Tag: 300-400

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

Insight into the biological impact of COVID-19 and its vaccines on human health was written by Ashwlayan, Vrish Dhwaj;Antlash, Chanchal;Imran, Mohd.;Asdaq, Syed Mohammed Basheeruddin;Alshammari, Mohammed Kanan;Alomani, Marwa;Alzahrani, Eman;Sharma, Divya;Tomar, Ritu;Arora, Mandeep Kumar. And the article was included in Saudi Journal of Biological Sciences in 2022.HPLC of Formula: 2492423-29-5 The following contents are mentioned in the article:

A review. COVID-19 (coronavirus disease-2019) is a contagious illness that has been declared a global epidemic by the World Health Organization (WHO). The coronavirus causes diseases ranging in severity from the common cold to severe respiratory diseases and death. Coronavirus primarily affects blood pressure by attaching to the angiotensin converting enzyme 2 (ACE 2) receptor. This virus has an impact on multiple organ systems, including the central nervous system, immune system, cardiovascular system, peripheral nervous system, gastrointestinal tract, endocrine system, urinary system, skin, and pregnancy. For the prevention of COVID-19, various vaccines such as viral-like particle vaccines, entire inactivated virus vaccines, viral vector vaccines, live attenuated virus vaccines, subunit vaccines, RNA vaccines, and DNA vaccines are now available. Some of the COVID-19 vaccines are reported to cause a variety of adverse effects that range from mild to severe in nature. SARS-CoV-2 replication is controlled by the RNA-Dependent RNA-Polymerase enzyme (RdRp). The availability of FDA-approved anti-RdRp drugs (Ribavirin, Remdesivir, Sofosbuvir, Galidesivir, and Tenofovir) as potent drugs against SARS-CoV-2 that tightly bind to its RdRp may aid in the treatment of patients and reduce the risk of the mysterious new form of COVID-19 viral infection. RdRp inhibitors, such as remdesivir (an anti-Ebola virus exptl. drug) and favipiravir (an anti-influenza drug), inhibit RdRp and thus slow the progression of COVID-19 and associated clin. symptoms, as well as significantly shorten recovery time. Molnupiravir, an orally active RdRp inhibitor and noval broad spectrum antiviral agent, is an iso-Pr pro-drug of EIDD-1931 for emergency use. Galidesivir′s in vitro and in vivo activities are limited to RNA of human public health concern. Top seeds for antiviral treatments with high potential to combat the SARS-CoV-2 strain include guanosine derivatives (IDX-184), setrobuvir, and YAK. The goal of this review is to compile scattered information on available COVID-19 vaccines and other treatments for protecting the human body from their harmful effects and to provide options for making better choices in a timely manner. This study involved multiple reactions and reactants, such as ((2R,3S,4R,5R)-3,4-Dihydroxy-5-((Z)-4-(hydroxyimino)-2-oxo-3,4-dihydropyrimidin-1(2H)-yl)tetrahydrofuran-2-yl)methyl isobutyrate (cas: 2492423-29-5HPLC of Formula: 2492423-29-5).

((2R,3S,4R,5R)-3,4-Dihydroxy-5-((Z)-4-(hydroxyimino)-2-oxo-3,4-dihydropyrimidin-1(2H)-yl)tetrahydrofuran-2-yl)methyl isobutyrate (cas: 2492423-29-5) 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. Commercial tetrahydrofuran contains substantial water that must be removed for sensitive operations, e.g. those involving organometallic compounds. Although tetrahydrofuran is traditionally dried by distillation from an aggressive desiccant, molecular sieves are superior.HPLC of Formula: 2492423-29-5

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

Efficacy of the use of mefenamic acid combined with standard medical care vs. standard medical care alone for the treatment of COVID-19: A randomized double-blind placebo-controlled trial was written by Guzman-Esquivel, Jose;Galvan-Salazar, Hector R.;Guzman-Solorzano, Hannah P.;Cuevas-Velazquez, Andrea C.;Guzman-Solorzano, Jose A.;Mokay-Ramirez, Karen A.;Paz-Michel, Brenda A.;Murillo-Zamora, Efren;Delgado-Enciso, Josuel;Melnikov, Valery;Delgado-Enciso, Osiris G.;Rodriguez-Sanchez, Iram P.;Martinez-Fierro, Margarita L.;Rojas-Larios, Fabian;Walle-Guillen, Mireya;Cardenas-Aguilar, Citlaly B.;Beas-Guzman, Oscar;Chaviano-Conesa, Daniel;Garcia-Garcia, Hossana S.;Delgado-Enciso, Ivan. And the article was included in International Journal of Molecular Medicine in 2022.Electric Literature of C13H19N3O7 The following contents are mentioned in the article:

Mefenamic acid is a non-steroidal anti-inflammatory drug exhibiting a wide range of anti-inflammatory, antipyretic, analgesic and probable antiviral activities. The present study evaluated the efficacy of treatment with mefenamic acid combined with standard medical care vs. standard medical care plus a placebo in ambulatory patients with coronavirus disease 2019 (COVID-19; nasal/oropharyngeal swabs reverse transcription-PCR test results pos. for severe acute respiratory syndrome coronavirus 2). The present study is a phase II prospective, two-arm, parallel-group, randomized, double-blind placebo-controlled clin. trial which analyzed 36 patients. Two aspects were evaluated during the 14-day follow-up period: (i) The time for reaching a patient acceptable symptom state (PASS), and (ii) the last day of each COVID-19 symptom presentation. Adverse effects were evaluated. The clin. severity for all the patients in the study was mild (88.9%) and moderate (11.1%). The control (placebo) group achieved PASS on day 8.0±1.3, compared with day 4.4±0.8 in the mefenamic acid group (P=0.020, Kaplan-Meier analyses using log-rank tests). Patients that received mefenamic acid plus standard medical care had a ~16-fold higher probability of achieving PASS on day 8 (adjusted RR, 15.57; 95% CI, 1.22-198.71; P = 0.035), compared with the placebo plus stan- dard medical care group. All symptoms lasted for fewer days in the mefenamic acid group, compared with the placebo group; however, only the symptoms of headache (P = 0.008), retro-orbital eye pain (P=0.049), and sore throat (P = 0.029) exhibited statistically significant differences. The experi- mental treatment produced no severe adverse effects. On the whole, the present study demonstrates that the administration of mefenamic acid markedly reduced the symptomatol. and time to reach PASS in ambulatory patients with COVID-19. Due to its probable antiviral effects and potent anti-inflam- matory mechanisms, mefenamic acid may prove to be useful in the treatment of COVID-19, in combination with other drugs, including the new antivirals (remdesivir, molnupiravir, or favipiravir). However, future studies are also required to confirm these findings. This study involved multiple reactions and reactants, such as ((2R,3S,4R,5R)-3,4-Dihydroxy-5-((Z)-4-(hydroxyimino)-2-oxo-3,4-dihydropyrimidin-1(2H)-yl)tetrahydrofuran-2-yl)methyl isobutyrate (cas: 2492423-29-5Electric Literature of C13H19N3O7).

((2R,3S,4R,5R)-3,4-Dihydroxy-5-((Z)-4-(hydroxyimino)-2-oxo-3,4-dihydropyrimidin-1(2H)-yl)tetrahydrofuran-2-yl)methyl isobutyrate (cas: 2492423-29-5) 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. Oxidations have also proved to be valuable and efficient approaches to chiral tetrahydrofuran derivatives.Electric Literature of C13H19N3O7

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

Accelerated first-in-human clinical trial of EIDD-2801/MK-4482 (molnupiravir), a ribonucleoside analog with potent antiviral activity against SARS-CoV-2 was written by Holman, Wendy;Holman, Wayne;McIntosh, Stacy;Painter, Wendy;Painter, George;Bush, Jim;Cohen, Oren. And the article was included in Trials in 2021.HPLC of Formula: 2492423-29-5 The following contents are mentioned in the article:

Abstract: A recently published article described the safety, tolerability, and pharmacokinetic profile of molnupiravir (Painter et al. 2021), a novel antiviral agent with potent activity against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease 2019 (COVID-19). Here, we report an unprecedented collaboration between sponsor, contract research organization (CRO), and regulatory authorities that enabled accelerated generation of these phase I data, including administration of the first-in-human (FIH) dose of molnupiravir within 5 days of receiving regulatory approval in the United Kingdom (UK). Single and multiple ascending dose (SAD and MAD, resp.) cohorts were dosed in randomized, double-blind, and placebo-controlled fashion, with a 6:2 active-to-placebo ratio in each cohort. A food-effect (FE) cohort included 10 subjects who were randomized to receive drug in the fasted or fed state followed by the fed or fasted state to complete a fed and fasted sequence for each subject. Dose escalation decisions were accelerated and MAD cohorts were initiated prior to completion of all SAD cohorts with the provision that the total daily dose in a MAD cohort would not exceed a dose proven to be safe and well-tolerated in a SAD cohort. Dosing in healthy volunteers was completed for eight single ascending dose (SAD) cohorts, seven multiple ascending dose (MAD) cohorts, and one food-effect (FE) cohort within approx. 16 wk of initial protocol submission to the Research Ethics Committee (REC) and Medicines and Healthcare products Regulatory Agency (MHRA). Working to standard industry timelines, the FIH study would have taken approx. 46 wk to complete and 33 wk to enable phase 2 dosing. Data from this study supported submission of a phase 2/3 clin. trial protocol to the US Food and Drug Administration (FDA) within 8 wk of initial protocol submission, with FDA comments permitting phase 2 study initiation within two addnl. weeks. In the setting of a global pandemic, this model of collaboration allows for accelerated generation of clin. data compared to standard processes, without compromising safety. This study involved multiple reactions and reactants, such as ((2R,3S,4R,5R)-3,4-Dihydroxy-5-((Z)-4-(hydroxyimino)-2-oxo-3,4-dihydropyrimidin-1(2H)-yl)tetrahydrofuran-2-yl)methyl isobutyrate (cas: 2492423-29-5HPLC of Formula: 2492423-29-5).

