Category: 24386-93-4

Effect of 5-iodotubercidin on proliferation and apoptosis in human colon cancer HT-29 cells and demethylation of deleted in liver cancer-1 gene was written by Zhang, Lingmin;Wang, Yaxu;Xie, Kai;Zeng, Linghai;Li, Quan. And the article was included in Di-San Junyi Daxue Xuebao in 2015.Computed Properties of C11H13IN4O4 The following contents are mentioned in the article:

Objective: To explore the effect of 5-iodotubercidin (ITU) on the proliferation and apoptosis in human colon cancer HT-29 cells and on the expression of deleted in liver cancer-1 (DLC-1) gene. Methods: HT-29 cells were treated with different concentrations of ITU (0.1, 0.5, 1, 2, 4, 6, 8, and 10 μmol/L) for 48 h, and the cell viability was studied by MTT assay. HT-29 cells were co-cultured with different concentrations of ITU (0, 2, 4, and 6 μmol/L) for 48 h, and the apoptosis rate was detected by flow cytometry. Meanwhile, the methylation levels of CpG islands at promoter region of DLC-1 gene were determined by bisulfite sequencing PCR (BSP). The DLC-1 mRNA expression levels were detected by reverse transcription-polymerase chain reaction (RT-PCR) and the DLC-1 protein expression levels were detected by Western blotting. Results: ITU distinctly inhibited the proliferation of HT-29 cells in a concentration-dependent manner in a certain range, and the 6 μmol/L group had the greatest effect, with IC₅₀ of 5.92 ± 0.62 μmol/L. The apoptotic rates of HT-29 cells treated with ITU (0, 2, 4, and 6 μmol/L) were (9.56 ± 2.21)%, (22.18 ± 3.16)%, (34.23 ± 3.16)%, and (40.5 ± 3.16)%, resp., which were increased in a concentration-dependent manner. The methylation rates of CpG islands at the promoter region of DLC-1 gene were 91.67%, 75.00%, 61.67%, and 43.33%, resp., after treatment with ITU (0, 2, 4, and 6 μmol/L). The results showed that ITU could decrease the methylation of DLC-1 gene promoter region. Little of DLC-1 mRNA and protein expression was detected in HT-29 cells, and ITU treatment increased the expression in a concentration-dependent manner. Conclusion: ITU could inhibit the proliferation of HT-29 cells and induce apoptosis through decreasing the methylation level of DLC-1 gene promoter region and increasing the DLC-1 gene expression. This study involved multiple reactions and reactants, such as (2R,3R,4S,5R)-2-(4-Amino-5-iodo-7H-pyrrolo[2,3-d]pyrimidin-7-yl)-5-(hydroxymethyl)tetrahydrofuran-3,4-diol (cas: 24386-93-4Computed Properties of C11H13IN4O4).

(2R,3R,4S,5R)-2-(4-Amino-5-iodo-7H-pyrrolo[2,3-d]pyrimidin-7-yl)-5-(hydroxymethyl)tetrahydrofuran-3,4-diol (cas: 24386-93-4) belongs to tetrahydrofuran derivatives. Tetrahydrofuran (THF) is a Lewis base that bonds to a variety of Lewis acids such as I2, phenols, triethylaluminum and bis(hexafluoroacetylacetonato)copper(II). Tetrahydrofuran reaction with hydrogen sulfide: In the presence of a solid acid catalyst, tetrahydrofuran reacts with hydrogen sulfide to give tetrahydrothiophene.Computed Properties of C11H13IN4O4

Referemce:
Tetrahydrofuran – Wikipedia,
Tetrahydrofuran | (CH2)3CH2O – PubChem

Screening of breast cancer stem cell inhibitors using a protein kinase inhibitor library was written by Choi, Hack Sun;Kim, Dal-Ah;Chung, Heesung;Park, In Ho;Kim, Bo Hye;Oh, Eok-Soo;Kang, Duk-Hee. And the article was included in Cancer Cell International in 2017.Safety of (2R,3R,4S,5R)-2-(4-Amino-5-iodo-7H-pyrrolo[2,3-d]pyrimidin-7-yl)-5-(hydroxymethyl)tetrahydrofuran-3,4-diol The following contents are mentioned in the article:

Background: Cancer stem cells (CSCs), a subpopulation in tumors, are known to cause drug resistance, tumor recurrence and metastasis. Based on the characteristic formation of mammospheres in in vitro conditions, the mammosphere formation assay has become an essential tool for quantifying CSC activity in breast cancer research. However, manual counting of mammospheres is a time-consuming process that is not amenable to high-throughput screening, and there are occasional inaccuracies in the process of determining the mammosphere diameter In this study, we proposed a novel automated counting method of mammosphere using the National Institute of Standards and Technol. (NIST)’s Integrated Colony Enumerator (NICE) with a screening of protein kinase library. Methods: Human breast cancer cell line MCF-7 was used for evaluation of tumor sphere efficiency, migration, and phenotype transition. Cell viability was assessed using MTT assay, and CSCs were identified by an anal. of CD44 expression and ALDEFLUOR assay using flow cytometry. Automated counting of mammosphere using NICE program was performed with a comparison to the result of manual counting. After identification of inhibitors to ameliorate CSC formation by screening a library of 79 protein kinase inhibitors using automated counting in primary, secondary and tertiary mammosphere assay, the effect of selected kinase inhibitors on migration, colony formation and epithelial-to-mesenchymal transition (EMT) of MCF-7 cells was investigated. Results: Automated counting of mammosphere using NICE program was an easy and less time-consuming process (<1 min for reading 6-well plate) which provided a comparable result with manual counting. Inhibition of calcium/calmodulin-dependent protein kinase II (CaMKII), Janus kinase-3 (JAK-3), and IκB kinase (IKK) were identified to decrease the formation of MCF-7-derived CSCs in primary, secondary and tertiary mammosphere assay. These protein kinase inhibitors alleviated TGF-β1-induced migration, colony formation and EMT of MCF-7 cells. Conclusions: We have developed a novel automated cell-based screening method which provided an easy, accurate and reproducible way for mammosphere quantification. This study is the first to show the efficacy of an automated medium-throughput mammosphere-counting method in CSC-related research with an identification of protein kinase inhibitors to ameliorate CSC formation. This study involved multiple reactions and reactants, such as (2R,3R,4S,5R)-2-(4-Amino-5-iodo-7H-pyrrolo[2,3-d]pyrimidin-7-yl)-5-(hydroxymethyl)tetrahydrofuran-3,4-diol (cas: 24386-93-4Safety of (2R,3R,4S,5R)-2-(4-Amino-5-iodo-7H-pyrrolo[2,3-d]pyrimidin-7-yl)-5-(hydroxymethyl)tetrahydrofuran-3,4-diol).

(2R,3R,4S,5R)-2-(4-Amino-5-iodo-7H-pyrrolo[2,3-d]pyrimidin-7-yl)-5-(hydroxymethyl)tetrahydrofuran-3,4-diol (cas: 24386-93-4) belongs to tetrahydrofuran derivatives. Tetrahydrofurans and furans are important oxygen-containing heterocycles that often exhibit interesting properties for biological applications or applications in the cosmetic industry. THF (Tetrahydrofuran) is also used as a starting material for the synthesis of poly(tetramethylene ether) glycol (PTMG), etc.Safety of (2R,3R,4S,5R)-2-(4-Amino-5-iodo-7H-pyrrolo[2,3-d]pyrimidin-7-yl)-5-(hydroxymethyl)tetrahydrofuran-3,4-diol

Referemce:
Tetrahydrofuran – Wikipedia,
Tetrahydrofuran | (CH2)3CH2O – PubChem

Cytotoxic effect of 5-aminoimidazole-4-carboxamide-1-beta-4-ribofuranoside (AICAR) on childhood acute lymphoblastic leukemia (ALL) cells: implication for targeted therapy was written by Sengupta, Tapas K.;Leclerc, Gilles M.;Kinser, Ting Ting Hsieh;Leclerc, Guy J.;Singh, Inderjit;Barredo, Julio C.. And the article was included in Molecular Cancer in 2007.Recommanded Product: 24386-93-4 The following contents are mentioned in the article:

Background: Acute lymphoblastic leukemia (ALL) is the most common hematol. malignancy affecting children. Despite significant progress and success in the treatment of ALL, a significant number of children continue to relapse and for them, outcome remains poor. Therefore, the search for novel therapeutic approaches is warranted. The aim of this study was to investigate the AMP activated protein kinase (AMPK) as a potential target in childhood acute lymphoblastic leukemia (ALL) subtypes characterized by non-random translocation signature profiles. We evaluated the effects of the AMPK activator AICAR on cell growth, cell cycle regulators and apoptosis of various childhood ALL cells. Results: We found that treatment with AICAR inhibited cell proliferation, induced cell cycle arrest in G1-phase, and apoptosis in CCRF-CEM (T-ALL), NALM6 (Bp-ALL), REH (Bp-ALL, TEL/AML1) and SupB15 (Bp-ALL, BCR/ABL) cells. These effects were abolished by treatment with the adenosine kinase inhibitor 5′-iodotubericidin prior to addition of AICAR indicating that AICAR’s cytotoxicity is mediated through AMPK activation. Moreover, we determined that growth inhibition exerted by AICAR was associated with activation of p38-MAPK and increased expression of the cell cycle regulators p27 and p53. We also demonstrated that AICAR mediated apoptosis through the mitochondrial pathway as revealed by the release of cytochrome C and cleavage of caspase 9. Addnl., AICAR treatment resulted in phosphorylation of Akt suggesting that activation of the PI3K/Akt pathway may represent a compensatory survival mechanism in response to apoptosis and/or cell cycle arrest. Combined treatment with AICAR and the mTOR inhibitor rapamycin resulted in additive antiproliferative activity ALL cells. Conclusion: AICAR-mediated AMPK activation was found to be a proficient cytotoxic agent in ALL cells and the mechanism of its anti-proliferative and apoptotic effect appear to be mediated via activation of p38-MAPK pathway, increased expression of cell cycle inhibitory proteins p27 and p53, and downstream effects on the mTOR pathway, hence exhibiting therapeutic potential as a mol. target for the treatment of childhood ALL. Therefore, activation of AMPK by AICAR represents a novel approach to targeted therapy, and suggests a role for AICAR in combination therapy with inhibitors of the PI3K/Akt/mTOR pathways for the treatment of childhood in ALL. This study involved multiple reactions and reactants, such as (2R,3R,4S,5R)-2-(4-Amino-5-iodo-7H-pyrrolo[2,3-d]pyrimidin-7-yl)-5-(hydroxymethyl)tetrahydrofuran-3,4-diol (cas: 24386-93-4Recommanded Product: 24386-93-4).

(2R,3R,4S,5R)-2-(4-Amino-5-iodo-7H-pyrrolo[2,3-d]pyrimidin-7-yl)-5-(hydroxymethyl)tetrahydrofuran-3,4-diol (cas: 24386-93-4) belongs to tetrahydrofuran derivatives. Tetrahydrofuran and dihydrofuran form the basic structural unit of many naturally occurring scaffolds like gambieric acid A and ciguatoxin, goniocin, and some biologically active molecules. THF (Tetrahydrofuran) is also used as a starting material for the synthesis of poly(tetramethylene ether) glycol (PTMG), etc.Recommanded Product: 24386-93-4

Referemce:
Tetrahydrofuran – Wikipedia,
Tetrahydrofuran | (CH2)3CH2O – PubChem

LASSBio-897 reduces lung injury induced by silica particles in mice: potential interaction with the A₂A receptor was written by Carvalho, Vinicius F.;Ferreira, Tatiana P. T.;de Arantes, Ana C. S.;Noeel, Francois;Tesch, Roberta;Sant’Anna, Carlos M. R.;Barreiro, Eliezer J. L.;Fraga, Carlos A. M.;Rodrigues e Silva, Patricia M.;Martins, Marco A.. And the article was included in Frontiers in Pharmacology in 2017.Application of 24386-93-4 The following contents are mentioned in the article:

Silicosis is a lethal fibro-granulomatous pulmonary disease highly prevalent in developing countries, for which no proper therapy is available. Among a small series of N-acylhydrazones, the safrole-derived compound LASSBio-897 (3-thienylidene-3, 4- methylenedioxybenzoylhydrazide) raised interest due to its ability to bind to the adenosine A₂A receptor. Here, we evaluated the anti-inflammatory and anti-fibrotic potential of LASSBio-897, exploring translation to a mouse model of silicosis and the A₂A receptor as a site of action. Pulmonary mechanics, inflammatory, and fibrotic changes were assessed 28 days after intranasal instillation of silica particles in Swiss-Webster mice. Glosensor cAMP HEK293G cells, CHO cells stably expressing human adenosine receptors and ligand binding assay were used to evaluate the pharmacol. properties of LASSBio-897 in vitro. Mol. docking studies of LASSBio-897 were performed using the genetic algorithm software GOLD 5.2. We found that the interventional treatment with the A₂A receptor agonist CGS 21680 reversed silica particle-induced airway hyper-reactivity as revealed by increased responses of airway resistance and lung elastance following aerosolized methacholine. LASSBio-897 (2 and 5 mg/kg, oral) similarly reversed pivotal lung pathol. features of silicosis in this model, reducing levels of airway resistance and lung elastance, granuloma formation and collagen deposition. In competition assays, LASSBio-897 decreased the binding of the selective A₂A receptor agonist [³H]-CGS21680 (IC₅₀ D 9.3μM). LASSBio-897 (50μM) induced modest cAMP production in HEK293G cells, but it clearly synergized the cAMP production by adenosine in a mechanism sensitive to the A₂A antagonist SCH 58261. This synergism was also seen in CHO cells expressing the A₂A, but not those expressing A₂B, A₁ or A₃ receptors. Based on the evidence that LASSBio-897 binds to A₂A receptor, mol. docking studies were performed using the A₂A receptor crystal structure and revealed possible binding modes of LASSBio-897 at the orthosteric and allosteric sites. These findings highlight LASSBio- 897 as a lead compound in drug development for silicosis, emphasizing the role of the A₂A receptor as its putative site of action. This study involved multiple reactions and reactants, such as (2R,3R,4S,5R)-2-(4-Amino-5-iodo-7H-pyrrolo[2,3-d]pyrimidin-7-yl)-5-(hydroxymethyl)tetrahydrofuran-3,4-diol (cas: 24386-93-4Application of 24386-93-4).

(2R,3R,4S,5R)-2-(4-Amino-5-iodo-7H-pyrrolo[2,3-d]pyrimidin-7-yl)-5-(hydroxymethyl)tetrahydrofuran-3,4-diol (cas: 24386-93-4) belongs to tetrahydrofuran derivatives. Solid acid catalysis, and the advantages often associated with their use, have been proved equally efficient for the synthesis of tetrahydrofurans or furans. Oxidations have also proved to be valuable and efficient approaches to chiral tetrahydrofuran derivatives.Application of 24386-93-4

Referemce:
Tetrahydrofuran – Wikipedia,
Tetrahydrofuran | (CH2)3CH2O – PubChem

Physiological Concentrations of Divalent Magnesium Ion Activate the Serine/Threonine Specific Protein Kinase ERK2 was written by Waas, William F.;Dalby, Kevin N.. And the article was included in Biochemistry in 2003.Category: tetrahydrofurans The following contents are mentioned in the article:

Extracellular regulated protein kinase 2 (ERK2) is a eukaryotic protein kinase whose activity is regulated by phorbol esters, serum, and growth factors, and displays enhanced activity in several human tumors. Despite its important biol. function, its mechanism of catalysis and mode of regulation are poorly understood. Recently, we showed that in the presence of 10 mM magnesium chloride, ERK2 phosphorylates the transcription factor Ets-1 through a random-ordered ternary-complex mechanism [Waas, W. F., and Dalby, K. N. (2002) J. Biol. Chem. 277, 12532]. Now we provide kinetic evidence that ERK2 must bind two divalent magnesium ions to facilitate catalysis at a physiol. relevant rate, because a second magnesium ion promotes both MgATP^2- binding and phosphoryl transfer. The velocity dependence on magnesium at saturating concentrations of the protein substrate, EtsΔ138, over a range of ATP^4- and Mg²⁺ ion concentrations, supports the notion that magnesium is an essential activator of ERK2. At high (≥1 mM) concentrations of ATP^4-, the velocity dependence on total Mg²⁺ is sigmoidal, but plateaus at high concentrations of free Mg²⁺, where the enzyme is fully activated. At concentrations of Mg²⁺ of ≤4 mM, the velocity dependence on ATP^4- displays a peak when the concentration of ATP^4- approaches that of total Mg²⁺ and tends to zero at high concentrations of ATP^4-, where the enzyme is predominantly unactivated. The observed velocity dependencies are consistent with the notion that ERK2·EtsΔ138 complexes and ATP^4- compete for the same pool of Mg²⁺ ions in solution No binding of ATP^4- (0-2.5 mM) by ERK2 (65 μM) can be detected using isothermal titration calorimetry at 27°, pH 8.0, and an ionic strength of 0.15 M (KCl), suggesting that the complex, MgATP^2-, is the true substrate for ERK2. In contrast, 5-iodotubericidin binds ERK2 tightly (K_d = 1 μM) and displays a competitive inhibition pattern toward MgATP^2- and a mixed pattern toward free Mg²⁺, suggesting that the binding of Mg²⁺ before MgATP^2- is not compulsory. This study involved multiple reactions and reactants, such as (2R,3R,4S,5R)-2-(4-Amino-5-iodo-7H-pyrrolo[2,3-d]pyrimidin-7-yl)-5-(hydroxymethyl)tetrahydrofuran-3,4-diol (cas: 24386-93-4Category: tetrahydrofurans).

(2R,3R,4S,5R)-2-(4-Amino-5-iodo-7H-pyrrolo[2,3-d]pyrimidin-7-yl)-5-(hydroxymethyl)tetrahydrofuran-3,4-diol (cas: 24386-93-4) belongs to tetrahydrofuran derivatives. Tetrahydrofurans and furans are important oxygen-containing heterocycles that often exhibit interesting properties for biological applications or applications in the cosmetic industry. Tetrahydrofuran can also be produced, or synthesised, via catalytic hydrogenation of furan. This process involves converting certain sugars into THF by digesting to furfural. An alternative to this method is the catalytic hydrogenation of furan with a nickel catalyst.Category: tetrahydrofurans

Referemce:
Tetrahydrofuran – Wikipedia,
Tetrahydrofuran | (CH2)3CH2O – PubChem

Inhibition of Adenosine Kinase Attenuates Acute Lung Injury* was written by Koehler, David;Streienberger, Ariane;Morote-Garcia, Julio C.;Granja, Tiago F.;Schneider, Mariella;Straub, Andreas;Boison, Detlev;Rosenberger, Peter. And the article was included in Critical Care Medicine in 2016.Formula: C11H13IN4O4 The following contents are mentioned in the article:

Objectives: Extracellular adenosine has tissue-protective potential in several conditions. Adenosine levels are regulated by a close interplay between nucleoside transporters and adenosine kinase. On the basis of the evidence of the role of adenosine kinase in regulating adenosine levels during hypoxia, we evaluated the effect of adenosine kinase on lung injury. Furthermore, we tested the influence of a pharmacol. approach to blocking adenosine kinase on the extent of lung injury. Design: Prospective exptl. animal study. Setting: University-based research laboratory Subjects: In vitro cell lines, wild-type and adenosine kinase mice. Interventions: We tested the expression of adenosine kinase during inflammatory stimulation in vitro and in a model of lipopolysaccharide inhalation in vivo. Studies using the adenosine kinase promoter were performed in vitro. Wild-type and adenosine kinase mice were subjected to lipopolysaccharide inhalation. Pharmacol. inhibition of adenosine kinase was performed in vitro, and its effect on adenosine uptake was evaluated. The pharmacol. inhibition was also performed in vivo, and the effect on lung injury was assessed. Measurements and main results: We observed the repression of adenosine kinase by proinflammatory cytokines and found a significant influence of nuclear factor kappa-light-chain-enhancer of activated B-cells on regulation of the adenosine kinase promoter. Mice with endogenous adenosine kinase repression (adenosine kinase) showed reduced infiltration of leukocytes into the alveolar space, decreased total protein and myeloperoxidase levels, and lower cytokine levels in the alveolar lavage fluid. The inhibition of adenosine kinase by 5-iodotubercidin increased the extracellular adenosine levels in vitro, diminished the transmigration of neutrophils, and improved the epithelial barrier function. The inhibition of adenosine kinase in vivo showed protective properties, reducing the extent of pulmonary inflammation during lung injury. Conclusions: Taken together, these data show that adenosine kinase is a valuable target for reducing the inflammatory changes associated with lung injury and should be pursued as a therapeutic option. This study involved multiple reactions and reactants, such as (2R,3R,4S,5R)-2-(4-Amino-5-iodo-7H-pyrrolo[2,3-d]pyrimidin-7-yl)-5-(hydroxymethyl)tetrahydrofuran-3,4-diol (cas: 24386-93-4Formula: C11H13IN4O4).

(2R,3R,4S,5R)-2-(4-Amino-5-iodo-7H-pyrrolo[2,3-d]pyrimidin-7-yl)-5-(hydroxymethyl)tetrahydrofuran-3,4-diol (cas: 24386-93-4) belongs to tetrahydrofuran derivatives. Tetrahydrofuran and dihydrofuran form the basic structural unit of many naturally occurring scaffolds like gambieric acid A and ciguatoxin, goniocin, and some biologically active molecules. THF (Tetrahydrofuran) is also used as a starting material for the synthesis of poly(tetramethylene ether) glycol (PTMG), etc.Formula: C11H13IN4O4

Referemce:
Tetrahydrofuran – Wikipedia,
Tetrahydrofuran | (CH2)3CH2O – PubChem

Adenosine actions are preserved in corpus cavernosum from obese and type II diabetic db/db mouse was written by Carneiro, Fernando Silva;Giachini, Fernanda R. C.;Lima, Victor V.;Carneiro, Zidonia N.;Leite, Romulo;Inscho, Edward W.;Tostes, Rita C.;Webb, R. Clinton. And the article was included in Journal of Sexual Medicine in 2008.Related Products of 24386-93-4 The following contents are mentioned in the article:

Introduction: Erectile dysfunction (ED) in diabetes is associated with autonomic neuropathy and endothelial dysfunction. Whereas the nonadrenergic-noncholinergic (NANC)/neurogenic nitric oxide pathway has received great attention in diabetes-associated ED, few studies have addressed sympathetic overactivity. Aim: To test the hypothesis that adenosine-induced inhibition of adrenergic-mediated contractile responses in mouse corpus cavernosum is impaired in the presence of diabetes. Methods: The db/db (obesity and type II diabetes caused by a leptin receptor mutation) mouse strain was used as a model of obesity and type II diabetes, and standard procedures were performed to evaluate functional cavernosal responses. Main Outcome Measures. Increased cavernosal responses to sympathetic stimulation in db/db mice are not associated with impaired prejunctional actions of adenosine. Results: Elec. field stimulation (EFS)-, but not phenylephrine (PE)-, induced contractions are enhanced in cavernosal strips from db/db mice in comparison with those from lean littermates. Direct effects of adenosine, 2-chloro-adenosine, A₁ receptor agonist C-8031 (N6 cyclopentyladenosine), and sodium nitroprusside are similar between the strips from lean and db/db mice, whereas relaxant responses to acetylcholine and NANC stimulation are significantly impaired in the cavernosal strips from db/db mice. 5′-Iodotubercidin (adenosine kinase inhibitor) and dipyridamole (inhibitor of adenosine transport), as well as the A₁ agonist C-8031, significantly and similarly inhibit contractions induced by stimulation of adrenergic nerves in the cavernosal strips from lean and db/db mice. Conclusions: Results from this study suggest that corpora cavernosa from obese and diabetic db/db mice display altered neural-mediated responses that would favor penile detumescence, i.e., increased contractile response to adrenergic nerve stimulation and decreased relaxant responses upon activation of NANC nerves. However, increased cavernosal responses to adrenergic nerve stimulation are not due to impaired neg. modulation of sympathetic neurotransmission by adenosine in this diabetic model. This study involved multiple reactions and reactants, such as (2R,3R,4S,5R)-2-(4-Amino-5-iodo-7H-pyrrolo[2,3-d]pyrimidin-7-yl)-5-(hydroxymethyl)tetrahydrofuran-3,4-diol (cas: 24386-93-4Related Products of 24386-93-4).

(2R,3R,4S,5R)-2-(4-Amino-5-iodo-7H-pyrrolo[2,3-d]pyrimidin-7-yl)-5-(hydroxymethyl)tetrahydrofuran-3,4-diol (cas: 24386-93-4) belongs to tetrahydrofuran derivatives. THF (Tetrahydrofuran) is water-miscible and has a low viscosity making it a highly versatile solvent used in a variety of industries. Tetrahydrofuran can also be produced, or synthesised, via catalytic hydrogenation of furan. This process involves converting certain sugars into THF by digesting to furfural. An alternative to this method is the catalytic hydrogenation of furan with a nickel catalyst.Related Products of 24386-93-4

Referemce:
Tetrahydrofuran – Wikipedia,
Tetrahydrofuran | (CH2)3CH2O – PubChem

Inhibition of adenosine metabolism induces changes in post-ictal depression, respiration, and mortality in genetically epilepsy prone rats was written by Kommajosyula, Srinivasa P.;Randall, Marcus E.;Faingold, Carl L.. And the article was included in Epilepsy Research in 2016.COA of Formula: C11H13IN4O4 The following contents are mentioned in the article:

A major cause of mortality in epilepsy patients is sudden unexpected death in epilepsy (SUDEP). Post-ictal respiratory dysfunction following generalized convulsive seizures is most commonly observed in witnessed cases of human SUDEP. DBA mouse models of SUDEP are induced by audiogenic seizures (AGSz) and show high incidences of seizure-induced death due to respiratory depression. The relatively low incidence of human SUDEP suggests that it may be useful to examine seizure-associated death in an AGSz model that rarely exhibits sudden death, such as genetically epilepsy-prone rats (GEPR-9s). Adenosine is released extensively during seizures and depresses respiration, which may contribute to seizure-induced death. The present study examined the effects of inhibiting adenosine metabolism on the durations of post-ictal depression (PID) and respiratory distress (RD), changes in blood oxygen saturation (% SpO₂), and the incidence of post-seizure mortality in GEPR-9s. Systemic administration of adenosine metabolism inhibitors, erythro-9-(2-hydroxy-3-nonyl) adenine (EHNA, 30 mg/kg) with 5-Iodotubericidin (5-ITU, 3 mg/kg) in GEPR-9s resulted in significant changes in the duration of AGSz-induced PID as compared to vehicle in both genders. These agents also significantly increased the duration of post-seizure RD and significantly decreased the mean% SpO₂ after AGSz, as compared to vehicle but only in females. Subsequently, we observed that the incidences of death in both genders 12-48 h post-seizure were significantly greater in drug vs. vehicle treatment. The incidence of death in females was also significantly higher than in males, which is consistent with the elevated seizure sensitivity of female GEPR-9s developmentally. These results support a potentially important role of elevated adenosine levels following generalized seizures in the increased incidence of death in GEPR-9s induced by adenosine metabolism inhibitors. These findings may also be relevant to human SUDEP, in light of the elevated adenosine levels that occur post-ictally in humans and its respiratory depressant actions. This study involved multiple reactions and reactants, such as (2R,3R,4S,5R)-2-(4-Amino-5-iodo-7H-pyrrolo[2,3-d]pyrimidin-7-yl)-5-(hydroxymethyl)tetrahydrofuran-3,4-diol (cas: 24386-93-4COA of Formula: C11H13IN4O4).

(2R,3R,4S,5R)-2-(4-Amino-5-iodo-7H-pyrrolo[2,3-d]pyrimidin-7-yl)-5-(hydroxymethyl)tetrahydrofuran-3,4-diol (cas: 24386-93-4) belongs to tetrahydrofuran derivatives. THF (Tetrahydrofuran) is a stable compound with relatively low boiling point and excellent solvency. Oxidations have also proved to be valuable and efficient approaches to chiral tetrahydrofuran derivatives.COA of Formula: C11H13IN4O4

Referemce:
Tetrahydrofuran – Wikipedia,
Tetrahydrofuran | (CH2)3CH2O – PubChem

Astrogliosis in epilepsy leads to overexpression of adenosine kinase, resulting in seizure aggravation. was written by Fedele, Denise E;Gouder, Nicolette;Güttinger, Martin;Gabernet, Laetitia;Scheurer, Louis;Rülicke, Thomas;Crestani, Florence;Boison, Detlev. And the article was included in Brain : a journal of neurology in 2005.Application of 24386-93-4 The following contents are mentioned in the article:

Adenosine kinase (ADK) is considered to be the key regulator of the brain’s endogenous anticonvulsant, adenosine. In adult brain, ADK is primarily expressed in a subpopulation of astrocytes and striking upregulation of ADK in these cells has been associated with astrogliosis after kainic acid-induced status epilepticus (KASE) in the kainic acid mouse model of temporal lobe epilepsy. To investigate the causal relationship between KASE-induced astrogliosis, upregulation of ADK and seizure activity, we have developed a novel mouse model [the Adktm1(-/-)-Tg(UbiAdk) mouse] lacking the endogenous astrocytic enzyme due to a targeted disruption of the endogenous gene, but containing an Adk transgene under the control of a human ubiquitin promoter. Mutant Adktm1(-/-)-Tg(UbiAdk) mice were characterized by increased brain ADK activity and constitutive overexpression of transgenic ADK throughout the brain, with particularly high levels in hippocampal pyramidal neurons. This ADK overexpression was associated with increased baseline levels of locomotion. Most importantly, two-thirds of the mutant mice analysed exhibited spontaneous seizure activity in the hippocampus and cortex. This was the direct consequence of transgene expression, since this seizure activity could be prevented by systemic application of the ADK inhibitor 5-iodotubercidin. Intrahippocampal injection of kainate in the mutant mice resulted in astrogliosis to the same extent as that observed in wild-type mice despite the absence of endogenous astrocytic ADK. Therefore, KASE-induced upregulation of endogenous ADK in wild-type mice is a consequence of astrogliosis. However, seizures in kainic acid-injected mutants displayed increased intra-ictal spike frequency compared with wild-type mice, indicating that, once epilepsy is established, increased levels of ADK aggravate seizure severity. We therefore conclude that therapeutic strategies that augment the adenosine system after astrogliosis-induced upregulation of ADK constitute a neurochemical rationale for the prevention of seizures in epilepsy. This study involved multiple reactions and reactants, such as (2R,3R,4S,5R)-2-(4-Amino-5-iodo-7H-pyrrolo[2,3-d]pyrimidin-7-yl)-5-(hydroxymethyl)tetrahydrofuran-3,4-diol (cas: 24386-93-4Application of 24386-93-4).

(2R,3R,4S,5R)-2-(4-Amino-5-iodo-7H-pyrrolo[2,3-d]pyrimidin-7-yl)-5-(hydroxymethyl)tetrahydrofuran-3,4-diol (cas: 24386-93-4) belongs to tetrahydrofuran derivatives. THF (Tetrahydrofuran) is a stable compound with relatively low boiling point and excellent solvency. THF (Tetrahydrofuran) is also used as a starting material for the synthesis of poly(tetramethylene ether) glycol (PTMG), etc.Application of 24386-93-4

Referemce:
Tetrahydrofuran – Wikipedia,
Tetrahydrofuran | (CH2)3CH2O – PubChem

Interactions of 5- iodotubercidin with binding site of serine/threonine – protein kinase Haspin; an ONIOM approach study was written by Hadad, Babak Khjalili;Sadeh, Hadis Soltani;Arman, Foroozan;Esmaeilzadeh, Fatemeh. And the article was included in Recent Advances in Electrical Engineering Series in 2012.Synthetic Route of C11H13IN4O4 The following contents are mentioned in the article:

Each daughter cell has to receive the correct complement of chromosomes in mitosis. Some of mitotic kinases are critical to manage individualization of chromosomes. Haspin is newly discovered kinase with regulatory effect. Haspin protein has serine/ threonine kinase activity. Thr 3 of Histone H3 is the only substrate of Haspin to do phosphorylation. Highly potent and selective ligands are developed using organo non-metallic inhibitors. Non- metal centers prepare a big chem. chamber. Uncontrolled growth, survival and metastasis are some characteristics of cancer. These are caused because of perturbation of regulatory signaling pathways specially, kinases. Chems. specifically inhibits such regulators, are targets for chemotherapy. Haspin (PDB ID: 3IQ7) is analyzed in present research. H-bond and Hydrophobic pocket interactions are studied with both docking and ONIOM methods. 5- Iodotubercidin-the mimetic structure of ATP- is one of effective inhibitors. To increase the efficacy and its attraction to binding site of the Haspin, it is suggested to modify the structure of drug to increase H-bond attraction. The main engaged amino acids in binding site that are responsible to produce H- bonds, are Glu⁶⁰⁶, Gly⁶⁰⁸, Asp⁶¹¹ and Gly⁶⁵³. By modifying the drug it is possible to increase some sites, to engage more amino acids, close to present pocket. Gln⁶¹⁴, Arg⁶¹⁶ are closest functional amino acids based on primary structure. The same process will be done for hydrophobic pocket where Ile⁴⁹⁰, Gly⁴⁹¹, Val⁴⁹⁸, Ala⁵⁰⁹, Phe⁶⁰⁹, Leu⁶⁵⁶, and He⁶⁸⁶ are the main amino acids. Phe⁴⁹⁵, Phe⁴⁹⁹, He⁶⁸⁵, Val⁵⁰⁸ and Phe⁶⁰⁵ are suggested to be the next targets. Oxygen and fluorine are found more effective than iodine to make the system more stable. It is suggested to use the oxygen or fluorine as two electroneg. elements instead of the iodine. This study involved multiple reactions and reactants, such as (2R,3R,4S,5R)-2-(4-Amino-5-iodo-7H-pyrrolo[2,3-d]pyrimidin-7-yl)-5-(hydroxymethyl)tetrahydrofuran-3,4-diol (cas: 24386-93-4Synthetic Route of C11H13IN4O4).

(2R,3R,4S,5R)-2-(4-Amino-5-iodo-7H-pyrrolo[2,3-d]pyrimidin-7-yl)-5-(hydroxymethyl)tetrahydrofuran-3,4-diol (cas: 24386-93-4) belongs to tetrahydrofuran derivatives. Tetrahydrofuran (THF), or oxolane, is mainly used as a precursor to polymers. Being polar and having a wide liquid range, THF is a versatile solvent. Oxidations have also proved to be valuable and efficient approaches to chiral tetrahydrofuran derivatives.Synthetic Route of C11H13IN4O4

Referemce:
Tetrahydrofuran – Wikipedia,
Tetrahydrofuran | (CH2)3CH2O – PubChem