2-Hydroxy-N-phenylbenzamides. N-phenyl substituted salicylamides. Derivatives have been used as fungicides, anti-mildew agents and topical antifungal agents. In concentrated form may cause irritation of skin and mucous membranes.
Organic salts and esters of benzenesulfonic acid.
The infiltrating of tissue specimens with paraffin, as a supporting substance, to prepare for sectioning with a microtome.
Exclusive legal rights or privileges applied to inventions, plants, etc.
A plastic substance deposited by insects or obtained from plants. Waxes are esters of various fatty acids with higher, usually monohydric alcohols. The wax of pharmacy is principally yellow wax (beeswax), the material of which honeycomb is made. It consists chiefly of cerotic acid and myricin and is used in making ointments, cerates, etc. (Dorland, 27th ed)
A genus of zygomycetous fungi of the family Mucoraceae, order MUCORALES.
Liquids that dissolve other substances (solutes), generally solids, without any change in chemical composition, as, water containing sugar. (Grant & Hackh's Chemical Dictionary, 5th ed)
The relative amounts of various components in the body, such as percentage of body fat.
Agents that modify interfacial tension of water; usually substances that have one lipophilic and one hydrophilic group in the molecule; includes soaps, detergents, emulsifiers, dispersing and wetting agents, and several groups of antiseptics.
A sport in which weights are lifted competitively or as an exercise.
These compounds stimulate anabolism and inhibit catabolism. They stimulate the development of muscle mass, strength, and power.
The ability of a substance to be dissolved, i.e. to form a solution with another substance. (From McGraw-Hill Dictionary of Scientific and Technical Terms, 6th ed)
Strongly cationic polymer that binds to certain proteins; used as a marker in immunology, to precipitate and purify enzymes and lipids. Synonyms: aziridine polymer; Epamine; Epomine; ethylenimine polymer; Montrek; PEI; Polymin(e).
Compounds formed by the joining of smaller, usually repeating, units linked by covalent bonds. These compounds often form large macromolecules (e.g., BIOPOLYMERS; PLASTICS).
An anionic surfactant, usually a mixture of sodium alkyl sulfates, mainly the lauryl; lowers surface tension of aqueous solutions; used as fat emulsifier, wetting agent, detergent in cosmetics, pharmaceuticals and toothpastes; also as research tool in protein biochemistry.
Preparation of TOOTH surfaces, and of materials bonded to teeth or DENTAL IMPLANTS, with agents and methods which roughen the surface to facilitate adhesion. Agents include phosphoric or other acids (ACID ETCHING, DENTAL) and methods include LASERS.
Sulfonic acid derivatives that are substituted with an aliphatic hydrocarbon group.
The temperature at which a substance changes from one state or conformation of matter to another.
Hard, amorphous, brittle, inorganic, usually transparent, polymerous silicate of basic oxides, usually potassium or sodium. It is used in the form of hard sheets, vessels, tubing, fibers, ceramics, beads, etc.
A change of a substance from one form or state to another.
Differential thermal analysis in which the sample compartment of the apparatus is a differential calorimeter, allowing an exact measure of the heat of transition independent of the specific heat, thermal conductivity, and other variables of the sample.
The property of objects that determines the direction of heat flow when they are placed in direct thermal contact. The temperature is the energy of microscopic motions (vibrational and translational) of the particles of atoms.
Method of tissue preparation in which the tissue specimen is frozen and then dehydrated at low temperature in a high vacuum. This method is also used for dehydrating pharmaceutical and food products.
The field of medicine concerned with understanding the biochemical basis of health and disease and involved in developing diagnostic and therapeutic methods that utilize MOLECULAR BIOLOGY techniques.
An enzyme that catalyzes the methylation of the epsilon-amino group of lysine residues in proteins to yield epsilon mono-, di-, and trimethyllysine. EC 2.1.1.43.
Tumors or cancer of the SALIVARY GLANDS.
A tube-like invagination of the EPIDERMIS from which the hair shaft develops and into which SEBACEOUS GLANDS open. The hair follicle is lined by a cellular inner and outer root sheath of epidermal origin and is invested with a fibrous sheath derived from the dermis. (Stedman, 26th ed) Follicles of very long hairs extend into the subcutaneous layer of tissue under the SKIN.
Differentiated epithelial cells of the INTESTINAL MUCOSA, found in the basal part of the intestinal crypts of Lieberkuhn. Paneth cells secrete GROWTH FACTORS, digestive enzymes such as LYSOZYME and antimicrobial peptides such as cryptdins (ALPHA-DEFENSINS) into the crypt lumen.
Highly proliferative, self-renewing, and colony-forming stem cells which give rise to NEOPLASMS.
Purifying or cleansing agents, usually salts of long-chain aliphatic bases or acids, that exert cleansing (oil-dissolving) and antimicrobial effects through a surface action that depends on possessing both hydrophilic and hydrophobic properties.
Substances or materials used in the course of housekeeping or personal routine.
Liquids that are suitable for drinking. (From Merriam Webster Collegiate Dictionary, 10th ed)
Facilities which provide information concerning poisons and treatment of poisoning in emergencies.
Hospital department which administers all activities pertaining to the hospital laundry service.
Substances and drugs that lower the SURFACE TENSION of the mucoid layer lining the PULMONARY ALVEOLI.
Size and composition of the family.
Various material objects and items in the home. It includes temporary or permanent machinery and appliances. It does not include furniture or interior furnishings (FURNITURE see INTERIOR DESIGN AND FURNISHINGS; INTERIOR FURNISHINGS see INTERIOR DESIGN AND FURNISHINGS).
Exploitation through misrepresentation of the facts or concealment of the purposes of the exploiter.
The prediction or projection of the nature of future problems or existing conditions based upon the extrapolation or interpretation of existing scientific data or by the application of scientific methodology.
Concept referring to the standardized fees for services rendered by health care providers, e.g., laboratories and physicians, and reimbursement for those services under Medicare Part B. It includes acceptance by the physician.
Substances intended to be applied to the human body for cleansing, beautifying, promoting attractiveness, or altering the appearance without affecting the body's structure or functions. Included in this definition are skin creams, lotions, perfumes, lipsticks, fingernail polishes, eye and facial makeup preparations, permanent waves, hair colors, toothpastes, and deodorants, as well as any material intended for use as a component of a cosmetic product. (U.S. Food & Drug Administration Center for Food Safety & Applied Nutrition Office of Cosmetics Fact Sheet (web page) Feb 1995)
A combustible, gaseous mixture of low-molecular weight PARAFFIN hydrocarbons, generated below the surface of the earth. It contains mostly METHANE and ETHANE with small amounts of PROPANE; BUTANES; and higher hydrocarbons, and sometimes NITROGEN; CARBON DIOXIDE; HYDROGEN SULFIDE; and HELIUM. (from McGraw-Hill Dictionary of Scientific and Technical Terms, 6th ed)
The aggregate enterprise of manufacturing and technically producing chemicals. (From Random House Unabridged Dictionary, 2d ed)
The facilitation of a chemical reaction by material (catalyst) that is not consumed by the reaction.
The generic name for the group of aliphatic hydrocarbons Cn-H2n+2. They are denoted by the suffix -ane. (Grant & Hackh's Chemical Dictionary, 5th ed)
A chemical reaction in which an electron is transferred from one molecule to another. The electron-donating molecule is the reducing agent or reductant; the electron-accepting molecule is the oxidizing agent or oxidant. Reducing and oxidizing agents function as conjugate reductant-oxidant pairs or redox pairs (Lehninger, Principles of Biochemistry, 1982, p471).

