Category: 54-47-7

Screening for hypophosphatasia: does biochemistry lead the way? was written by Held, Corinna Melanie;Guebelin, Anic;Krebs, Andreas;Sass, Joern Oliver;Wurm, Michael;Lausch, Ekkehart;van der Werf-Grohmann, Natascha;Schwab, Karl Otfried. And the article was included in Journal of Pediatric Endocrinology and Metabolism in 2022.Name: (4-Formyl-5-hydroxy-6-methylpyridin-3-yl)methyl dihydrogen phosphate The following contents are mentioned in the article:

Objectives: Patients with childhood hypophosphatasia (HPP) often have unspecific symptoms. It was our aim to identify patients with mild forms of HPP by laboratory data screening for decreased alk. phosphatase (AP) within a pediatric population. We conducted a retrospective hospital-based data screening for AP activity below the following limits: Girls: ≤12 years: <125 U/L; >12 years: <50 U/L Boys: ≤14 years: <125 U/L; >14 years: <70 U/L. Screening pos. patients with otherwise unexplained hypophosphatasemia were invited for further diagnostics: Re-test of AP activity, pyridoxal 5-phosphate (PLP) in hemolyzed whole blood, phosphoethanolamine (PEA) in serum and urine, and inorganic pyrophosphate in urine. Sequencing of the ALPL gene was performed in patients with clin. and/or laboratory abnormalities suspicious for HPP. We assessed a total of 14,913 samples of 6,731 patients and identified 393 screening-pos. patients. The majority of patients were excluded due to known underlying diseases causing AP depression. Of the 30 patients who participated in the study, three had a decrease in AP activity in combination with an increase in PLP and PEA. A heterozygous ALPL mutation was detected in each of them: One patient with a short stature was diagnosed with childhood-HPP and started with enzyme replacement therapy. The remaining two are considered as mutation carriers without osseous manifestation of the disease. A diagnostic algorithm based on decreased AP is able to identify patients with ALPL mutation after exclusion of the differential diagnoses of hypophosphatasemia and with addnl. evidence of increased AP substrates. 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). 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

Screening for hypophosphatasia: does biochemistry lead the way? was written by Held, Corinna Melanie;Guebelin, Anic;Krebs, Andreas;Sass, Joern Oliver;Wurm, Michael;Lausch, Ekkehart;van der Werf-Grohmann, Natascha;Schwab, Karl Otfried. And the article was included in Journal of Pediatric Endocrinology and Metabolism in 2022.Category: pyridine-derivatives The following contents are mentioned in the article:

Objectives: Patients with childhood hypophosphatasia (HPP) often have unspecific symptoms. It was our aim to identify patients with mild forms of HPP by laboratory data screening for decreased alk. phosphatase (AP) within a pediatric population. We conducted a retrospective hospital-based data screening for AP activity below the following limits: Girls: ≤12 years: <125 U/L; >12 years: <50 U/L Boys: ≤14 years: <125 U/L; >14 years: <70 U/L. Screening pos. patients with otherwise unexplained hypophosphatasemia were invited for further diagnostics: Re-test of AP activity, pyridoxal 5-phosphate (PLP) in hemolyzed whole blood, phosphoethanolamine (PEA) in serum and urine, and inorganic pyrophosphate in urine. Sequencing of the ALPL gene was performed in patients with clin. and/or laboratory abnormalities suspicious for HPP. We assessed a total of 14,913 samples of 6,731 patients and identified 393 screening-pos. patients. The majority of patients were excluded due to known underlying diseases causing AP depression. Of the 30 patients who participated in the study, three had a decrease in AP activity in combination with an increase in PLP and PEA. A heterozygous ALPL mutation was detected in each of them: One patient with a short stature was diagnosed with childhood-HPP and started with enzyme replacement therapy. The remaining two are considered as mutation carriers without osseous manifestation of the disease. A diagnostic algorithm based on decreased AP is able to identify patients with ALPL mutation after exclusion of the differential diagnoses of hypophosphatasemia and with addnl. evidence of increased AP substrates. This study involved multiple reactions and reactants, such as (4-Formyl-5-hydroxy-6-methylpyridin-3-yl)methyl dihydrogen phosphate (cas: 54-47-7Category: pyridine-derivatives).

(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). Pyridine groups exist in countless molecules, and their applications include catalysis, drug design, molecular recognition, and natural product synthesis.Category: pyridine-derivatives

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.HPLC of Formula: 54-47-7 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: 54-47-7HPLC of Formula: 54-47-7).

