Category: 1750-45-4

In homogeneous catalysis, the catalyst is in the same phase as the reactant. The number of collisions between reactants and catalyst is at a maximum.In a patent, 1750-45-4, name is 5-Chloro-6-hydroxybenzo[d]oxazol-2(3H)-one, introducing its new discovery. Product Details of 1750-45-4

Preliminary characterization of a murine model for 1-bromopropane neurotoxicity: Role of cytochrome P450

Neurotoxicity of 1-bromopropane (1-BP) has been reported in both human cases and animal studies. To date, neurotoxicity of 1-BP has been induced in rats but not in mice due to the lethal hepatotoxicity of 1-BP. Oxidization by cytochromes P450 and conjugation with glutathione (GSH) are two critical metabolism pathways of 1-BP and play important roles in toxicity of 1-BP. The aim of the present study was to establish a murine model of 1-BP neurotoxicity, by reducing the hepatotoxicity of 1-BP with 1-aminobenzotriazole (1-ABT); a commonly used nonspecific P450s inhibitor. The results showed that subcutaneous or intraperitoneal injection of 1-ABT at 50?mg/kg body weight BID (100?mg/kg BW/day) for 3?days, inhibited about 92?96% of hepatic microsomal CYP2E1 activity, but only inhibited about 62?64% of CYP2E1 activity in brain microsomes. Mice treated with 1-ABT survived even after exposure to 1200?ppm 1-BP for 4 weeks and histopathological studies showed that treatment with 1-ABT protected mice from 1-BP-induced hepatic necrosis, hepatocyte degeneration, and hemorrhage. After 4-week exposure to 1-BP, the brain weight of 1-ABT(+)/1200?ppm 1-BP group was decreased significantly. In 1-ABT-treated groups, expression of hippocampal Ran protein and cerebral cortical GRP78 was dose-dependently increased by exposure to 1-BP. We conclude that the control of hepatic P450 activity allows the observation of effects of 1-BP on the murine brain at a higher concentration by reduction of hepatotoxicity. The study suggests that further experiments with liver-specific control of P450 activity using gene technology might provide better murine models for 1-bromopropane-induced neurotoxicity.

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Benzoxazole | C7H5NO – PubChem

Chemistry is traditionally divided into organic and inorganic chemistry. Formula: C7H4ClNO3, The former is the study of compounds containing at least one carbon-hydrogen bonds.In a patent£¬Which mentioned a new discovery about 1750-45-4

Inhibition of Magnolol and Honokiol on Cytochrome P450 Enzymes in Rat and Human Liver Microsomes

Objective: The purpose of this work is to evaluate the in vitro inhibitory effect of magnolol (MN) and honokiol (HN) on rat/human cytochrome P450 (CYP) enzymes (1A2/1A2, 2D/2D6, 3A/3A4, 2E1/2E1, and 2C/2C9). Methods: Rat liver microsomes (RLM) and human liver microsomes (HLM) were used as the enzyme sources. After the probe substrate of each CYP isoforms was co-incubated individually with MN or HN in RLM or HLM, the metabolite production of each probe substrate in RLM and HLM incubation medium was determined and used to evaluate the activity of corresponding CYP isoforms. Results: MN inhibited rat CYP1A2 and human CYP3A4 with the IC50 values of 10.0 and 56.2 mumol/L, respectively. HN inhibited rat CYP1A2 and CYP2E1, human CYP1A2 and CYP3A4 with the IC50 values of 12.1, 12.6, 17.8, and 43.9 mumol/L, respectively. Conclusion: HN is a moderate or weak inhibitor of human CYP1A2. Both MN and HN are weak or non inhibitors of the other tested human CYP isoforms. The results suggest that no significant metabolic interaction seems likely to occur when the substrate drugs of CYP isoforms tested in the present work are co-administered with MN and HN.

