Disease relevance of LS-25344

• Furthermore, chronic administration of 0.2% ABA in the diet did not result in detectable toxicity and/or carcinogenic effects [1].
• A single i.p. injection of ABA at greater than 150 mg/kg body weight (B.W.) enhanced dose-dependently the induction of gamma-GTP positive foci in rat liver initiated by 20 mg/kg B.W. of DEN [1].
• In this study, a synthetic peptide (FRETN 89-98), containing residues 89-98 of lambda N protein and a fluorescence donor (anthranilamide) and quencher (3-nitrotyrosine), has been examined for ATP-dependent degradation by E. coli and human Lon proteases [2].
• A series of novel unsymmetrical anthranilamide-containing HIV protease inhibitors was designed [3].
• 2-Aminobenzamide, an inhibitor of ADP-ribosylation, antagonizes induced DNA hypomethylation during differentiation of murine Friend erythroleukemia cells by N'-methylnicotinamide [4].

High impact information on LS-25344

• These most comprehensive CoMFA and CoMSIA models are useful in understanding the structure-activity relationships of anthranilamide derivatives as well as aid in the design of novel derivatives with enhanced modulation of P-gp activity [5].
• Two readily synthesized anthranilamide, VEGF receptor tyrosine kinase inhibitors have been prepared and evaluated as angiogenesis inhibitors [6].
• While several analogues had potent in vitro and in vivo activities indicative of potential atypical antipsychotic activity, anthranilamide 77 (1192U90) ddemonstrated a superior pharmacological profile [7].
• Based on the above results, ABA was used as a representative ADPRT inhibitor for clarifying the mechanisms underlying the effects [1].
• Liver cell necrosis was not detectable either by analysis of serum enzymes or histologically 1, 3, 5, 7 and 14 days after 20 mg/kg B.W. of DEN with or without administration of 600 mg/kg B.W. of ABA [1].

Chemical compound and disease context of LS-25344

• Among them, the compound having a (3,4-difluorobenzyl)(2-hydroxyethyl)amino group at one end and a 2-aminobenzamide group at the other of molecule showed the most promising profile as an anticancer drug candidate, since it had a comparatively low toxicity as did MS-275 against a normal fibroblast cell CCD-1059SK [8].
• Subchronic toxicity, metabolism, and pharmacokinetics of the aminobenzamide anticonvulsant ameltolide (LY201116) in rhesus monkeys [9].

Biological context of LS-25344

• The most efficient is based on the cyclization of phenacyl anthranilamide 2a in the presence of (poly)phosphoric acid [10].
• Reductive amination using 2-aminobenzamide resulted in an opened reducing-terminal sugar ring and suppression of the cross-ring fragment ions carrying information associated with that ring [11].
• Rat liver SOD stimulated anthranilamide hydroxylation by the reconstituted system in proportion to its amount below a protein concentration of 1 microgram/ml [12].
• Anthranilamide analogues such as 23 are potent and highly selective muscarinic M2 antagonists that also show good oral bioavailability and in vivo activity [13].
• The 2-aminobenzamide series inhibitors generally had the potency in cell growth inhibitions comparable to that of MS-275 [8].

Anatomical context of LS-25344

• The characteristics of the enzyme in mung bean microsomal membranes and the usefulness of fluorogenic 2AB-labeled galactooligosaccharides for the assay of GalT are discussed [14].
• At a given SOD activity level, there was no difference among the rat liver SOD, Cu,Zn-SOD from bovine erythrocytes, and Mn-SOD from Serratia marcescens in their ability to stimulate anthranilamide hydroxylation not only by rat liver microsomes, but also by the reconstituted cytochrome P-450-containing monooxygenase system [12].
• Although 2-aminobenzamide does not seem to affect normal DNA methylation in cultured cells, the observed DNA hypomethylation in cells cultured for 24 h with 5 mM N'-methylnicotinamide was antagonized over 50% by equimolar 2-aminobenzamide [4].
• We prepared recombinant human TPO produced in Chinese hamster ovary (CHO) cells and analyzed the sugar chain structures quantitatively using 2-aminobenzamide labeling, sequential glycosidase digestion and matrix-assisted laser desorption ionization time-of-flight mass spectrometry (MALDI-TOF/MS) [15].
• Hydroxylation of anthranilamide was found to be catalyzed by drugs hydroxylation system but not by the microsomes alone, and is a specific reaction activated by a protein component contained in the soluble fraction [16].

Associations of LS-25344 with other chemical compounds

• ADPRT inhibitors investigated were 3-aminobenzamide (ABA), 5-methylnicotinamide (MNAM), and thymidine [1].
• Using 1H nuclear magnetic resonance spectroscopy, and beta-galactosidase and endo-beta-(1-->4)-galactanase treatments of the enzymatically formed 2AB-labeled galactooligosaccharides, the newly incorporated Gal residues were shown to be beta-(1-->4) linked [14].
• The AB and PHN derivatives formed abundant [M + H]+ and [M - H]- ions in ESI, and by matrix-assisted laser desorption/ionization (MALDI) produced abundant [M + Na]+ ions [17].
• Microanalysis of glycosaminoglycan-derived oligosaccharides labeled with a fluorophore 2-aminobenzamide by high-performance liquid chromatography: application to disaccharide composition analysis and exosequencing of oligosaccharides [18].
• Reversed-phase HPLC and derivatization by reductive amination using 2-aminobenzamide were finally applied to characterize a glycan pool enzymatically released from glycoproteins [19].

Gene context of LS-25344

• O-glycans were released from CF and ND mucins and derivatized with 2-aminobenzamide (2-AB), separated by ion exchange chromatography, and quantified by fluorescence [20].
• Aminobenzamide inhibited ADP-ribosylation of only HMG 2 in young but all HMGs except HMG 2 in the old [21].
• In a similar fashion, the 2AB-labeled O-glycans derived from APP were determined to be mono- and disialylated core type 1 structures [22].
• In short-term 51Cr-release assays with several mouse and human tumor cell lines, the inhibitors aminobenzamide (ABA) and nicotinamide (NA) of ADP-ribosylation sensitized HER-2/neu-nonoverexpressing cells (CaOV-3 and MCF-7) but not HER-2/neu-overexpressing cells (SKOV-3 and SKBR-3) to TNF [23].
• Latencies of haloperidol-, cis-N-(1-benzyl-2-methyl-pyrrolidin-3-yl)-2-methoxy-5-chloro-4-met hyl- aminobenzamide (YM-09151-2)- and sulpiride-, dopamine D2 receptor antagonists, treated groups did not differ from that seen in the PCP-treated group [24].

Analytical, diagnostic and therapeutic context of LS-25344

• To adequately resolve deficiencies affecting the first steps of lipid-linked oligosaccharide formation, we have used a non-radioactive procedure employing the fluorescence detection of 2-aminobenzamide-coupled oligosaccharides after HPLC separation [25].
• The magnitude of the effect was similar to that observed when partial hepatectomy (PH) was performed instead of ABA administration [1].
• Fluorescent labelled derivatives formed by reductive amination of neutral oligosaccharides with 2-aminobenzamide have been chromatographed on PGC-HPLC and by BioGel P4 gel filtration [26].
• A sensitive and rapid bioassay of homogalacturonan synthase using 2-aminobenzamide-labeled oligogalacturonides [27].
• MATERIALS AND METHODS: Cells (asynchronous, logarithmic phase) were pre-incubated with 2 mM aminobenzamide at 37 or 25 degrees C, X-irradiated with 10 Gy and allowed to repair DNA breaks for 15, 60 and 120 min at 37 or 25 degrees C. The remaining double-strand break were estimated by the neutral comet assay [28].

References