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           Search results for: Anthranilic Acid-13C6 C13C6H7NO2 CAS: 335081-06-6   

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Structure-based design of functionalized 2-substituted and 1,2-disubstituted benzimidazole derivatives and their antibacterial efficacy.

The aim of this present study was to synthesize 2-substituted and 1,2-disubstituted benzimidazole derivatives to investigate their diversity for possible future drug design. The structure-based design of precursors 2-(1H-benzimidazol-2-yl)aniline , 2-(3,5-dinitro phenyl)-1H-benzimidazole and 2-benzyl-1H-benzimidazole were achieved by the condensation reaction of -phenylenediamine with anthranilic acid, 3,5-dinitrophenylbenzoic acid, and phenylacetic acid, respectively. The precursors , and , upon reaction with six different electrophile-releasing agents, furnished the corresponding 2-substituted benzimidazole, and 1,2-disubstituted benzimidazole derivatives and , respectively. The structural identity of the targeted compounds was authenticated by elemental analytical data and spectral information from FT-IR, UV, H, and C NMR. The outcome of the findings from the screening unveiled 2-benzyl-1-(phenylsulfonyl)-1H-benzimidazole as the most active derivative with lowest MIC value of 15.63 µg/mL.

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CRISPR/Cas9 mediated G4946E substitution in the ryanodine receptor of Spodoptera exigua confers high levels of resistance to diamide insecticides.

Diamide insecticides selectively activate insect ryanodine receptors (RyRs), inducing uncontrolled release of calcium ions, and causing muscle contraction, paralysis and eventually death. The RyR substitution associated with diamide resistance has been identified in three lepidopteran pests, Plutella xylostella, Tuta absoluta and Chilo suppressalis. Recently, the T. absoluta RyR mutation was knocked into the model insect Drosophila melanogaster by CRISPR/Cas9 mediated genome editing and provided in vivo functional confirmation for its role in diamide resistance. In the present study, we successfully introduced the RyR mutation with CRISPR/Cas9 technology into a lepidopteran pest of global importance, Spodoptera exigua. The genome-edited strain (named 4946E) homozygous for the SeRyR mutation exhibited 223-, 336- and >1000-fold resistance to chlorantraniliprole, cyantraniliprole and flubendiamide, respectively when compared to the wild type strain (WHS) of S. exigua. Reciprocal crossing experiments revealed that the target-site resistance in strain 4946E underlies an autosomal and almost recessive mode of inheritance for anthranilic diamides, whereas it was completely recessive for flubendiamide. Our results not only provided in vivo functional validation of the RyR mutation in conferring high levels of resistance to diamide insecticides for the first time in a controlled genetic background of a lepidopteran pest, but also revealed slight differences on the level of resistance between anthranilic diamides (chlorantraniliprole and cyantraniliprole) and flubendiamide conferred by the SeRyR mutation.

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Comparison of isocratic retention models for hydrophilic interaction liquid chromatographic separation of native and fluorescently labeled oligosaccharides.

In this work, we have investigated retention of maltooligosaccharides and their fluorescent derivatives in hydrophilic interaction liquid chromatography using four different stationary phases. The non-derivatized maltooligosaccharides (maltose to maltoheptaose) and their derivatives with 2-aminobenzoic acid, 2-aminobenzamide, 2-aminopyridine and 8-aminonaphthalene-1,3,6-trisulfonic acid were analyzed on silica gel, aminopropyl silica, amide (carbamoyl-bonded silica) and ZIC-HILIC zwitterionic sulfobetain bonded phase. The partitioning of the analytes between the bulk mobile phase and adsorbed water-rich layer, polar and ionic interactions of analytes with stationary phase have been evaluated and compared. The effects of the mobile phase additives (0.1% (v/v) of acetic acid and ammonium acetate in concentration range 5-30 mmol L(-1)) on retention were described. The suitability of different models for prediction of retention was tested including linear solvent strength model, quadratic model, mixed-mode model, and empirical Neue-Kuss model. The mixed-mode model was extended to the parameter describing the contribution of monomeric glucose unit to the retention of non-derivatized and derivatized maltooligosaccharides, which was used for evaluation of contribution of both, oligosaccharide backbone and end-group to retention.

