenia/osteoporosis and/or bone fragility and low serum alk. phosphatase (sALP). Twenty-two patients with at least two sALP values below the reference range were retrospectively enrolled after exclusion of secondary causes. Data about clin. features, mineral and bone markers, serum pyridoxal-5′-phosphate (PLP), urine phosphoethanolamine (PEA), lumbar and femur bone densitometry, and column X-ray were collected. Peripheral blood DNA of each participant was analyzed to detect ALPL gene anomalies. Pathogenic ALPL variants (pALPL) occurred in 23% and benign variants in 36% of patients (bALPL), while nine patients harbored wild-type alleles (wtALPL). Fragility fractures and dental anomalies were more frequent in patients harboring pALPL and bALPL than in wtALPL patients. Of note, wtALPL patients comprised women treated with tamoxifen for hormone-sensitive breast cancer. Mineral and bone markers were similar in the three groups. Mean urine PEA levels were significantly higher in patients harboring pALPL than those detected in patients harboring bALPL and wtALPL; by contrast, serum PLP levels were similar in the three groups. A 6-points score, considering clin. and biochem. features, was predictive of pALPL detection [P = 0.060, OR 1.92 (95% CI 0.972, 3.794)], and more significantly of pALPL or bALPL [P = 0.025, OR 14.33 (95% CI 1.401, 14.605)]. In osteopenic/osteoporotic patients, single clin. or biochem. factors did not distinguish hypophosphatasemic patients harboring pALPL or bALPL from those harboring wtALPL. Occurrence of multiple clin. and biochem. features is predictive of ALPL anomalies, and, therefore, they should be carefully identified. Tamoxifen emerged as a hypophosphatasemic drug. This study involved multiple reactions and reactants, such as (4-Formyl-5-hydroxy-6-methylpyridin-3-yl)methyl dihydrogen phosphate (cas: 54-47-7Name: (4-Formyl-5-hydroxy-6-methylpyridin-3-yl)methyl dihydrogen phosphate).

(4-Formyl-5-hydroxy-6-methylpyridin-3-yl)methyl dihydrogen phosphate (cas: 54-47-7) belongs to pyridine derivatives. Pyridine’s the lone pair does not contribute to the aromatic system but importantly influences the chemical properties of pyridine, as it easily supports bond formation via an electrophilic attack. Pyridine groups exist in countless molecules, and their applications include catalysis, drug design, molecular recognition, and natural product synthesis.Name: (4-Formyl-5-hydroxy-6-methylpyridin-3-yl)methyl dihydrogen phosphate

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Clinical, biochemical and genetic findings in adult patients with chronic hypophosphatasemia was written by Guarnieri, V.;Sileri, F.;Indirli, R.;Guabello, G.;Longhi, M.;Dito, G.;Verdelli, C.;Corbetta, S.. And the article was included in Journal of Endocrinological Investigation in 2022.Product Details of 54-47-7 The following contents are mentioned in the article:

The study aimed to define the clin., biochem. and genetic features of adult patients with osteopenia/osteoporosis and/or bone fragility and low serum alk. phosphatase (sALP). Twenty-two patients with at least two sALP values below the reference range were retrospectively enrolled after exclusion of secondary causes. Data about clin. features, mineral and bone markers, serum pyridoxal-5′-phosphate (PLP), urine phosphoethanolamine (PEA), lumbar and femur bone densitometry, and column X-ray were collected. Peripheral blood DNA of each participant was analyzed to detect ALPL gene anomalies. Pathogenic ALPL variants (pALPL) occurred in 23% and benign variants in 36% of patients (bALPL), while nine patients harbored wild-type alleles (wtALPL). Fragility fractures and dental anomalies were more frequent in patients harboring pALPL and bALPL than in wtALPL patients. Of note, wtALPL patients comprised women treated with tamoxifen for hormone-sensitive breast cancer. Mineral and bone markers were similar in the three groups. Mean urine PEA levels were significantly higher in patients harboring pALPL than those detected in patients harboring bALPL and wtALPL; by contrast, serum PLP levels were similar in the three groups. A 6-points score, considering clin. and biochem. features, was predictive of pALPL detection [P = 0.060, OR 1.92 (95% CI 0.972, 3.794)], and more significantly of pALPL or bALPL [P = 0.025, OR 14.33 (95% CI 1.401, 14.605)]. In osteopenic/osteoporotic patients, single clin. or biochem. factors did not distinguish hypophosphatasemic patients harboring pALPL or bALPL from those harboring wtALPL. Occurrence of multiple clin. and biochem. features is predictive of ALPL anomalies, and, therefore, they should be carefully identified. Tamoxifen emerged as a hypophosphatasemic drug. This study involved multiple reactions and reactants, such as (4-Formyl-5-hydroxy-6-methylpyridin-3-yl)methyl dihydrogen phosphate (cas: 54-47-7Product Details of 54-47-7).