Aromatic L-amino acid decarboxylase: conformational change in the flexible region around Arg334 is required during the transaldimination process. (1/1033)

Aromatic L-amino acid decarboxylase (AADC) catalytic mechanism has been proposed to proceed through two consecutive intermediates (i.e., Michaelis complex and the external aldimine). Limited proteolysis of AADC that preferentially digested at the C-terminal side of Arg334 was slightly retarded in the presence of dihydroxyphenyl acetate that formed a stable Michaelis complex. On the contrary, AADC was scarcely digested in the presence of L-dopa methyl ester that formed a stable external aldimine. Similar protection by the substrate analogs was observed in the chemical modification experiment. From these results, we concluded that the region around Arg334 must be exposed and flexible in the unliganded state, and forming the Michaelis complex generated a subtle conformational change, then underwent marked conformational change during the subsequent transaldimination process prerequisite to forming the external aldimine. For further analyses, we constructed a mutant gene encoding in tandem the two peptides of AADC cleaved at the Asn327-Met328 bond inside the putative flexible region. The gene product, fragmentary AADC, was still active with L-dopa as substrate, but its k(cat) value was decreased 57-fold, and the Km value was increased 9-fold compared with those of the wild-type AADC. The absorption spectra of the fragmentary AADC in the presence of L-dopa methyl ester showed shift in the equilibrium of the transaldimination from the external aldimine to the Michaelis complex. Tryptic digestion of the fragmentary AADC removed seven amino acid residues, Met328-Arg334, and resulted in complete inactivation. Susceptibility of the fragmentary enzyme to trypsin was not changed by L-dopa methyl ester revealing the loss of appropriate conformational change in the flexible region induced by substrate binding. From these results we propose that the conformational change in the flexible region is required during the transaldimination process.  (+info)

Trefoil peptide TFF2 (spasmolytic polypeptide) potently accelerates healing and reduces inflammation in a rat model of colitis. (2/1033)

BACKGROUND: The trefoil peptides are major secretory products of mucus cells of the gastrointestinal tract and show increased expression after inflammatory or ulcerative damage. Recombinant human TFF2 (spasmolytic polypeptide) has been shown to be cytoprotective, and enhances repair in models of gastric injury. AIMS: To test the healing effects of recombinant human (h)TFF2 in a rat model of chronic colitis. METHODS: Colitis was induced by intracolonic administration of dinitrobenzene sulphonic acid in ethanol. Mucosal repair was quantified macroscopically, microscopically by image analysis of tissue histology, and by measuring myeloperoxidase activity. RESULTS: Initial validation studies showed that maximal injury and inflammation occurred at the end of the first week after colitis induction (active phase), and that spontaneous healing was complete by eight weeks. Once daily intrarectal application of hTFF2 (2.5 mg/kg; approximately 0.5 mg/rat) for five days after maximal damage had been sustained, reduced both microscopic and macroscopic injury by 80% and inflammatory index by 50% compared with vehicle controls. In addition, endogenous concentrations of rat TFF2 and TFF3 (intestinal trefoil factor) were increased in the active phase of colitis and were reduced to basal levels by hTFF2 treatment. CONCLUSIONS: This study has shown that hTFF2 enhances the rate of colonic epithelial repair, and reduces local inflammation in a rat model of colitis, and suggests that luminal application of trefoil peptides may have therapeutic potential in the treatment of inflammatory bowel disease.  (+info)

KNR4, a suppressor of Saccharomyces cerevisiae cwh mutants, is involved in the transcriptional control of chitin synthase genes. (3/1033)

The KNR4 gene, originally isolated by complementation of a K9 killer-toxin-resistant mutant displaying reduced levels of both 1,3-beta-glucan and 1,3-beta-glucan synthase activity, was recloned from a YCp50 genomic library as a suppressor of Saccharomyces cerevisiae calcofluor-white-hypersensitive (cwh) mutants. In these mutants, which were characterized by increased chitin levels, the suppressor effect of KNR4 resulted, for some of them, in a lowering of polymer content to close to wild-type level, with no effect on the contents of beta-glucan and mannan. In all cases, this effect was accompanied by a strong reduction in mRNA levels corresponding to CHS1, CHS2 and CHS3, encoding chitin synthases, without affecting expression of FKS1 and RHO1, two genes encoding the catalytic subunit and a regulatory component of 1,3-beta-glucan synthase, respectively. Overexpression of KNR4 also inhibited expression of CHS genes in wild-type strains and in two other cwh mutants, whose sensitivity to calcofluor white was not suppressed by this gene. The physiological relevance of the KNR4 transcriptional effect was addressed in two different ways. In a wild-type strain exposed to alpha-factor, overexpression of this gene inhibited CHS1 induction and delayed shmoo formation, two events which are triggered in response to the pheromone, whereas it did not affect bud formation and cell growth in a chs1 chs2 double mutant. A chimeric protein made by fusing green fluorescent protein to the C terminus of Knr4p which fully complemented a knr4delta mutation was found to localize in patches at presumptive bud sites in unbudded cells and at the incipient bud site during bud emergence. Taken together, these results demonstrate that KNR4 has a regulatory role in chitin deposition and in cell wall assembly. A mechanism by which this gene affects expression of CHS genes is proposed.  (+info)

Nitrite determination in human plasma and synovial fluid using reactions of nitric oxide with 3, 5-dibromo-4-nitrosobenzenesulphonate (DBNBS). (4/1033)