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Protein A (Liquid form) Protein A (Liquid form) Protein A (Liquid form) Protein A (Liquid form) NATIVE HUMAN PROLACTIN, P Ofloxacin CAS Number [824 Native Human Lactoferrin, NATIVE HUMAN PROLACTIN, P Cellufine Formyl , 50 ml Cellufine Formyl Media Cellufine Formyl , 500 ml Cellufine Formyl Media

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Benzenesulfonamides incorporating bulky aromatic/heterocyclic tails with potent carbonic anhydrase inhibitory activity.

Three series of sulfonamides incorporating long, bulky tails were obtained by applying synthetic strategies in which substituted anthranilic acids, quinazolines and aromatic sulfonamides have been used as starting materials. They incorporate long, bulky diamide-, 4-oxoquinazoline-3-yl- or quinazoline-4-yl moieties in their molecules, and were investigated for the inhibition of four physiologically relevant carbonic anhydrase (CA, EC 4.2.1.1) isoforms, the cytosolic human (h) hCA I and II, as well as the transmembrane hCA IX and XII. Most of the new sulfonamides showed excellent inhibitory effects against the four isoforms, with KIs of 7.6-322nM against hCA I, of 0.06-85.4nM against hCA II; of 6.7-152nM against hCA IX and of 0.49-237nM against hCA XII; respectively. However no relevant isoform-selective behavior has been observed for any of them, although hCA II and XII, isoforms involved in glaucoma-genesis were the most inhibited ones. The structure-activity relationship for inhibiting the four CAs with these derivatives is discussed in detail.

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Reductive ring closure methodology toward heteroacenes bearing a dihydropyrrolo[3,2-b]pyrrole core: scope and limitation.

A newly developed reductive ring closure methodology to heteroacenes bearing a dihydropyrrolo[3,2-b]pyrrole core was systematically studied for its scope and limitation. The methodology involves (i) the cyclization of an o-aminobenzoic acid ester derivative to give an eight-membered cyclic dilactam, and (ii) the conversion of the dilactams into the corresponding diimidoyl chloride, which undergoes (iii) reductive ring closure to install the dihydropyrrolo[3,2-b]pyrrole core. The first step of the methodology plays the key role due to its substrate limitation, which suffers from the competition of oligomerization and hydrolysis. All the dilactams could successfully convert to the corresponding diimidoyl chlorides, most of which succeeded to give the dihydropyrrolo[3,2-b]pyrrole core. The influence of the substituents and the elongation of conjugated length on the photophysical properties of the obtained heteroacenes were then investigated systematically using UV-vis spectroscopy and cyclic voltammetry. It was found that chlorination and fluorination had quite a different effect on the photophysical properties of the heteroacene, and the ring fusing pattern also had a drastic influence on the band gap of the heteroacene. The successful preparation of a series of heteroacenes bearing a dihydropyrrolo[3,2-b]pyrrole core would provide a wide variety of candidates for further fabrication of organic field-effect transistor devices.

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Hepatitis B Core Antigen Hepatitis B Core Antigen Hepatitis B Core Antigen Hepatitis B Core Antigen HCV core recombinant anti HCV core recombinant anti HCV core recombinant anti HCV core recombinant anti HBV core recombinant anti HBV core recombinant anti HCV core 2 119aa recombin HCV core 24 antigen.

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Dual fluorescence of N-phenylanthranilic acid: Effect of solvents, pH and beta-cyclodextrin.

Spectral characteristics of N-phenylanthranilic acid (NPAA) have been studied in different solvents, pH and beta-cyclodextrin (beta-CD) and compared with anthranilic acid (2-aminobenzoic acid, 2ABA). In all solvents a dual fluorescence is observed in NPAA, whereas 2ABA gives single emission. Combining the results observed in the absorption, fluorescence emission and fluorescence excitation spectra, it is found that strong intramolecular hydrogen bonding (IHB) interactions present in NPAA molecule. The inclusion complex of NPAA with beta-CD is analysed by UV-vis, fluorimetry, FT-IR, (1)H NMR, scanning electron microscope and AM 1 method. The above spectral studies show that NPAA forms a 1:1 inclusion complex with beta-CD and COOH group present in the beta-CD cavity. A mechanism is proposed to explain the inclusion process.