(4-Formyl-5-hydroxy-6-methylpyridin-3-yl)methyl dihydrogen phosphate (cas: 54-47-7) belongs to pyridine derivatives. The pyridine ring occurs in many important compounds, including agrochemicals, pharmaceuticals, and vitamins. Pyridine, its benzo and pyridine-based compounds play diverse roles in organic chemistry. Pyridine-based materials are valued for their optical and physical properties as well as their medical potential. Product Details of 54-47-7

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Molecular insight into gene response of diorcinol- and rubrolide-treated biofilms of the emerging pathogen Stenotrophomonas maltophilia was written by Gudzuhn, Mirja;Alio, Ifey;Moll, Raphael;de Vries, Jessica;Boehlich, Jacob;Assmann, Maik;Janneschuetz, Jasmin;Schuetzenmeister, Nina;Himmelbach, Axel;Poehlein, Anja;Daniel, Rolf;Streit, Wolfgang R.. And the article was included in Microbiology Spectrum in 2022.Recommanded Product: 54-47-7 The following contents are mentioned in the article:

Stenotrophomonas maltophilia is a multidrug-resistant human opportunistic pathogen. S. maltophilia contributes to disease progression in cystic fibrosis patients and is found in wounds and infected tissues and on catheter surfaces. Due to its well-known multidrug resistance, it is difficult to treat S. maltophilia infections. Strain-specific susceptibility to antimicrobials has also been reported in several studies. Recently, three fungal diorcinols and 14 rubrolides were shown to reduce S. maltophilia K279a biofilm formation. Based on these initial findings, we were interested to extend this approach by testing a larger number of diorcinols and rubrolides and to understand the mol. mechanisms behind the observed antibiofilm effects. Of 52 tested compounds, 30 were able to significantly reduce the biofilm thickness by up to 85% ± 15% and had strong effects on mature biofilms. All compounds with antibiofilm activity also significantly affected the biofilm architecture. Addnl. RNA-sequencing data of diorcinol- and rubrolide-treated biofilm cells of two clin. isolates (454 and K279) identified a small set of shared genes that were affected by these potent antibiofilm compounds Among these, genes for iron transport, general metabolism, and membrane biosynthesis were most strongly and differentially regulated. A further hierarchical clustering and detailed structural inspection of the diorcinols and rubrolides implied that a prenyl group as side chain of one of the Ph groups of the diorcinols and an increasing degree of bromination of chlorinated rubrolides were possibly the cause of the strong antibiofilm effects. This study gives a deep insight into the effects of rubrolides and diorcinols on biofilms formed by the important global pathogen S. maltophilia. This study involved multiple reactions and reactants, such as (4-Formyl-5-hydroxy-6-methylpyridin-3-yl)methyl dihydrogen phosphate (cas: 54-47-7Recommanded Product: 54-47-7).