(4-Formyl-5-hydroxy-6-methylpyridin-3-yl)methyl dihydrogen phosphate (cas: 54-47-7) belongs to pyridine derivatives. 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.HPLC of Formula: 54-47-7

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Membrane lipid phosphorus reusing and antioxidant protecting played key roles in wild soybean resistance to phosphorus deficiency compared with cultivated soybean was written by Chen, Jing;Zhou, Ji;Li, Mingxia;Li, Mu;Hu, Yunan;Zhang, Tao;Shi, Lianxuan. And the article was included in Plant and Soil in 2022.Category: pyridine-derivatives The following contents are mentioned in the article:

Crop yield and quality are generally limited by poor soils, which is a key limiting factor for sustainable development in modern agriculture. Wild soybean (Glycine soja) is an excellent wild resource, with tolerance to adverse environments, especially poor soil. This study aimed to reveal the key mol. mechanism of wild soybean to resist phosphorus deficiency in soil. Differences in the types, amounts and metabolic pathways of small mol. metabolites and gene expression were compared and multi-omics integration anal. was performed between wild and cultivated soybean (Glycine max) seedling roots under sufficient and artificially simulated low-phosphorus in this study. Results Under low-phosphorus stress, wild soybean seedlings experienced less growth inhibition and rootspecific growth compared with cultivated soybean. Genes encoding sulfoquinovosyl transferase (SQD2), catechol O-methyltransferase (COMT), glutathione S-transferase (GST) and peroxidase (POD) were upregulated; levels of glutamic acid, glycine, putrescine, phenylalanine, tyrosine, catechol and neohesperidin were increased; and levels of glycerol-3-phosphate decreased. Integrated anal. showed that the above genes and metabolites were involved in glutathione metabolism, glycerolipid metabolism and phenylpropane biosynthesis. Conclusions These metabolic pathways are involved in phosphorus reuse, while membrane lipid remodeling and reactive oxygen species scavenging are carried out to maintain membrane stability and ensure plant survival under phosphorus deficiency. This study provides new ideas for the study of mechanism of tolerance to phosphorus deficiency in wild soybean and lays the theor. foundation for developing varieties of cultivated soybean that tolerate poor soils. This study involved multiple reactions and reactants, such as (4-Formyl-5-hydroxy-6-methylpyridin-3-yl)methyl dihydrogen phosphate (cas: 54-47-7Category: pyridine-derivatives).

(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. 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. Category: pyridine-derivatives

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Membrane lipid phosphorus reusing and antioxidant protecting played key roles in wild soybean resistance to phosphorus deficiency compared with cultivated soybean was written by Chen, Jing;Zhou, Ji;Li, Mingxia;Li, Mu;Hu, Yunan;Zhang, Tao;Shi, Lianxuan. And the article was included in Plant and Soil in 2022.Related Products of 54-47-7 The following contents are mentioned in the article:

Crop yield and quality are generally limited by poor soils, which is a key limiting factor for sustainable development in modern agriculture. Wild soybean (Glycine soja) is an excellent wild resource, with tolerance to adverse environments, especially poor soil. This study aimed to reveal the key mol. mechanism of wild soybean to resist phosphorus deficiency in soil. Differences in the types, amounts and metabolic pathways of small mol. metabolites and gene expression were compared and multi-omics integration anal. was performed between wild and cultivated soybean (Glycine max) seedling roots under sufficient and artificially simulated low-phosphorus in this study. Results Under low-phosphorus stress, wild soybean seedlings experienced less growth inhibition and rootspecific growth compared with cultivated soybean. Genes encoding sulfoquinovosyl transferase (SQD2), catechol O-methyltransferase (COMT), glutathione S-transferase (GST) and peroxidase (POD) were upregulated; levels of glutamic acid, glycine, putrescine, phenylalanine, tyrosine, catechol and neohesperidin were increased; and levels of glycerol-3-phosphate decreased. Integrated anal. showed that the above genes and metabolites were involved in glutathione metabolism, glycerolipid metabolism and phenylpropane biosynthesis. Conclusions These metabolic pathways are involved in phosphorus reuse, while membrane lipid remodeling and reactive oxygen species scavenging are carried out to maintain membrane stability and ensure plant survival under phosphorus deficiency. This study provides new ideas for the study of mechanism of tolerance to phosphorus deficiency in wild soybean and lays the theor. foundation for developing varieties of cultivated soybean that tolerate poor soils. 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 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). 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.Related Products of 54-47-7