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Phenethyl 1 thio beta D g PSAP (Prostate Specific PSAP (Prostate Specific PSAP (Prostate Specific Boric Acid - Borate Buff Boric Acid - Borate Buff Phosphotungstic Acid Hem Phosphotungstic Acid Hem Phosphomolybdic Phosphot Phosphomolybdic Phosphot Phosphomolybdic Phosphot Phosphomolybdic Acid Sol

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Toxicology and carcinogenesis studies of naphthalene (cas no. 91-20-3) in F344/N rats (inhalation studies).

Naphthalene is used as an intermediate in the synthesis of phthalic and anthranilic acids, naphthols, naphthylamines, sulfonic acid, synthetic resins, celluloid, and hydronaphthalenes; it is also used in the preparation of anthraquinone, indigo, salicylic acid, and 1-naphthyl-N-methylcarbamate insecticide. It is an ingredient in some moth repellants and toilet bowl deodorants; it is also used in veterinary medicine in antiseptics for irrigating animal wounds and as an external medication to control lice on livestock and poultry. Naphthalene was selected for study by the National Toxicology Program because previous inhalation studies with naphthalene in mice were positive and existing studies in rats were either considered inadequate or were conducted via routes other than inhalation. Male and female F344/N rats were exposed to naphthalene (greater than 99% pure) by inhalation for 2 years. Genetic toxicology studies were conducted in Salmonella typhimurium and cultured Chinese hamster ovary cells. 2-YEAR STUDY: Groups of 49 male and 49 female rats were exposed to naphthalene by inhalation at concentrations of 0, 10, 30, or 60 ppm for 6 hours plus T90 (12 minutes) per day, 5 days per week for 105 weeks. Additional groups of nine male and nine female rats were exposed to 10, 30, or 60 ppm for up to 18 months for evaluation of toxicokinetic parameters. Survival, Body Weights, and Gross Observations: The survival of all exposed groups of male and female rats was similar to that of the chamber controls. Mean body weights of all exposed groups of males were less than those of the chamber control group throughout most of the study. Masses were observed in the nose of male and female rats. These masses frequently partially occluded the nasal passages or obliterated the normal architecture of the nasal turbinates. Pathology Findings: The incidences of neuroblastoma of the olfactory epithelium, a rare neoplasm, occurred with positive trends in males and females. Because this neoplasm did not occur in chamber control rats or in male rats exposed to 10 ppm and because this neoplasm has not been seen in the historical chamber control rats in NTP 2-year inhalation studies, the increased incidences of neuroblastoma were considered to be related to naphthalene exposure. In males, the incidences of adenoma of the respiratory epithelium of the nose, another rare neoplasm, occurred with a positive trend and were significantly increased in all exposed groups; none occurred in the chamber controls. In females, these neoplasms occurred in the 30 and 60 ppm groups but not in the chamber control or 10 ppm groups. Because these neoplasms did not occur in the chamber controls and have not been observed in the historical chamber control rats in NTP 2-year inhalation studies, the incidences of nasal adenoma were considered to be related to naphthalene exposure. Increased incidences of nonneoplastic lesions of the nose associated with exposure to naphthalene included atypical hyperplasia, atrophy, chronic inflammation, and hyaline degeneration of the olfactory epithelium; hyperplasia, squamous metaplasia, hyaline degeneration, and goblet cell hyperplasia of the respiratory epithelium; and glandular hyperplasia and squamous metaplasia. Toxicokinetic Results Model: A physiologically based toxicokinetic model was developed to characterize the disposition of inhaled naphthalene in rats. Because of its low vapor pressure and high blood-to-air partition coefficient, essentially all of the naphthalene that is absorbed into the general circulation is metabolized. At the exposure concentrations used in the 2-year study, approximately 20% to 30% of the inhaled dose was metabolized by male and female rats. Naphthalene that was not absorbed during exposure was assumed to be exhaled. The respective estimated daily doses metabolized by rats exposed to 10, 30, or 60 ppm for 6 hours (i.e., the internalized doses) are 3.6, 10.7, and 20.1 mg naphthalene/kg body weight for males and 3.9, 11.4, and 20.6 mg/kg for females.