(4-Formyl-5-hydroxy-6-methylpyridin-3-yl)methyl dihydrogen phosphate (cas: 54-47-7) belongs to pyridine derivatives. Pyridine’s the lone pair does not contribute to the aromatic system but importantly influences the chemical properties of pyridine, as it easily supports bond formation via an electrophilic attack. Several pyridine derivatives play important roles in biological systems. While its biosynthesis is not fully understood, nicotinic acid (vitamin B3) occurs in some bacteria, fungi, and mammals.Recommanded Product: 54-47-7

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Molecular insight into gene response of diorcinol- and rubrolide-treated biofilms of the emerging pathogen Stenotrophomonas maltophilia was written by Gudzuhn, Mirja;Alio, Ifey;Moll, Raphael;de Vries, Jessica;Boehlich, Jacob;Assmann, Maik;Janneschuetz, Jasmin;Schuetzenmeister, Nina;Himmelbach, Axel;Poehlein, Anja;Daniel, Rolf;Streit, Wolfgang R.. And the article was included in Microbiology Spectrum in 2022.Synthetic Route of C8H10NO6P The following contents are mentioned in the article:

Stenotrophomonas maltophilia is a multidrug-resistant human opportunistic pathogen. S. maltophilia contributes to disease progression in cystic fibrosis patients and is found in wounds and infected tissues and on catheter surfaces. Due to its well-known multidrug resistance, it is difficult to treat S. maltophilia infections. Strain-specific susceptibility to antimicrobials has also been reported in several studies. Recently, three fungal diorcinols and 14 rubrolides were shown to reduce S. maltophilia K279a biofilm formation. Based on these initial findings, we were interested to extend this approach by testing a larger number of diorcinols and rubrolides and to understand the mol. mechanisms behind the observed antibiofilm effects. Of 52 tested compounds, 30 were able to significantly reduce the biofilm thickness by up to 85% ± 15% and had strong effects on mature biofilms. All compounds with antibiofilm activity also significantly affected the biofilm architecture. Addnl. RNA-sequencing data of diorcinol- and rubrolide-treated biofilm cells of two clin. isolates (454 and K279) identified a small set of shared genes that were affected by these potent antibiofilm compounds Among these, genes for iron transport, general metabolism, and membrane biosynthesis were most strongly and differentially regulated. A further hierarchical clustering and detailed structural inspection of the diorcinols and rubrolides implied that a prenyl group as side chain of one of the Ph groups of the diorcinols and an increasing degree of bromination of chlorinated rubrolides were possibly the cause of the strong antibiofilm effects. This study gives a deep insight into the effects of rubrolides and diorcinols on biofilms formed by the important global pathogen S. maltophilia. This study involved multiple reactions and reactants, such as (4-Formyl-5-hydroxy-6-methylpyridin-3-yl)methyl dihydrogen phosphate (cas: 54-47-7Synthetic Route of C8H10NO6P).

(4-Formyl-5-hydroxy-6-methylpyridin-3-yl)methyl dihydrogen phosphate (cas: 54-47-7) belongs to pyridine derivatives. In contrast to benzene, Pyridine’s electron density is not evenly distributed over the ring, reflecting the negative inductive effect of the nitrogen atom. Pyridine groups exist in countless molecules, and their applications include catalysis, drug design, molecular recognition, and natural product synthesis.Synthetic Route of C8H10NO6P

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Metabolic adjustments of blood-stage Plasmodium falciparum in response to sublethal pyrazoleamide exposure was written by Tewari, Shivendra G.;Kwan, Bobby;Elahi, Rubayet;Rajaram, Krithika;Reifman, Jaques;Prigge, Sean T.;Vaidya, Akhil B.;Wallqvist, Anders. And the article was included in Scientific Reports in 2022.Recommanded Product: (4-Formyl-5-hydroxy-6-methylpyridin-3-yl)methyl dihydrogen phosphate The following contents are mentioned in the article:

Due to the recurring loss of antimalarial drugs to resistance, there is a need for novel targets, drugs, and combination therapies to ensure the availability of current and future countermeasures. Pyrazoleamides belong to a novel class of antimalarial drugs that disrupt sodium ion homeostasis, although the exact consequences of this disruption in Plasmodium falciparum remain under investigation. In vitro experiments demonstrated that parasites carrying mutations in the metabolic enzyme PfATP4 develop resistance to pyrazoleamide compounds However, the underlying mechanisms that allow mutant parasites to evade pyrazoleamide treatment are unclear. Here, we first performed experiments to identify the sublethal dose of a pyrazoleamide compound (PA21A092) that caused a significant reduction in growth over one intraerythrocytic developmental cycle (IDC). At this drug concentration, we collected transcriptomic and metabolomic data at multiple time points during the IDC to quantify gene- and metabolite-level alterations in the treated parasites. To probe the effects of pyrazoleamide treatment on parasite metabolism, we coupled the time-resolved omics data with a metabolic network model of P. falciparum. We found that the drug-treated parasites adjusted carbohydrate metabolism to enhance synthesis of myoinositol-a precursor for phosphatidylinositol biosynthesis. This metabolic adaptation caused a decrease in metabolite flux through the pentose phosphate pathway, causing a decreased rate of RNA synthesis and an increase in oxidative stress. Our model analyses suggest that downstream consequences of enhanced myoinositol synthesis may underlie adjustments that could lead to resistance emergence in P. falciparum exposed to a sublethal dose of a pyrazoleamide drug. This study involved multiple reactions and reactants, such as (4-Formyl-5-hydroxy-6-methylpyridin-3-yl)methyl dihydrogen phosphate (cas: 54-47-7Recommanded Product: (4-Formyl-5-hydroxy-6-methylpyridin-3-yl)methyl dihydrogen phosphate).

(4-Formyl-5-hydroxy-6-methylpyridin-3-yl)methyl dihydrogen phosphate (cas: 54-47-7) belongs to pyridine derivatives. In contrast to benzene, Pyridine’s electron density is not evenly distributed over the ring, reflecting the negative inductive effect of the nitrogen atom. Halopyridines are particularly attractive synthetic building blocks in a variety of cross-coupling methods, including the Suzuki-Miyaura cross-coupling reaction.Recommanded Product: (4-Formyl-5-hydroxy-6-methylpyridin-3-yl)methyl dihydrogen phosphate

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Exploring the potential toxicological mechanisms of vine tea on the liver based on network toxicology and transcriptomics was written by Xiao, Fangyu;Qiu, Jihua;Zhao, Ying. And the article was included in Frontiers in Pharmacology in 2022.HPLC of Formula: 54-47-7 The following contents are mentioned in the article:

This study focuses on whether vine tea contains potentially toxic components that trigger hepatotoxicity as a mechanism of action, which further provides some reference for the consumption and guides future product development of vine tea. The chem. components of vine tea were collected from the reported literature and the toxicol. information matched with the CTD database was collected, and the dataset of potential toxic components was established. The toxic components were submitted to the PharmMapper server to obtain potential targets. At the same time, the relevant targets were searched in the CTD database and GeneCards database with keywords such as “Hepatic Toxicity,” “Liver Damage,” and “Drug-induced liver injury.” After intersection, the potential hepatotoxic targets of vine tea were obtained. The protein interactions of potential hepatotoxic targets of vine tea were analyzed by the STRING database. Protein-protein interaction (PPI) networks were constructed by Cytoscape3.6.1 software. The GO mol. function and KEGG pathway of hepatotoxic targets were enriched by the R package to screen the key targets. The role of the components and key targets was analyzed by the LEDOCK program. The data from GEO database were mined for the functional correlation characterized by cell transcriptional expression caused by vine tea as a disturbance factor. This study has searched 34 potential toxic components and 57 potential hepatotoxic targets of vine tea, and the result showed that these targets were mainly involved in oxidative stress, cell metabolism, and apoptosis to affect the liver. Vine tea has the interrelationship of multi-components, multi-targets, and multi-pathways. At the cellular level, the toxic components of vine tea, mainly flavonoids, may promote oxidative stress, promote oxidation to produce free radicals, guide apoptosis, and affect cell metabolism and other cytotoxic mechanisms. However, this hepatotoxicity is related to the dose, duration of vine tea, and individual differences. This study revealed the potential hepatotoxic components of vine tea and provides a reference for further research and development of related functional products. This study involved multiple reactions and reactants, such as (4-Formyl-5-hydroxy-6-methylpyridin-3-yl)methyl dihydrogen phosphate (cas: 54-47-7HPLC of Formula: 54-47-7).