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Benzoxazole | C7H5NO – PubChem

Related Products of 1750-45-4, A catalyst don’t appear in the overall stoichiometry of the reaction it catalyzes, but it must appear in at least one of the elementary reactions in the mechanism for the catalyzed reaction. 1750-45-4, Name is 5-Chloro-6-hydroxybenzo[d]oxazol-2(3H)-one, molecular formula is C7H4ClNO3. In a Article£¬once mentioned of 1750-45-4

Stimulation of Cl- secretion by chlorzoxazone

We previously demonstrated that 1-ethyl-2-benzimidazolone (1-EBIO) directly activates basolateral membrane calcium-activated K+ channels (K(Ca)), thereby stimulating Cl- secretion across several epithelia. In our pursuit to identify potent modulators of Cl- secretion that may be useful to overcome the Cl-secretory defect in cystic fibrosis (CF), we have identified chlorzoxazone [5-chloro-2(3H)-benzoxazolone], a clinically used centrally acting muscle relaxant, as a stimulator of Cl- secretion in several epithelial cell types, including T84, Calu-3, and human bronchial epithelium. The Cl- secretory response induced by chlorzoxazone was blocked by charybdotoxin (CTX), a known blocker of K(Ca). In nystatin-permeabilized monolayers, chlorzoxazone stimulated a basolateral membrane I(K), which was inhibited by CTX and also stimulated an apical /(Cl) that was inhibited by glibenclamide, indicating that the G(Cl) responsible for this /(Cl) may be cystic fibrosis transmembrane conductance regulator (CFTR). In membrane vesicles prepared from T84 cells, chlorzoxazone stimulated 86Rb+ uptake in a CTX-sensitive manner. In excised, inside-out patches, chlorzoxazone activated an inwardly-rectifying K+ channel, which was inhibited by CTX. 6- Hydroxychlorzoxazone, the major metabolite of chlorzoxazone, did not activate K(Ca), whereas zoxazolamine (2-amino-5-chlorzoxazole) showed a similar response profile as chlorzoxazone. In normal human nasal epithelium, chlorzoxazone elicited hyperpolarization of the potential difference that was similar in magnitude to isoproterenol. However, in the nasal epithelium of CF patients with the DeltaF508 mutation of CFTR, there was no detectable Cl- secretory response to chlorzoxazone. These studies demonstrate that chlorzoxazone stimulates transepithelial Cl- secretion in normal airway epitheliumun vitro and in vivo, and suggest that stimulation requires functional CFTR in the epithelia.

Balanced chemical reaction does not necessarily reveal either the individual elementary reactions by which a reaction occurs or its rate law.Related Products of 1750-45-4. In my other articles, you can also check out more blogs about 1750-45-4

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Benzoxazole – Wikipedia,
Benzoxazole | C7H5NO – PubChem

1750-45-4, Name is 5-Chloro-6-hydroxybenzo[d]oxazol-2(3H)-one, belongs to benzoxazole compound, is a common compound. category: benzoxazoleIn an article, once mentioned the new application about 1750-45-4.

Effects of Radix Astragali and Radix Rehmanniae, the components of an anti-diabetic foot ulcer herbal formula, on metabolism of model CYP1A2, CYP2C9, CYP2D6, CYP2E1 and CYP3A4 probe substrates in pooled human liver microsomes and specific CYP isoforms

The present study investigated the effects of Radix Astragali (RA) and Radix Rehmanniae (RR), the major components of an anti-diabetic foot ulcer herbal formula (NF3), on the metabolism of model probe substrates of human CYP isoforms, CYP1A2, CYP2C9, CYP2D6, CYP2E1 and CYP3A4, which are important in the metabolism of a variety of xenobiotics. The effects of RA or RR on human CYP1A2 (phenacetin O-deethylase), CYP2C9 (tolbutamide 4-hydroxylase), CYP2D6 (dextromethorphan O-demethylase), CYP2E1 (chlorzoxazone 6-hydroxylase) and CYP3A4 (testosterone 6beta-hydroxylase) activities were investigated using pooled human liver microsomes. NF3 competitively inhibited activities of CYP2C9 (IC50 = 0.98 mg/ml) and CYP3A4 (IC50 = 0.76 mg/ml), with Ki of 0.67 and 1.0 mg/ml, respectively. With specific human CYP2C9 and CYP3A4 isoforms, NF3 competitively inhibited activities of CYP2C9 (IC 50 = 0.86 mg/ml) and CYP3A4 (IC50 = 0.88 mg/ml), with Ki of 0.57 and 1.6 mg/ml, respectively. Studies on RA or RR individually showed that RR was more important in the metabolic interaction with the model CYP probe substrates. RR dose-dependently inhibited the testosterone 6beta-hydroxylation (Ki = 0.33 mg/ml) while RA showed only minimal metabolic interaction potential with the model CYP probe substrates studied. This study showed that RR and the NF3 formula are metabolized mainly by CYP2C9 and/or CYP3A4, but weakly by CYP1A2, CYP2D6 and CYP2E1. The relatively high Ki values of NF3 (for CYP2C9 and CYP3A4 metabolism) and RR (for CYP3A4 metabolism) would suggest a low potential for NF3 to cause herb-drug interaction involving these CYP isoforms.