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Toxicology and Carcinogenesis Studies of Naphthalene (CAS No. 91-20-3) in B6C3F1 Mice (Inhalation Studies).

Naphthalene, a white, crystalline powder, is used as a moth repellent and in the manufacture of phthalic and anthranilic acids, naphthylamines, and synthetic resins. The 2-year studies were conducted by exposing groups of male and female B6C3F1 mice to naphthalene (>99% pure) vapor for 6 hours daily, 5 days per week, for 104 weeks. Genetic toxicology studies were conducted in Salmonella typhimurium and Chinese hamster ovary cells. 2-Year Studies: Groups of male and female mice were exposed to atmospheres containing 0 (75 mice per group), 10 (75 mice per group), or 30 ppm (150 mice per group) naphthalene. Mice from each group were included for 14-day hematology evaluations (male: 0 ppm, 5 animals; 10 ppm, 4; 30 ppm, 10; female: 0 ppm, 4; 10 ppm, 5; 30 ppm, 10). Mean body weights of exposed mice were slightly lower than those of controls throughout the studies. Survival of male control mice was significantly less than that of exposed mice; the lower survival was the result of wound trauma and secondary infections related to fighting among the group-housed mice (0 ppm, 26/70, 37%; 10 ppm, 52/69, 75%; 30 ppm, 118/133, 89%). Survival of exposed female mice was similar to that of controls (59/69, 86%; 57/65, 88%; 102/135, 76%). Neoplastic and Nonneoplastic Effects in the 2-Year Studies: No increase in tumor incidence related to naphthalene administration was observed in male mice. In females, the incidence of pulmonary alveolar/bronchiolar adenomas was significantly greater in the high-dose group than in the controls (5/69, 7%; 2/65, 3%; 28/135, 21%). One other high-dose female had an alveolar/bronchiolar carcinoma. The combined incidence of alveolar/ bronchiolar adenomas and carcinomas in the high-dose females was above those for control female B6C3F1 mice from NTP feed, water, and inhalation studies (91/1,166, 7.8%, range 0%-16%). These lung tumors were attributed to naphthalene exposure. Nonneoplastic lesions attributed to naphthalene exposure were observed in the nose and lungs of mice of both sexes. In the nose, naphthalene exposure was associated with an increase in the incidence and severity of chronic inflammation, metaplasia of the olfactory epithelium, and hyperplasia of respiratory epithelium. Chronic inflammation in the lung was associated with chemical exposure. Genetic Toxicology: Naphthalene was negative for the induction of gene mutations in Salmonella typhimurium strains TA100, TA1535, TA1537, and TA98 with and without exogenous metabolic activation (S9). In cytogenetic tests with Chinese hamster ovary cells, naphthalene induced sister chromatid exchanges with and without S9 activation. Exposure to naphthalene induced a significant increase in chromosomal aberrations in Chinese hamster ovary cells in the presence of S9. Conclusions: Under the conditions of these 2-year inhalation studies, there was no evidence of carcinogenic activity of naphthalene in male B6C3F1 mice exposed to 10 or 30 ppm. There was some evidence of carcinogenic activity of naphthalene in female B6C3F1 mice, based on increased incidences of pulmonary alveolar/ bronchiolar adenomas. In both male and female mice, naphthalene caused increased incidences and severity of chronic inflammation, metaplasia of the olfactory epithelium, and hyperplasia of the respiratory epithelium in the nose and chronic inflammation in the lungs. Synonyms: Naphthalin, Naphthene, Tar Camphor

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