DBNBS (3,5-dibromo-4-nitrosobenzenesulphonate) reacts with nitric oxide (NO) produced from nitrite ions in acid solution to give a radical with a characteristic electron spin resonance spectrum, attributable to a 'DBNBS-NO' product, and comprising a triplet with alphaN=0.96 mT. This is identical with the spectrum obtained when NO, introduced from the gas phase, reacts with DBNBS. Under certain conditions, an additional signal is observed, attributable to oxidation of DBNBS to the radical cation, DBNBS*+ (a triplet with alphaN=1.32 mT). Conditions are described for the determination of nitrite, which avoid this DBNBS oxidation. The height of the low-field signal from the DBNBS-NO product is directly proportional to the nitrite concentration up to about 0.08 mM nitrite. The method has been applied to the measurement of nitrite concentrations in whole blood, plasma and synovial fluid taken from rheumatoid arthritis patients. In order to avoid the oxidation of DBNBS when analysing biological samples of this type, it is necessary to treat the specimen by ultrafiltration as soon as possible after collection and before addition of DBNBS.  (+info)

Deletion of new covalently linked cell wall glycoproteins alters the electrophoretic mobility of phosphorylated wall components of Saccharomyces cerevisiae. (5/1033)

The incorporation of radioactive orthophosphate into the cell walls of Saccharomyces cerevisiae was studied. 33P-labeled cell walls were extensively extracted with hot sodium dodecyl sulfate (SDS). Of the remaining insoluble radioactivity more than 90% could be released by laminarinase. This radioactive material stayed in the stacking gel during SDS-polyacrylamide gel electrophoresis but entered the separating gel upon treatment with N-glycosidase F, indicating that phosphate was linked directly or indirectly to N-mannosylated glycoproteins. The phosphate was bound to covalently linked cell wall proteins as mannose-6-phosphate, the same type of linkage shown previously for soluble mannoproteins (L. Ballou, L. M. Hernandez, E. Alvarado, and C. E. Ballou, Proc. Natl. Acad. Sci. USA 87:3368-3372, 1990). From the phosphate-labeled glycoprotein fraction released by laminarinase, three cell wall mannoproteins, Ccw12p, Ccw13p and Ccw14p, were isolated and identified by N-terminal sequencing. For Ccw13p (encoded by DAN1 [also called TIR3]) and Ccw12p the association with the cell wall has not been described before; Ccw14p is identical with cell wall protein Icwp (I. Moukadiri, J. Armero, A. Abad, R. Sentandreu, and J. Zueco, J. Bacteriol. 179:2154-2162, 1997). In ccw12, ccw13, or ccw14 single or double mutants neither the amount of radioactive phosphate incorporated into cell wall proteins nor its position in the stacking gel was changed. However, the triple mutant brought about a shift of the 33P-labeled glycoprotein components from the stacking gel into the separating gel. The disruption of CCW12 results in a pronounced sensitivity of the cells to calcofluor white and Congo red. In addition, the ccw12 mutant shows a decrease in mating efficiency and a defect in agglutination.  (+info)

Perturbations in the control of cellular arachidonic acid levels block cell growth and induce apoptosis in HL-60 cells. (6/1033)

Our previous studies demonstrated that inhibitors of arachidonate-phospholipid remodeling [i.e. the enzyme CoA-independent transacylase (CoA-IT)] decrease cell proliferation and induce apoptosis in neoplastic cells. The goal of the current study was to elucidate the molecular events associated with arachidonate-phospholipid remodeling that influence cell proliferation and survival. Initial experiments revealed the essential nature of cellular arachidonate to the signaling process by demonstrating that HL-60 cells depleted of arachidonate were more resistant to apoptosis induced by CoA-IT inhibition. In cells treated with CoA-IT inhibitors a marked increase in free arachidonic acid and AA-containing triglycerides were measured. TG enrichment was likely due to acylation of arachidonic acid into diglycerides and triglycerides via de novo glycerolipid biosynthesis. To determine the potential of free fatty acids to affect cell proliferation, HL-60 cells were incubated with varying concentrations of free fatty acids; exogenously provided 20-carbon polyunsaturated fatty acids caused a dose-dependent inhibition of cell proliferation, whereas oleic acid was without effect. Blocking 5-lipoxygenase or cyclooxygenases had no effect on the inhibition of cell proliferation induced by arachidonic acid or CoA-IT inhibitors. An increase in cell-associated ceramides (mainly in the 16:0-ceramide fraction) was measured in cells exposed to free arachidonic acid or to CoA-IT inhibitors. This study, in conjunction with other recent studies, suggests that perturbations in the control of cellular arachidonic acid levels affect cell proliferation and survival.  (+info)

Saccharomyces cerevisiae mid2p is a potential cell wall stress sensor and upstream activator of the PKC1-MPK1 cell integrity pathway. (7/1033)

The MID2 gene of Saccharomyces cerevisiae encodes a protein with structural features indicative of a plasma membrane-associated cell wall sensor. MID2 was isolated as a multicopy activator of the Skn7p transcription factor. Deletion of MID2 causes resistance to calcofluor white, diminished production of stress-induced cell wall chitin under a variety of conditions, and changes in growth rate and viability in a number of different cell wall biosynthesis mutants. Overexpression of MID2 causes hyperaccumulation of chitin and increased sensitivity to calcofluor white. alpha-Factor hypersensitivity of mid2Delta mutants can be suppressed by overexpression of upstream elements of the cell integrity pathway, including PKC1, RHO1, WSC1, and WSC2. Mid2p and Wsc1p appear to have overlapping roles in maintaining cell integrity since mid2Delta wsc1Delta mutants are inviable on medium that does not contain osmotic support. A role for MID2 in the cell integrity pathway is further supported by the finding that MID2 is required for induction of Mpk1p tyrosine phosphorylation during exposure to alpha-factor, calcofluor white, or high temperature. Our data are consistent with a role for Mid2p in sensing cell wall stress and in activation of a response that includes both increased chitin synthesis and the Mpk1p mitogen-activated protein kinase cell integrity pathway. In addition, we have identified an open reading frame, MTL1, which encodes a protein with both structural and functional similarity to Mid2p.  (+info)

Chs7p, a new protein involved in the control of protein export from the endoplasmic reticulum that is specifically engaged in the regulation of chitin synthesis in Saccharomyces cerevisiae. (8/1033)

The Saccharomyces cerevisiae CHS7 gene encodes an integral membrane protein located in the ER which is directly involved in chitin synthesis through the regulation of chitin synthase III (CSIII) activity. In the absence of CHS7 product, Chs3p, but not other secreted proteins, is retained in the ER, leading to a severe defect in CSIII activity and consequently, to a reduced rate of chitin synthesis. In addition, chs7 null mutants show the yeast phenotypes associated with a lack of chitin: reduced mating efficiency and lack of the chitosan ascospore layer, clear indications of Chs7p function throughout the S. cerevisiae biological cycle. CHS3 overexpression does not lead to increased levels of CSIII because the Chs3p excess is retained in the ER. However, joint overexpression of CHS3 and CHS7 increases the export of Chs3p from the ER and this is accompanied by a concomitant increase in CSIII activity, indicating that the amount of Chs7p is a limiting factor for CSIII activity. Accordingly, CHS7 transcription is increased when elevated amounts of chitin synthesis are detected. These results show that Chs7p forms part of a new mechanism specifically involved in Chs3p export from the ER and consequently, in the regulation of CSIII activity.  (+info)

TY - JOUR. T1 - The multikinase inhibitor Sorafenib enhances glycolysis and synergizes with glycolysis blockade for cancer cell killing. AU - Barba, Marta. AU - Bernardini, Camilla. AU - Scatena, Roberto. AU - Maulucci, Giuseppe. AU - Pani, Giovambattista. AU - Gasbarrini, Antonio. AU - Tesori, Valentina. AU - Pontoglio, Alessandro. AU - Puglisi, Maria Ausiliatrice. AU - Piscaglia, Anna Chiara. AU - Castellini, Laura. AU - Spelbrink, Johannes N.. PY - 2015. Y1 - 2015. N2 - Although the only effective drug against primary hepatocarcinoma, the multikinase inhibitor Sorafenib (SFB) usually fails to eradicate liver cancer. Since SFB targets mitochondria, cell metabolic reprogramming may underlie intrinsic tumor resistance. To characterize cancer cell metabolic response to SFB, we measured oxygen consumption, generation of reactive oxygen species (ROS) and ATP content in rat LCSC (Liver Cancer Stem Cells) -2 cells exposed to the drug. Genome wide analysis of gene expression was performed by ...
Sodium 5-methoxy-2-methyl-4-(3-oxobutanamido)benzenesulfonate 133167-77-8 NMR spectrum, Sodium 5-methoxy-2-methyl-4-(3-oxobutanamido)benzenesulfonate H-NMR spectral analysis, Sodium 5-methoxy-2-methyl-4-(3-oxobutanamido)benzenesulfonate C-NMR spectral analysis ect.
sodium,2,5-bis(methoxycarbonyl)benzenesulfonate 31314-30-4 NMR spectrum, sodium,2,5-bis(methoxycarbonyl)benzenesulfonate H-NMR spectral analysis, sodium,2,5-bis(methoxycarbonyl)benzenesulfonate C-NMR spectral analysis ect.
Surfactants are often used in supramolecular chemistry, due to their ability to self-organize. Surfactant molecules aggregate spontaneously and reversibly to adopt a defined intermolecular arrangement. In this work, general phase behavior, adsorption and association in aqueous mixtures of dodecylammonium chloride, DACl and sodium 4-(1-pentylheptyl)benzenesulfonate, NaDBS, were studied by a combination of techniques including surface tension and conductivity measurements, light scattering and optical microscopy. The strong synergistic properties of the system were brought out with the Regular Solution Theory.Various colloidal objects are observed in wide range of composition: conventional small vesicles, large giant multilamellar or multivesicular vesicles. An excess of NaDBS provides extremely large tubular and elongated multilamellar vesicles. The new catanionic 1:1 complex, dodecylammonium 4-(1-pentylheptyl) benzenesulfonate, formed in the equimolar conditions is a result of intramolecular ...
Reaction mass of potassium, sodium 2-[(E)-(2,4-diamino-6-carboxy-3-[(E)-(4-{[2-(sulfonatooxy)ethyl] sulfonyl}phenyl)diazenyl]-5-{(E)-phenyldiazenyl}phenyl)diazenyl]benzenesulfonate (1:5.8:3.4), polyvinylsulfonyl and potassium, sodium 2-[(E)-{2,4-diamino-6-carboxy-3,5-bis[(E)-(4-{[2- (sulfonatooxy)ethyl]sulfonyl} phenyl)diazenyl]phenyl}diazenyl]-benzenesulfonate (1:5.8:2.4), vinylsulfonyl- and potassium, sodium 2-[(E)-(2,4-diamino-6-carboxy-5-[(E)-(4-{[2-(sulfonatooxy)ethyl] sulfonyl}phenyl)diazenyl]-3-{(E)-phenyl]diazenyl}phenyl)diazenyl]-benzenesulfonate (1:5.8:3.4), polyvinylsulfonyl- and potassium, sodium 2-[(E)-(2,4-diamino-6-carboxy-3,5-bis{(E)- phenyldiazenyl}phenyl)diazenyl]-benzenesulfonate (1:5.8:6.8), polyvinylsulfonyl ...
Sodium benzenesulfonate | C6H5NaO3S | CID 517327 - structure, chemical names, physical and chemical properties, classification, patents, literature, biological activities, safety/hazards/toxicity information, supplier lists, and more.
Sodium 5-chloro-2-(4-chloro-2-nitrophenoxy)benzenesulfonate/ACM85136034 can be provided in Alfa Chemistry. We are dedicated to provide our customers the best products and services.
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Hepatocellular carcinoma (HCC) is the fifth most common neoplasia, In former times, treatment of advanced HCC with conventional antineoplastic drugs did not result in satisfactory outcomes: recently , in this patient population the oral multikinase inhibitor sorafenib has been able to induce a statistically significant improvement of overall survival. .Similarly to other anti-angiogenic drugs employed in other tumour types, also sorafenib seldom induces the dimensional tumour shrinking usually observed with conventional cytotoxic drugs: data gathered from studies carried out with sorafenib and other competitors under development do not report any complete response in HCV-induced HCC.Case presentationAn 84-year old man with a long-lasting history of chronic HCV hepatitis was referred to our Institution for an ultrasonography investigation of a focal hepatic lesion. To better characterize the liver disease and clearly define the diagnosis of the focal hepatic lesion, the patient was hospitalized ...
The mean elimination half-life of sorafenib was approximately 25 to 48 hours. Multiple doses of NEXAVAR for 7 days resulted in a 2.5- to 7-fold accumulation compared to a single dose. Steady-state plasma sorafenib concentrations were achieved within 7 days, with a peak-to-trough ratio of mean concentrations of less than 2. The steady-state concentrations of sorafenib following administration of 400 mg NEXAVAR twice daily were evaluated in DTC, RCC and HCC patients. Patients with DTC have mean steady-state concentrations that are 1.8-fold higher than patients with HCC and 2.3-fold higher than those with RCC. The reason for increased sorafenib concentrations in DTC patients is unknown.. Absorption and Distribution: After administration of NEXAVAR tablets, the mean relative bioavailability was 38-49% when compared to an oral solution. Following oral administration, sorafenib reached peak plasma levels in approximately 3 hours. With a moderate-fat meal (30% fat; 700 calories), bioavailability was ...
The multi-kinase inhibitor sorafenib (tradename Nexavar®, Bayer) has been recently approved by the FDA for the treatment of non-resectable hepatocarcinoma and advanced renal carcinoma.
Background: Traditional systemic chemotherapy does not provide survival benefits in patients with hepatocellular carcinoma (HCC). Molecular targeted therapy shows promise for HCC treatment, however, the duration of effectiveness for targeted therapies is finite and combination therapies offer the potential for improved effectiveness.. Methods: Sorafenib, a multikinase inhibitor, and YC-1, a soluble guanylyl cyclase (sGC) activator, were tested in HCC by proliferation assay, cell cycle analysis and western blot in vitro and orthotopic and ectopic HCC models in vivo.. Results: In vitro, combination of sorafenib and YC-1 synergistically inhibited proliferation and colony formation of HepG2, BEL-7402 and HCCLM3 cells. The combination also induced S cell cycle arrest and apoptosis, as observed by activated PARP and caspase 8. Sorafenib and YC-1 respectively suppressed the expression of phosphorylated STAT3 (p-STAT3) (Y705) in a dose-and time-dependent manner. Combination of sorafenib and YC-1 ...
The multikinase inhibitor and FDA\approved medication dovitinib (Dov) crosses the bloodCbrain barrier and was recently used as single medication application in clinical trials for GB patients with repeated disease. comet assays, and improved Gigabyte cell apoptosis. Pretreatment of Gigabyte cells with Dov (Dov priming) previous to TMZ treatment decreased Gigabyte cell viability self-employed of g53 position. Sequential treatment including Dov priming and switching treatment cycles with TMZ and Dov considerably decreased lengthy\term Gigabyte cell success in MGMT+ individual Gigabyte cells. Our outcomes may possess instant medical ramifications to improve TMZ response in individuals with LIN28+/HMGA2+ Gigabyte, self-employed of their MGMT methylation position. and mouse xenograft research shown a significant advantage in using a mixed treatment of Dov with platinum eagle substances in digestive tract malignancy (Gaur antiproliferative activity in human being endometrial malignancy cells (Eritja ...
B-Raf is a multi- drug target serine/threonine protein kinase, involved in the transduction of mitogenic signals from the cell membrane to the nucleus. Mutated B-Raf causes overactive downstream signaling via MEK and ERK, leading to excessive cell proliferation and survival, independent of growth factors causing cancers such as Pancreatic carcinoma. A novel bi-aryl urea- Sorafenib, is a potent inhibitor of Raf-1 that has been approved for the treatment of a number of cancers including pancreatic cancer. The present investigation was designed to identify the potential off-targets of Sorafenib which could be responsible for its reported undesirable side effects. Molecular docking was used to test the efficacy of structural analogs of Sorafenib against B-Raf using FlexX and it was found that the analog with CID:10151557 had a high potency with minimum number of clashes, low lipophilic score and high match score, similar to Sorafenib. To identify the potential off-target/s of Sorafenib, macromolecular
PRIMARY OBJECTIVES:. I. The primary endpoint is the response rate (CR+PR) for each stratum of sarcoma patients treated with sorafenib as defined by RECIST.. SECONDARY OBJECTIVES:. I. Progression-free survival (defined as CR + PR + SD, assessed at 3 months or 6 months).. II. Overall survival. III. Pharmacokinetics of sorafenib in this patient population (all sites will participate).. IV. Frequency of B-raf mutations in the patients sarcomas treated as part of this study and correlation with response or resistance to sorafenib (all sites will participate).. V. Ras-raf kinase pathway activation in pre-treatment existing tumor specimens (paraffin section immunohistochemistry; all sites will participate).. VI. At MSKCC only: Pre and post treatment specimen changes in downstream events of ras signaling, specifically inhibition of ERK phosphorylation. Only patients with angiosarcoma and MPNST will undergo biopsy (up to 10 patients).. VII. At MSKCC only: Circulating Endothelial Cells (CECs), ...
PRIMARY OBJECTIVES:. I. The primary endpoint is the response rate (CR+PR) for each stratum of sarcoma patients treated with sorafenib as defined by RECIST.. SECONDARY OBJECTIVES:. I. Progression-free survival (defined as CR + PR + SD, assessed at 3 months or 6 months).. II. Overall survival. III. Pharmacokinetics of sorafenib in this patient population (all sites will participate).. IV. Frequency of B-raf mutations in the patients sarcomas treated as part of this study and correlation with response or resistance to sorafenib (all sites will participate).. V. Ras-raf kinase pathway activation in pre-treatment existing tumor specimens (paraffin section immunohistochemistry; all sites will participate).. VI. At MSKCC only: Pre and post treatment specimen changes in downstream events of ras signaling, specifically inhibition of ERK phosphorylation. Only patients with angiosarcoma and MPNST will undergo biopsy (up to 10 patients).. VII. At MSKCC only: Circulating Endothelial Cells (CECs), ...
Sorafenib is a multikinase inhibitor targeting several serine/threonine and receptor tyrosine kinases. The drug is marketed as Nexavar and is used in the treatment of renal cell carcinoma (Kidney cancer). It is also being studied as treatment in other types of cancer.
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Sorafenib is a multikinase inhibitor of Raf-1, B-Raf and VEGFR-2 with IC50 of 6 nM, 22 nM and 90 nM in cell-free assays, respectively.
Learn about the no-cost, support services available for patients taking NEXAVAR (sorafenib). Visit hcp.nexavar-us.com to see full safety and Prescribing Information.
This trial will compare the tolerability and pharmacokinetics of sorafenib alone or in combination with golvatinib as first-line therapy in patients with
This trial will compare the tolerability and pharmacokinetics of sorafenib alone or in combination with golvatinib as first-line therapy in patients with
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WHITE PHARMACEUTICALS - Exporter, Importer, Distributor, Supplier, Trading Company of Soranib - Sorafenib based in New Delhi, India
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Antidiabetic is used for the management of Kind 2 diabetes mellitus in adults, as an adjunct to eating regimen and exercise and generally with different drugs for diabetes like metformin. taking nexavar with other medications are available that can treat your condition. Even brief-term oral sorafenib appears to effectively shut intratumoral shunts in patients with HCC and thus might enable transarterial therapy of these sufferers.. ...
Oncotarget | https://doi.org/10.18632/oncotarget.6104 Jun Li, Lehua Shi, Xiaofeng Zhang, Bin Sun, Yefa Yang, Naijian Ge, Huiying Liu, Xia Yang, Lei Chen, Haihua Qian, Mengchao Wu, Zhengfeng Yin
DI-fusion, le Dépôt institutionnel numérique de lULB, est loutil de référencementde la production scientifique de lULB.Linterface de recherche DI-fusion permet de consulter les publications des chercheurs de lULB et les thèses qui y ont été défendues.
DI-fusion, le Dépôt institutionnel numérique de lULB, est loutil de référencementde la production scientifique de lULB.Linterface de recherche DI-fusion permet de consulter les publications des chercheurs de lULB et les thèses qui y ont été défendues.
Looking for online definition of calcofluor white stain in the Medical Dictionary? calcofluor white stain explanation free. What is calcofluor white stain? Meaning of calcofluor white stain medical term. What does calcofluor white stain mean?
Recent evidence suggests that the development of castration resistant prostate cancer (CRPCa) is commonly associated with an aberrant, ligand-independent activation of the androgen receptor (AR). A putative mechanism allowing prostate cancer (PCa) cells to grow under low levels of androgens, is the expression of constitutively active, C-terminally truncated AR lacking the AR-ligand binding domain (LBD). Due to the absence of a LBD, these receptors, termed ARΔLBD, are unable to respond to any form of anti-hormonal therapies. In this study we demonstrate that the multikinase inhibitor sorafenib inhibits AR as well as ARΔLBD-signalling in CRPCa cells. This inhibition was paralleled by proteasomal degradation of the AR- and ARΔLBD-molecules. In line with these observations, maximal antiproliferative effects of sorafenib were achieved in AR and ARΔLBD-positive PCa cells. The present findings warrant further investigations on sorafenib as an option for the treatment of advanced AR-positive PCa.
We examined whether the multikinase inhibitor sorafenib and histone deacetylase inhibitors (HDACI) interact to kill pancreatic carcinoma cells and determined the impact of inhibiting BCL-2 family function on sorafenib and HDACI lethality. The lethality of sorafenib was enhanced in pancreatic tumor cells in a synergistic fashion by pharmacologically achievable concentrations of the HDACIs vorinostat or sodium valproate. Overexpression of cellular FLICE-like inhibitory protein (c-FLIP-s) or knockdown of CD95 suppressed the lethality of the sorafenib/HDACI combination (sorafenib + HDACI). In immunohistochemical analyses or using expression of fluorescence-tagged proteins, treatment with sorafenib and vorinostat together (sorafenib + vorinostat) promoted colocalization of CD95 with caspase 8 and CD95 association with the endoplasmic reticulum markers calnexin, ATG5, and Grp78/BiP. In cells lacking CD95 expression or in cells expressing c-FLIP-s, the lethality of sorafenib + HDACI exposure was ...
T-0902611 benzenesulfonate is a cytomegalovirus replication inhibitor that may be useful in the treatment of cytomegalovirus infections.
Sorafenib (Nexavar), is a multikinase inhibitor, which has demonstrated both antiproliferative and antiangiogenic properties in vitro and in vivo, inhibiting the activity of targets present in the tumoral cells (c-RAF [proto-oncogene serine/threonine-protein kinase], BRAF, (V600E)BRAF, c-KIT, and FMS-like tyrosine kinase 3) and in tumor vessels (c-RAF, vascular endothelial growth factor receptor [VEGFR]-2, VEGFR-3, and platelet-derived growth factor receptor β). Sorafenib was initially approved for the treatment of hepatocellular carcinoma and advanced renal cell carcinoma. Experimental studies have demonstrated that sorafenib has both antiproliferative and antiangiogenic properties in vitro and in vivo, against thyroid cancer cells. Furthermore, several completed (or ongoing) studies have evaluated the long-term efficacy and tolerability of sorafenib in patients with papillary, follicular and medullary aggressive thyroid cancer. The results of the different studies showed good clinical ...
We hypothesized that 1) increased HT and HFSR were markers for increased response duration in individuals treated with bevacizumab and/or sorafenib; 2) that since these toxicities are likely derived from the activity of bevacizumab and sorafenib, the development of HT would increase the risk of also developing HFSR; and 3) that VEGFR2 genotypic variation may be responsible for alterations in the activity of bevacizumab and/or sorafenib therapy that would manifest in associations with toxicity or clinical outcome following treatment with these agents. The results of the present study confirm a previously published study where HFSR development was noted to be related to PFS in patients with various solid tumors receiving doses of sorafenib between 300-600 mg bid [17], and a small study that HT is related to bevacizumab response [18]. Moreover, those receiving combination therapy with bevacizumab and sorafenib that developed hypertension enjoyed a greater than 5-fold increase in overall survival ...
Looking for online definition of sorafenib in the Medical Dictionary? sorafenib explanation free. What is sorafenib? Meaning of sorafenib medical term. What does sorafenib mean?
This study reports on the efficacy and mechanism of action of the small-molecule multikinase inhibitor foretinib in preclinical models of ovarian cancer metastasis. Our data suggest 4 principal mechanisms for how foretinib inhibits ovarian cancer growth and metastasis. In ovarian cancer cell lines, the inhibitor: (i) blocked activation of c-Met signaling; (ii) reduced proliferation mediated by a G2-M cell-cycle arrest; (iii) induced cell death through a 2-step mechanism in which cells detach followed by a caspase-dependent form of anoikis; and (iv) reduced proliferation, adhesion, migration, and invasion during early tumor development. In mouse models of ovarian cancer metastasis, foretinib reduced tumor burden and metastasis mediated by reduced angiogenesis, proliferation, and increased apoptosis. The multiple activities of foretinib are consistent with the numerous effects that have been attributed to c-Met and angiogenesis in the context of cancer (3).. Foretinib targets c-Met and VEGFR-2 ...
Dose study of the multikinase inhibitor, LY2457546, in patients with relapsed acute myeloid leukemia to assess safety, pharmacokinetics, and pharmacodynamics Volker Wacheck1, Michael Lahn2, Gemma Dickinson3, Wolfgang Füreder4, Renata Meyer4, Susanne Herndlhofer4, Thorsten Füreder1, Georg Dorfner5, Sada Pillay2, Valérie André6, Timothy P Burkholder7, Jacqueline K Akunda8, Leann Flye-Blakemore9, Dirk Van Bockstaele9, Richard F Schlenk10, Wolfgang R Sperr4, Peter Valent4,111Department of Clinical Pharmacology, Medical University of Vienna, Währinger Gürtel, Vienna, Austria; 2Early Oncology Clinical Investigation, Eli Lilly and Company, Indianapolis, IN, USA; 3Department of Pharmacokinetics, Eli Lilly and Company, Erl Wood Research Centre, Windlesham, Surrey, UK; 4Department of Internal Medicine I, Division of Hematology and Hemostaseology, Medical University of Vienna, Währinger Gürtel, Vienna, Austria; 5Eli Lilly GesmbH, Medical Department, Vienna, Austria; 6Department of Statistics, Eli Lilly and
Regorafenib (BAY 73-4506) is a novel, orally active multikinase inhibitor that is well tolerated in preclinical mouse models as well as clinically according to Phase I - III trials performed. The toxicity profile is comparable with other oral multikinase inhibitors with similar molecular targets. Re …
The combination of NU7441 and sorafenib enhanced the accumulation of cells in G1 phase and significantly reduced the proportion of cells in S and G2M phases, in FLT3-ITD MV4-11 cells but not WT-FLT3 HL-60 cells (Fig. S7). NU7441 and sorafenib concurrently increased the proportion of MV4-11 cells in sub-G1, indicating cell death (Fig. S7). This was confirmed by Annexin V analysis, which revealed a synergistic induction of apoptosis with NU7441 combined with sorafenib, in MV4-11 but not HL60 cells (Fig. 2a). Similarly, DNA-PK inhibitors (NU7441, CC-115, or M3814) and FLT3 inhibitors (sorafenib, midostaurin) synergistically induced apoptosis in Ba/F3 FLT3-ITD cells, but not Ba/F3 EV cells (Fig. 2a).. To investigate the clinical relevance of DNA-PK and FLT3 inhibitor combinations, drug sensitivity was assessed by Annexin V flow cytometry in human AML blasts ex vivo. NU7441 combined with sorafenib was synergistic in both wildtype and mutant-FLT3 blasts (Figs. 2b and S8A). In contrast, mutant-FLT3 ...
Patient characteristics included hepatitis C/B (SIRT, n=55/13; sorafenib, n=49/15); ECOG 0/1 (SIRT, n=145/92; sorafenib, n=139/83); BCLC A/B/C (SIRT, n=9/66/162; sorafenib n=12/61/149); Child Pugh A(5-6)/B7/unknown (SIRT, n=196/39/2; sorafenib, n=187/35/0); bilobar (SIRT, n=50; sorafenib, n=35); macrovascular invasion (SIRT, n=149; sorafenib, n=128); AFP (SIRT, median 87 ng/mL, sorafenib, median 80.0 ng/mL) ...
Purpose: Foretinib is an oral multikinase inhibitor targeting Met, RON, Axl, and VEGFR. We conducted a phase I, first-time-in-human, clinical trial using escalating doses of oral foretinib. Primary objectives were to identify a maximum tolerated dose and determine the safety profile of foretinib. Secondary objectives included evaluation of plasma pharmacokinetics, long-term safety after repeated administration, preliminary antitumor activity, and pharmacodynamic activity. Experimental Design: Patients had histologically confirmed metastatic or unresectable solid tumors for which no standard measures existed. All patients received foretinib orally for 5 consecutive days every 14 days. Dose escalation followed a conventional 3+3 design. Results: Forty patients were treated in eight dose cohorts. The maximum tolerated dose was defined as 3.6 mg/kg, with a maximum administered dose of 4.5 mg/kg. Dose-limiting toxicities included grade 3 elevations in aspartate aminotransferase and lipase. ...
After eking out marginal benefit to our patients with HCC for several years with predominantly single-agent doxorubicin and other anthracycline use, we noted that the biologic agent sorafenib rose above the fray. Phase 2 trial data with sorafenib required forward-thinking interpretation of clinical data that included very small response rates. Although response rates were low, a provocative clinical benefit potential for sorafenib in HCC led to completion of the first large randomized trial showing a survival benefit of systemic therapy.. The SHARP trial, presented at ASCO 2007 and published in 2008, showed a superior overall survival with sorafenib therapy (10.7 months) versus placebo (7.9 months).. The SHARP trial focused on patients with overall good liver function (based on Child-Pugh class A), as have many of the therapies to date for this malignancy. Most patients had bilirubin below 2.0 mg/dL, albumin greater than 3.5 g/dL, INR ,1.7 and the absence of significant ascites or hepatic ...
1% collagenase for 3 hrs at room temperature and 1. 5 kUml DNase I for the last 5 min in キナーゼ 阻害剤 L 15 medium followed by pipetting. The cell suspension was wa
Background Recent decades show major improvements in survival rates after cardiac arrest. that Speer4a these guidelines were not usually applied. The most common routine is a follow-up visit at a cardiac reception unit. If the need for neurological or psychological support are discovered the routines are not explicit. In addition, family users are not usually included in the follow-up. Conclusions Although efforts are already made to improve post cardiac arrest care and follow-up, many hospitals need to focus more on this part of cardiac arrest treatment. In addition, evidence-based national guidelines will have to be developed and implemented in order to achieve a more uniform care and follow-up for survivors and their family members. This national survey highlights this need, and might be helpful in the implementation of such guidelines. Electronic supplementary material The online version of this article (doi:10.1186/s12912-016-0123-0) contains supplementary material, which is available to ...
Bernd Kasper, MD, PhD, professor, Universitätsmedizin Mannheim, Mannheim, discusses imatinib (Gleevac) versus sorafenib (Nexavar) as treatments for patients with sarcoma.
Open-label, multi-center extension treatment protocol to allow access to tivozanib and sorafenib for subjects who have participated on the AV-951-09-301
The IUPHAR/BPS Guide to Pharmacology. sorafenib ligand page. Quantitative data and detailed annnotation of the targets of licensed and experimental drugs.
UPDATE: The latest blog and transcript of Bayer CEO Marijn Dekkers full quote on the Indian compulsory license of Nexavar at the December Financial Times event is now available.]. Continue Reading →. ...
Just a quick question. Am I right in thinking that ALL current PSPs can be downgraded and/or permanent CFW installed? Thanks.
Sigma-Aldrich offers abstracts and full-text articles by [Youn Kyoung Jeong, Mi-Sook Kim, Ji Young Lee, Eun Ho Kim, Wonwoo Kim, Hunjoo Ha, Jae-Hoon Jeong].
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The Russian Orthodox Church posed a number of questions to the investigators and the state commission, which have remained unanswered
The article describes an interesting aquarium inhabitant, such as the shrimp Amano. This crustacean has its own unique features of existence, which
Benzenesulfonates. *Benzenesulfonic acids. Hidden categories: *Articles without InChI source. *Chemical pages without ...
Benzenesulfonates. *Food colorings. *Naphthalenesulfonates. *Organic sodium salts. Hidden categories: *CS1 maint: BOT: original ...
Benzenesulfonates. Hidden categories: *Articles with changed EBI identifier. *ECHA InfoCard ID from Wikidata ...
In early 2008, a noninferiority study versus vancomycin or metronidazole for Clostridium difficile associated diarrhea (CDAD) found that about half of the patients in the tolevamer group did not complete the treatment, versus 25% in the vancomycin and 29% in the metronidazole groups. CDAD recurrence in patients reaching clinical success was reduced significantly by tolevamer (6% recurrence rate), vancomycin (18%) and metronidazole (19%). However, the good result of tolevamer is partly due to the high drop-out rate in this group. Since tolevamer did not reach its primary endpoint in this study, its development was halted.[14] ...
... LI Xiu-Lan, ZHANG Lei, GONG Qing-Tao, ZHANG Lu, ... Interfacial Dilational Properties of Tri-Substituted Alkyl Benzene Sulfonates[J].Acta Phys. -Chim. Sin., 2010, 26(03): 631-637 ...
Linear Alkyl Benzene Sulfonates. Normal alpha olefins react with benzene via Lewis acid catalysis to form linear alkyl benzenes ... LABs). Sulfonation and subsequent neutralization of LAB result in linear alkyl benzene sulfonates, which are commonly used in ...
Benzenesulfonates. *Benzenesulfonates: administration & dosage. *Cisplatin. *Cisplatin: administration & dosage. * ...
Benzenesulfonates / therapeutic use * Benzimidazoles / therapeutic use * Breast Neoplasms / drug therapy* * Breast Neoplasms / ...
Benzenesulfonates * Ligands * Folic Acid * Hydroxymethyl and Formyl Transferases * Phosphoribosylaminoimidazolecarboxamide ...
... sodium or potassium alkyl benzene sulfonates; sodium alkyl glyceryl ether sulfonates; sodium coconut oil fatty acid ...
Also useful are the sodium keryl benzene sulfonates. The amidoalkane sulfonates are characterized by the structure of an amide ... One group of these compounds, the sodium polypropylene benzene sulfonates, is described in United States Patent No. 2,477,383 ...
Surface Dilational Properties of Sodium 4-(1-methyl)-Alkyl Benzene Sulfonates: Effect of Alkyl Chain Length. Zhang, Ji-Chao / ...
Benzenesulfonates / pharmacology*. Biological Transport, Active / drug effects. Chlorides / blood*. Dinitrofluorobenzene / ... 0/Anion Exchange Protein 1, Erythrocyte; 0/Benzenesulfonates; 0/Chlorides; 0/NBD-taurine; 0/Nicotinic Acids; 0/Oxadiazoles; ...
3-ethyl-1-methyl-1H-imidazol-3-ium 4-(C11-13-sec-alkyl benzenesulfonates). IUPAC names 3 ... 3-ethyl-1-methyl-1H-imidazol-3-ium 4-(C11-13-sec-alkyl benzenesulfonates) ...
Such linear alkyl benzene sulfonates are known as "LAS". Such surfactants and their preparation are described for example in U. ... Specific, non-limiting examples of anionic surfactants useful herein include: a) Cn-Cis alkyl benzene sulfonates (LAS); b) C10- ...
Linear benzene sulfonates Studies in Animals The absorption, distribution, metabolism and elimination of LAS has been studied ...
Anionic Surfactants: Alkyl Sulfonates, Alkyl Benzene Sulfonates, etc.. Antistatic capabilities of these surfactants are ...
Mixtures of alkyl benzenesulfonates and ethoxylated alkylphenols may be employed.. The first polymer or the second polymer may ...
Benzenesulfonates (administration & dosage, therapeutic use) *Carcinoma, Renal Cell (blood supply, drug therapy, pathology) ...
These were called branched-chain alkyl benzene sulfonates . Like soap, they could take hard minerals out of water, leaving it ... They were replaced by straight-chain alkyl benzene sulfonates, such as Sodium dodecylbenzinesulfonate and sodium ... Linear Alkyl benzene sulfonates (LAS). Straight-chain, anionic surfactants. Somewhat slow to biodegrade. Most common ... Alkyl benzene sulfonates (ABS). Branched-chain, anionic surfactants. Slow to biodegrade. Seldom used. ...
Alkyl Benzene Sulfonates. R10ArSO3M. where R10 is an alkyl group of 8 to 18 carbon atoms, Ar is a benzene ring (C6H4) and M is ...
... aryl substituted benzenesulfonates); aldehydes (e.g., glutaraldehyde); peroxymonosulfate; Fentons reagent (a mixture of iron ...
Only 1 of 7 benzenesulfonates and 2 of 5 benzene-sulfonamides proved amenable to anaerobic metabolism. The authors found 37-75 ...
Seventy pyridazolon-4-ylidenehydrazinyl benzenesulfonates were prepared and evaluated in enzyme assays. The binding modes of ...
Particularly preferred surfactants for use herein include alkyl benzene sulfonates, alkyl sulfates, alkyl polyethoxy sulfates ...
Linear Alkyl Benzene Sulfonates (LAS): These synthetic petrochemicals are normally listed as anionic surfactants on labels, ...
... provides a detailed quantitative appraisal of the market of chemicals used in HI&I cleaning products, including current and forecast demand by major product, pricing analysis, competitive analysis, competitive landscape, and supplier share.
C.sub.16 alkyl benzene sulfonates; C.sub.10 -C.sub.20 paraffin sulfonates; alpha olefin sulfonates containing about 10-24 ...
Classified as benzenesulfonates, they can assemble themselves into a supramolecular structure. The molecules then form discs, ...
Long chain mono-olefins find utility in the manufacture of linear alkylated benzene sulfonates, which are used in the detergent ...
Effect of linear alkyl benzene sulfonates (LAS) on the fate of phenanthrene in a model ecosystem (water-lava-plant-air) ...
4-dinitrophenyl X-substituted benzenesulfonates with alicyclic secondary amines. ...
Monitoring benzenesulfonates (BS) and naphthalenesulfonates (NS) took place in five municipal sewage treatment plants (STP). A ...
8. The cleaning composition of claim 1 wherein the anionic surfaceant is said C9 -C15 alkyl benzene sulfonates or said C10 -C20 ... The cleaning composition of claim 9 wherein the anionic surfaceant is said C9 -C15 alkyl benzene sulfonates or said C10 -C20 ... wherein said anionic surfactant is selected from the group consisting of C9-15 alkyl benzene sulfonates, C10-20 alkane ... wherein said anionic surfactant is selected from the group consisting of C9-15 alkyl benzene sulfonates, C10-20 alkane ...
  • These substances are usually alkyl benzenesulfonates, a family of compounds that are similar to soap but are more soluble in hard water, because the polar sulfonate (of detergents) is less likely than the polar carboxyl (of soap) to bind to calcium and other ions found in hard water. (niir.org)
  • The first general method for the Pd-catalyzed amination of aryl tosylates and benzenesulfonates was developed utilizing ligand 1, which belongs to a new generation of biaryl monophosphine ligands. (scienceopen.com)
  • Only 1 of 7 benzenesulfonates and 2 of 5 benzene-sulfonamides proved amenable to anaerobic metabolism. (epa.gov)
  • The molecules in question with the working names A-Na and Azo-Na are promising substances that are classified as benzenesulfonates. (mipt.ru)