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Assessing the neurotoxicity of airborne nano-scale particulate matter in human iPSC-derived neurons using a transcriptomics benchmark dose model was written by Zhang, Zhengbao;Li, Xiang;Jiang, Shuyun;Qiu, Chunfang;Guo, Ping;Wang, Ziwei;Xu, Chi;Zhang, Liying;Ma, Xingyu;Chen, Shen;Xing, Xiumei;Chen, Liping;Wang, Qing;Ma, Huimin;Zeng, Xiaowen;Chen, Wen;Li, Daochuan. And the article was included in Toxicology and Applied Pharmacology in 2022.Safety of (4-Formyl-5-hydroxy-6-methylpyridin-3-yl)methyl dihydrogen phosphate The following contents are mentioned in the article:

Airborne nano-scale particulate matter (nPM) exposure is a risk factor for neurol. diseases. However, to date, there has been no comprehensive evaluation of ambient nPMs neurotoxicity. We examined the toxic effects of nPM on human neurons derived from induced pluripotent stem cells (iPSCs) at doses ranging from 0 to 200μg/mL, and employed whole-genome RNA-sequencing in different dose groups to gain further insight into the neurotoxicity of ambient nPM. Our findings showed that nPM was absorbed by neurons, and induced a variety of toxic effects. The apical benchmark dose lower confidence bound (aBMDL) values of each effect endpoint were ranked as follows, in ascending order: mitochondrial membrane potential, neurite length, early apoptosis, cell viability. BMD anal. based on transcriptomic data revealed that the point of departure (PoD) of the 20 pathways with the lowest p-values (0.75μg/mL), the top 20 upstream regulators (0.79μg/mL) and the neurol. diseases (0.77μg/mL) could be appropriate for nPM neurotoxicity evaluation. The transcriptomic PoDs (tPoDs) were similar to apical PoDs (aPoDs) since their absolute fold differences were within 10-fold. Further anal. of the transcriptomic data revealed that nPM exposure could disturb the pathways related to ferroptosis, neurotransmitters, xenobiotic metabolism, etc., which might be critical in regulating nPM neurotoxicity. We also found that low-dose nPM induced cytokine signaling pathways, while high doses of nPM activated cell-cycle regulation and DNA repair pathways. Our results indicate that BMD modeling based on transcriptomic data could be useful in illustrating the neurotoxic mechanism, and also could be a promising method for evaluating the potential health risks of nPM. This study involved multiple reactions and reactants, such as (4-Formyl-5-hydroxy-6-methylpyridin-3-yl)methyl dihydrogen phosphate (cas: 54-47-7Safety of (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. 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.Safety of (4-Formyl-5-hydroxy-6-methylpyridin-3-yl)methyl dihydrogen phosphate

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Assessing the neurotoxicity of airborne nano-scale particulate matter in human iPSC-derived neurons using a transcriptomics benchmark dose model was written by Zhang, Zhengbao;Li, Xiang;Jiang, Shuyun;Qiu, Chunfang;Guo, Ping;Wang, Ziwei;Xu, Chi;Zhang, Liying;Ma, Xingyu;Chen, Shen;Xing, Xiumei;Chen, Liping;Wang, Qing;Ma, Huimin;Zeng, Xiaowen;Chen, Wen;Li, Daochuan. And the article was included in Toxicology and Applied Pharmacology in 2022.Related Products of 54-47-7 The following contents are mentioned in the article:

Airborne nano-scale particulate matter (nPM) exposure is a risk factor for neurol. diseases. However, to date, there has been no comprehensive evaluation of ambient nPMs neurotoxicity. We examined the toxic effects of nPM on human neurons derived from induced pluripotent stem cells (iPSCs) at doses ranging from 0 to 200μg/mL, and employed whole-genome RNA-sequencing in different dose groups to gain further insight into the neurotoxicity of ambient nPM. Our findings showed that nPM was absorbed by neurons, and induced a variety of toxic effects. The apical benchmark dose lower confidence bound (aBMDL) values of each effect endpoint were ranked as follows, in ascending order: mitochondrial membrane potential, neurite length, early apoptosis, cell viability. BMD anal. based on transcriptomic data revealed that the point of departure (PoD) of the 20 pathways with the lowest p-values (0.75μg/mL), the top 20 upstream regulators (0.79μg/mL) and the neurol. diseases (0.77μg/mL) could be appropriate for nPM neurotoxicity evaluation. The transcriptomic PoDs (tPoDs) were similar to apical PoDs (aPoDs) since their absolute fold differences were within 10-fold. Further anal. of the transcriptomic data revealed that nPM exposure could disturb the pathways related to ferroptosis, neurotransmitters, xenobiotic metabolism, etc., which might be critical in regulating nPM neurotoxicity. We also found that low-dose nPM induced cytokine signaling pathways, while high doses of nPM activated cell-cycle regulation and DNA repair pathways. Our results indicate that BMD modeling based on transcriptomic data could be useful in illustrating the neurotoxic mechanism, and also could be a promising method for evaluating the potential health risks of nPM. 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. Pyridines are an important class of heterocycles and occur in polysubstituted forms in many naturally occurring biologically active compounds, drug molecules and chiral ligands. Reduced pyridines, namely tetrahydropyridines, dihydropyridines and piperidines, are found in numerous natural and synthetic compounds. The synthesis and reactivity of these compounds have often been driven by the fact many of these compounds have interesting and unique pharmacological properties. Related Products of 54-47-7

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Biochemical characterization of the first step in sulfonolipid biosynthesis in Alistipes finegoldii was written by Radka, Christopher D.;Miller, Darcie J.;Frank, Matthew W.;Rock, Charles O.. And the article was included in Journal of Biological Chemistry in 2022.Application In Synthesis of (4-Formyl-5-hydroxy-6-methylpyridin-3-yl)methyl dihydrogen phosphate The following contents are mentioned in the article:

Sulfonolipids are unusual lipids found in the outer membranes of Gram-neg. bacteria in the phylum Bacteroidetes. Sulfonolipid and its deacylated derivative, capnine, are sulfur analogs of ceramide-1-phosphate and sphingosine-1-phosphate, resp.; thus, sulfonolipid biosynthesis is postulated to be similar to the sphingolipid biosynthetic pathway. Here, we identify the first enzyme in sulfonolipid synthesis in Alistipes finegoldii as the product of the alfi_1224 gene, cysteate acyl-acyl carrier protein (ACP) transferase (SulA). We show SulA catalyzes the condensation of acyl-ACP and cysteate (3-sulfo-alanine) to form 3-ketocapnine. Acyl-CoA is a poor substrate. We show SulA has a bound pyridoxal phosphate (PLP) cofactor that undergoes a spectral red shift in the presence of cysteate, consistent with the transition of the lysine-aldimine complex to a substrate-aldimine complex. Furthermore, the SulA crystal structure shows the same prototypical fold found in bacterial serine palmitoyltransferases (Spts), enveloping the PLP cofactor bound to Lys251. We observed the SulA and Spt active sites are identical except for Lys281 in SulA, which is an alanine in Spt. Addnl., SulA(K281A) is catalytically inactive but binds cysteate and forms the external aldimine normally, highlighting the structural role of the Lys281 side chain in walling off the active site from bulk solvent. Finally, the electropos. groove on the protein surface adjacent to the active site entrance provides a landing pad for the electroneg. acyl-ACP surface. Taken together, these data identify the substrates, products, and mechanism of SulA, the PLP-dependent condensing enzyme that catalyzes the first step in sulfonolipid synthesis in a gut commensal bacterium. This study involved multiple reactions and reactants, such as (4-Formyl-5-hydroxy-6-methylpyridin-3-yl)methyl dihydrogen phosphate (cas: 54-47-7Application In Synthesis of (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 conjugated system of six π electrons that are delocalized over the ring. The molecule is planar and, thus, follows the Hückel criteria for aromatic systems. Halopyridines are particularly attractive synthetic building blocks in a variety of cross-coupling methods, including the Suzuki-Miyaura cross-coupling reaction.Application In Synthesis of (4-Formyl-5-hydroxy-6-methylpyridin-3-yl)methyl dihydrogen phosphate

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Pyridoxal-5-phosphate induced cardioprotection in aging associated with up-expression of cystathionine-γ-lyase, 3-mercaptopyruvate sulfurtransferase, and ATP-sensitive potassium channels was written by Mys, Lidiia;Goshovska, Yulia;Strutynska, Nataliia;Fedichkina, Raisa;Korkach, Yuliia;Strutynskyi, Ruslan;Sagach, Vadim. And the article was included in European Journal of Clinical Investigation in 2022.Application of 54-47-7 The following contents are mentioned in the article:

In the present work, we investigated the cardioprotective potential of pyridoxal-5-phosphate (PLP) in old rats as a cofactor of enzymes that synthesize hydrogen sulfide (H₂S). PLP was administered per os in a dose of 0.7 mg per kg daily for 2 wk. Rats were divided into three groups (adult, old and old +PLP) of 20 animals. The cardiac mRNA levels of genes encoding H₂S-synthesizing enzymes cystathionine-γ-lyase (CSE) and 3-mercaptopyruvate sulfurtransferase (3-MST), uncoupling proteins (UCP3), subunits of ATP-sensitive potassium (K_ATP) channels were determined using real-time polymerase chain reaction anal. We also studied the effect of PLP-administration on the content of H₂S, oxidative stress, the activities of inducible and constitutive NO-synthase (iNOS, cNOS), arginase and nitrate reductase in the heart homogenates as well as cardiac resistance to ischemia-reperfusion in Langendorff-isolated heart model. It was shown that PLP restored mRNA levels of CSE, 3-MST and UCP3 genes, and H₂S content and also significantly increased the expression of SUR2 and Kir6.1 (2.2 and 3.3 times, resp.) in the heart of old rats. PLP significantly reduced the formation of superoxide, malondialdehyde, diene conjugates as well as the activity of iNOS and arginase. PLP significantly increased constitutive synthesis of NO and prevented reperfusion disturbances of the heart function after ischemia. Thus, PLP-administration in old rats was associated with up-expression of CSE, 3-MST, UCP3 and SUR2 and Kir6.1 subunits of K_ATP channels, and also increased cNOS activity and reduced oxidative stress and prevented reperfusion dysfunction of the heart in ischemia-reperfusion. This study involved multiple reactions and reactants, such as (4-Formyl-5-hydroxy-6-methylpyridin-3-yl)methyl dihydrogen phosphate (cas: 54-47-7Application 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. 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.Application of 54-47-7

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem

Pyridoxal-5-phosphate induced cardioprotection in aging associated with up-expression of cystathionine-γ-lyase, 3-mercaptopyruvate sulfurtransferase, and ATP-sensitive potassium channels was written by Mys, Lidiia;Goshovska, Yulia;Strutynska, Nataliia;Fedichkina, Raisa;Korkach, Yuliia;Strutynskyi, Ruslan;Sagach, Vadim. And the article was included in European Journal of Clinical Investigation in 2022.Product Details of 54-47-7 The following contents are mentioned in the article:

In the present work, we investigated the cardioprotective potential of pyridoxal-5-phosphate (PLP) in old rats as a cofactor of enzymes that synthesize hydrogen sulfide (H₂S). PLP was administered per os in a dose of 0.7 mg per kg daily for 2 wk. Rats were divided into three groups (adult, old and old +PLP) of 20 animals. The cardiac mRNA levels of genes encoding H₂S-synthesizing enzymes cystathionine-γ-lyase (CSE) and 3-mercaptopyruvate sulfurtransferase (3-MST), uncoupling proteins (UCP3), subunits of ATP-sensitive potassium (K_ATP) channels were determined using real-time polymerase chain reaction anal. We also studied the effect of PLP-administration on the content of H₂S, oxidative stress, the activities of inducible and constitutive NO-synthase (iNOS, cNOS), arginase and nitrate reductase in the heart homogenates as well as cardiac resistance to ischemia-reperfusion in Langendorff-isolated heart model. It was shown that PLP restored mRNA levels of CSE, 3-MST and UCP3 genes, and H₂S content and also significantly increased the expression of SUR2 and Kir6.1 (2.2 and 3.3 times, resp.) in the heart of old rats. PLP significantly reduced the formation of superoxide, malondialdehyde, diene conjugates as well as the activity of iNOS and arginase. PLP significantly increased constitutive synthesis of NO and prevented reperfusion disturbances of the heart function after ischemia. Thus, PLP-administration in old rats was associated with up-expression of CSE, 3-MST, UCP3 and SUR2 and Kir6.1 subunits of K_ATP channels, and also increased cNOS activity and reduced oxidative stress and prevented reperfusion dysfunction of the heart in ischemia-reperfusion. 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. 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. Product Details of 54-47-7

Referemce:
Pyridine – Wikipedia,
Pyridine | C5H5N – PubChem