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Benzoxazole – Wikipedia,
Benzoxazole | C7H5NO – PubChem

Related Products of 1750-45-4, The reaction rate of a catalyzed reaction is faster than the reaction rate of the uncatalyzed reaction at the same temperature.1750-45-4, Name is 5-Chloro-6-hydroxybenzo[d]oxazol-2(3H)-one, molecular formula is C7H4ClNO3. In a Article£¬once mentioned of 1750-45-4

Evaluation of the synergistic effect of allium sativum, eugenia jambolana, momordica charantia, ocimum sanctum, and psidium guajava on hepatic and intestinal drug metabolizing enzymes in rats

Aims/Background: This study was to investigated the synergistic effect of polyherbal formulations (PHF) of Allium sativum L., Eugenia jambolana Lam., Momordica charantia L., Ocimum sanctum Linn., and Psidium guajava L. in the inhibition/induction of hepatic and intestinal cytochrome P450 (CYPs) and Phase-II conjugated drug metabolizing enzymes (DMEs). Consumption of these herbal remedy has been extensively documented for diabetes treatment in Ayurveda. Methodology: PHF of these five herbs was prepared, and different doses were orally administered to Sprague?Dawley rats of different groups except control group. Expression of mRNA and activity of DMEs were examined by real-time polymerase chain reaction and high performance liquid chromatography in isolated liver and intestine microsomes in PHF pretreated rats. Results: The activities of hepatic and intestinal Phase-II enzyme levels increased along with mRNA levels except CYP3A mRNA level. PHF administration increases the activity of hepatic and intestinal UDP-glucuronyltransferase and glutathione S-transferase in response to dose and time; however, the activity of hepatic sulfotransferase increased at higher doses. Conclusions: CYPs and Phase-II conjugated enzymes levels can be modulated in dose and time dependent manner. Observations suggest that polyherbal formulation might be a possible cause of herb-drug interaction, due to changes in pharmacokinetic of crucial CYPs and Phase-II substrate drug.

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Benzoxazole – Wikipedia,
Benzoxazole | C7H5NO – PubChem

Application of 1750-45-4, The reaction rate of a catalyzed reaction is faster than the reaction rate of the uncatalyzed reaction at the same temperature.1750-45-4, Name is 5-Chloro-6-hydroxybenzo[d]oxazol-2(3H)-one, molecular formula is C7H4ClNO3. In a Article£¬once mentioned of 1750-45-4

A diversified library of bacterial and fungal bifunctional cytochrome P450 enzymes for drug metabolite synthesis

Innovative biohydroxylation catalysts for the preparation of drug metabolites were developed from scratch. A set of bacterial and fungal sequences of putative and already known bifunctional P450 enzymes was identified by protein sequence alignments, expressed in Escherichia coli and characterised. Notably, a fungal self-sufficient cytochrome P450 (CYP) from Aspergillus fumigatus turned out to be especially stable during catalyst preparation and application and also in presence of organic co-solvents. To enhance the catalytic activity and broaden the substrate specificity of those variants with high expression levels prominent single mutations were introduced. Selected improved variants were then used as lyophilised bacterial lysates for the synthesis of 4′-hydroxydiclofenac and 6-hydroxychlorzoxazone, the two metabolites of active pharmaceutical compounds diclofenac and chlorzoxazone representing the same metabolites as generated by human P450s.

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Benzoxazole – Wikipedia,
Benzoxazole | C7H5NO – PubChem

Electric Literature of 1750-45-4, Because a catalyst decreases the height of the energy barrier, its presence increases the reaction rates of both the forward and the reverse reactions by the same amount.1750-45-4, Name is 5-Chloro-6-hydroxybenzo[d]oxazol-2(3H)-one, molecular formula is C7H4ClNO3. In a article£¬once mentioned of 1750-45-4

Sodium tanshinone IIA sulfonate and its interactions with human CYP450s

1.Sodium tanshinone IIA sulfonate (STS) is a water-soluble derivative of tanshinone IIA, a famous Chinese medicine used for many years to treat cardiovascular disorders. However, the role of cytochrome P450 (CYP) enzymes in the metabolism of STS was unclear. In this study, we screened the main CYPs for the metabolism of STS and studied their interactions in vitro. 2.Seven CYPs were screened for the metabolism of STS by human liver microsomes (HLMs) or recombinant CYP isoforms. To determine the potential of STS to affect CYP-mediated phase I metabolism in humans, phenacetin (CYP1A2), coumarin (CYP2A6), tolbutamide (CYP2C9), metoprolol (CYP2D6), chlorzoxazone (CYP2E1), S-Mephenytoin (CYP2C19), and midazolam (CYP3A4) were used as the respective probe substrates. Enzyme kinetic studies were performed to investigate the mode of inhibition of the enzyme?substrate interactions. 3.STS inhibited the activity of CYP3A4 in a dose-dependent manner in the HLMs and CYP3A4 isoform. Other CYP isoforms, including CYP1A2, CYP2A6, CYP2C9, CYP2D6, CYP2E1, and CYP2C19, showed minimal or no effect on the metabolism of STS. 4.The results suggested that STS primarily inhibits the activities of CYP3A4 in vitro, and STS has the potential to perpetrate drug?drug interactions with other CYP3A4 substrates.

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Benzoxazole – Wikipedia,
Benzoxazole | C7H5NO – PubChem

In heterogeneous catalysis, the catalyst is in a different phase from the reactants. Application In Synthesis of 5-Chloro-6-hydroxybenzo[d]oxazol-2(3H)-one, At least one of the reactants interacts with the solid surface in a physical process called adsorption in such a way. 1750-45-4, name is 5-Chloro-6-hydroxybenzo[d]oxazol-2(3H)-one. In an article£¬Which mentioned a new discovery about 1750-45-4

The tyrosine kinase inhibitor nilotinib selectively inhibits cyp2c8 activities in human liver microsomes

The tyrosine kinase inhibitor nilotinib was examined for its inhibition of cytochrome P450s (CYPs) in human liver microsomes and in human CYPs expressed in a baculovirus-insect cell system. Nilotinib demonstrated preferential inhibition of CYP2C8-mediated paclitaxel 6alpha-hydroxylation, rosiglitazone hydroxylation and amodiaquine N-deethylation in human liver microsomes, with IC50 values of 0.4, 7.5 and 0.7 muM, respectively. The IC 50 value of nilotinib for paclitaxel 6alpha-hydroxylation was 20-fold lower than that of the other five tyrosine-kinase inhibitors tested. Nilotinib appears to display competitive inhibition against paclitaxel 6alpha-hydroxylation and amodiaquine N-deethylation, with estimated mean Ki values of 0.90 and 0.15 muM in human liver microsomes and 0.10 and 0.61 muM in recombinant human CYP2C8, respectively. These results are consistent with those of molecular docking simulations, where paclitaxel could not access the CYP2C8 catalytic site in the presence of nilotinib, but the binding of midazolam, a substrate of CYP3A4, to the catalytic site of CYP3A4 was not affected by nilotinib. The demonstrated inhibitory activity of nilotinib against CYP2C8 at concentrations less than those observed in patients who received nilotinib therapy is of potential clinical relevance and further in vivo exploration is warranted.

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Benzoxazole – Wikipedia,
Benzoxazole | C7H5NO – PubChem

1750-45-4, Name is 5-Chloro-6-hydroxybenzo[d]oxazol-2(3H)-one, belongs to benzoxazole compound, is a common compound. SDS of cas: 1750-45-4In an article, once mentioned the new application about 1750-45-4.

Metabolic drug-drug interaction potential of macrolactin a and 7-O-succinyl macrolactin a assessed by evaluating cytochrome P450 inhibition and induction and UDP-glucuronosyltransferase inhibition in Vitro

Macrolactin A (MA) and 7-O-succinyl macrolactin A (SMA), polyene macrolides containing a 24-membered lactone ring, show antibiotic effects superior to those of teicoplanin against vancomycin-resistant enterococci and methicillin-resistant Staphylococcus aureus. MA and SMA are currently being evaluated as antitumor agents in preclinical studies in Korea. We evaluated the potential of MA and SMA for the inhibition or induction of human liver cytochrome P450 (CYP) enzymes and UDP-glucuronosyltransferases (UGTs) in vitro to assess their safety as new molecular entities. We demonstrated that MA and SMA are potent competitive inhibitors of CYP2C9, with Ki values of 4.06 muM and 10.6 muM, respectively. MA and SMA also weakly inhibited UGT1A1 activity, with Ki values of 40.1 muM and 65.3 muM, respectively. However, these macrolactins showed no time-dependent inactivation of the nine CYPs studied. In addition, MA and SMA did not induce CYP1A2, CYP2B6, or CYP3A4/5. On the basis of an in vitro-in vivo extrapolation, our data strongly suggested that MA and SMA are unlikely to cause clinically significant drugdrug interactions mediated via inhibition or induction of most of the CYPs involved in drug metabolism in vivo, except for the inhibition of CYP2C9 by MA. Similarly, MA and SMA are unlikely to inhibit the activity of UGT1A1, UGT1A4, UGT1A6, UGT1A9, and UGT2B7 enzymes in vivo. Although further investigations will be required to clarify the in vivo interactions of MA with CYP2C9-targeted drugs, our findings offer a clearer understanding and prediction of drug-drug interactions for the safe use of MA and SMA in clinical practice. Copyright

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Benzoxazole – Wikipedia,
Benzoxazole | C7H5NO – PubChem

Electric Literature of 1750-45-4, Catalysts function by providing an alternate reaction mechanism that has a lower activation energy than would be found in the absence of the catalyst. In some cases, the catalyzed mechanism may include additional steps.In a article, 1750-45-4, molcular formula is C7H4ClNO3, introducing its new discovery.

Determination of brain cytochrome P450 2E1 activity in rat with the probe of chlorzoxazone by liquid chromatography-mass spectrometry

A simple and sensitive method was developed for the determination of cytochrome P450 2E1 (CYP2E1) activity based on the liquid chromatography-mass spectrometry (LC-MS) analysis of 6-hydroxychlorzoxazone generated by 6-hydroxylation of chlorzoxazone under specific catalysis of CYP2E1. In the proposed method, 2-benzoxazolinone was chosen as internal standard and isopropyl ether was used as extraction solvent for sample preparation. The inter-day and intra-day precisions at low, medium and high concentrations of 6-hydroxychlorzoxazone were below 20.0%, and the LOD (S/N = 3) was 0.05. ng/mL. This method was applied to analyze the CYP2E1 activity of rat in different brain regions including frontal cortex (FC), cerebellum (CB), brain stem (BS), hippocampus (HC), striatum (ST), thalamus (TH), and olfactory bulb (OB). The results confirmed that chlorzoxazone was a suitable probe for the determination of CYP2E1 activity in brain regions and samples with low content of CYP2E1.

The proportionality constant is the rate constant for the particular unimolecular reaction. the reaction rate is directly proportional to the concentration of the reactant. I hope my blog about 1750-45-4 is helpful to your research. Electric Literature of 1750-45-4

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Benzoxazole – Wikipedia,
Benzoxazole | C7H5NO – PubChem