((2R,3S,4R,5R)-3,4-Dihydroxy-5-((Z)-4-(hydroxyimino)-2-oxo-3,4-dihydropyrimidin-1(2H)-yl)tetrahydrofuran-2-yl)methyl isobutyrate (cas: 2492423-29-5) belongs to tetrahydrofuran derivatives.Tetrahydrofuran has many industry uses as a solvent including in natural and synthetic resins, high polymers, fat oils, rubber, polymer. Tetrahydrofuran reaction with hydrogen sulfide: In the presence of a solid acid catalyst, tetrahydrofuran reacts with hydrogen sulfide to give tetrahydrothiophene.HPLC of Formula: 2492423-29-5

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

TMPRSS2, a novel host-directed drug target against SARS-CoV-2 was written by Keller, Christian;Boettcher-Friebertshaeuser, Eva;Lohoff, Michael. And the article was included in Signal Transduction and Targeted Therapy in 2022.Category: tetrahydrofurans The following contents are mentioned in the article:

In a recent study in Nature, Shapira et al. reported that the peptidomimetic compound N-0385 inhibited SARS-CoV-2 infection in vitro in remarkably low concentrations by blocking the host cell protease TMPRSS2, which mediates proteolytic cleavage of the SARS-CoV-2 major surface glycoprotein spike(S). Antigenic escape by, e.g., the Omicron variant (B.1.1.529) may jeopardize passive immunization by monoclonal antibodies, calling for complementary concepts in prophylaxis and therapy. So far, these have concentrated on agents that directly interfere with viral replication, e.g., by inhibition of the viral 3CL proprotease (paxlovid), by inhibition of the RNA-dependent RNA polymerase (remdesivir), or by introducing copying errors (molnupiravir). Viral infection not only requires binding of S to its receptor angiotensin-converting enzyme 2 (ACE2) but also cleavage of S at two distinct sites by host cell proteases: First, furin (and related pro-protein convertases) cleaves at a polybasic site, generating the S1 and S2 subunits, which remainnon-covalently linked (S1/S2 site, Fig.1a). Mechanistically, TMPRSS2 inhibition results in incompletely cleaved, fusion-incompetent SARS-CoV-2 viruses that are unable to infect new host cells (Fig.1a). The data presented by Shapira et al. suggest spike maturation by inhibiting TMPRSS2 as a potent drug target in COVID-19 when the inhibitor is given before or early in infection. As an advantage over virus-directed therapies, host-directed targets have a low potential for resistance: The TMPRSS2 cleavage site of the SARS-CoV-2 spike protein has remained very conserved over the pandemic (Fig.1b), suggesting that N-0385 should retain a high potency against future variants of concern. Another advantage to target TMPRSS2 is its activating function in other viral infections (e.g., other corona viruses, influenza virus), which expands the field of potential applications for TMPRSS2 inhibitors. Broad-spectrum serine protease inhibitors against COVID-19 that were recently evaluated in clin. trials are i.v. nafamostat, a synthetic inhibitor, and aerosolized aprotinin, a protease inhibitor from bovine lung. This study involved multiple reactions and reactants, such as ((2R,3S,4R,5R)-3,4-Dihydroxy-5-((Z)-4-(hydroxyimino)-2-oxo-3,4-dihydropyrimidin-1(2H)-yl)tetrahydrofuran-2-yl)methyl isobutyrate (cas: 2492423-29-5Category: tetrahydrofurans).

((2R,3S,4R,5R)-3,4-Dihydroxy-5-((Z)-4-(hydroxyimino)-2-oxo-3,4-dihydropyrimidin-1(2H)-yl)tetrahydrofuran-2-yl)methyl isobutyrate (cas: 2492423-29-5) 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.Category: tetrahydrofurans

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