(4-Formyl-5-hydroxy-6-methylpyridin-3-yl)methyl dihydrogen phosphate (cas: 54-47-7) belongs to pyridine derivatives. Pyridine’s the lone pair does not contribute to the aromatic system but importantly influences the chemical properties of pyridine, as it easily supports bond formation via an electrophilic attack. One of the examples of pyridines is the well-known alkaloid lithoprimidine, which is an A3 adenosine receptor antagonist and N,N-dimethylaminopyridine (DMAP) analog, commonly used in organic synthesis.HPLC of Formula: 54-47-7

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Pyridoxine or pyridoxal-5-phosphate treatment for seizures in glycosylphosphatidylinositol deficiency: A cohort study. was written by Bayat, Allan;Aledo-Serrano, Angel;Gil-Nagel, Antonio;Korff, Christian M;Thomas, Ashley;Boßelmann, Christian;Weber, Yvonne;Gardella, Elena;Lund, Allan M;de Sain-van der Velden, Monique G M;Møller, Rikke S. And the article was included in Developmental medicine and child neurology in 2022.Related Products of 54-47-7 The following contents are mentioned in the article:

AIM: To investigate the short-term efficacy and safety of high-dose pyridoxine and pyridoxal 5-phosphate (P5P) in the treatment of inherited glycosylphosphatidylinositol (GPI) deficiency-associated epilepsy. METHOD: Participants with genetically confirmed GPI deficiency were treated with oral pyridoxine or P5P as compassionate use in an agreed-upon clinical regimen. Pyridoxine (20-30 mg/kg/day) was used for 3 months. Baseline evaluation included 4 weeks of prospective seizure data and one video electroencephalogram (EEG). Seizure frequency was captured daily. The EEG was repeated after reaching maximum dosage of pyridoxine. Pyridoxine was switched to P5P (20-30 mg/kg/day) if seizure burden was unchanged after 3 months’ treatment. Another EEG was done after 3 months of P5P treatment. Primary outcome measures were reduction of seizure frequency and EEG improvements. RESULTS: Seven participants (one female, six males; age range 5-23 year; mean age 11 years 10 months, SD 5 year 2 months) were included. The genetic causes of inherited GPI deficiency were phosphatidylinositol N-acetylglucosaminyltransferase subunit A/T/V deficiency. All had drug-resistant epilepsy and neurodevelopmental impairment. We observed more than 50% seizure frequency reduction in 2 out of 7 and less than 50% reduction in another 3 out of 7 participants. No participants reached seizure freedom. No remarkable changes in electrophysiological findings were observed in 6 out of 7 participants treated with pyridoxine or P5P when comparing the baseline and follow-up EEGs. INTERPRETATION: We observed no long-lasting electrophysiological improvements during treatment but pyridoxine may reduce seizure frequency or burden in inherited GPI deficiency. WHAT THIS PAPER ADDS: Inherited glycosylphosphatidylinositol (GPI) deficiency often causes early-onset and drug-resistant epilepsy. Vitamin B₆ is a potential disease-specific treatment; however, efficacy and safety are ill-defined. Pyridoxine may reduce seizure frequency or burden in inherited GPI deficiency. Pyridoxine and P5P could prove to be a useful treatment in some individuals with inherited GPI deficiency and epilepsy. This study involved multiple reactions and reactants, such as (4-Formyl-5-hydroxy-6-methylpyridin-3-yl)methyl dihydrogen phosphate (cas: 54-47-7Related Products of 54-47-7).

(4-Formyl-5-hydroxy-6-methylpyridin-3-yl)methyl dihydrogen phosphate (cas: 54-47-7) belongs to pyridine derivatives. Pyridine’s the lone pair does not contribute to the aromatic system but importantly influences the chemical properties of pyridine, as it easily supports bond formation via an electrophilic attack. Pyridine, its benzo and pyridine-based compounds play diverse roles in organic chemistry. Pyridine-based materials are valued for their optical and physical properties as well as their medical potential. Related Products of 54-47-7

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem