Disease relevance of Phenylanthranilic acid

• 5. The Cl- channel blockers diphenylamine-2-carboxylic acid (DPC, 1 mM) and 5-nitro-2-(3-phenylpropylamino)-benzoic acid (0.5 mM) abolished the ACh-evoked acidosis in both HCO3(-) -and acetate-buffered media [1].
• This reduction in [Cl-]i was completely inhibited by 10(-8)M FK453 (a selective A1 antagonist), 500ng/ml pertussis toxin (IAP), and 2.5mM N-phenylanthranilic acid (NPA) (a Cl- channel blocker) [2].
• N-phenylanthranilic acid (N-PAA; 4 mmol/kg/day p.o.) causes a diffuse renal papillary necrosis and a polyuria in 7 days [3].
• Four uncouplers of oxidative phosphorylation (UOP) (carbonyl cyanide m-chlorophenylhydrazone, 2,4-dinitrophenol, 4-hydroxybenzylidenemalonitrile and N-phenylanthranilic acid) have been found to alter the shape of the radiation survival curves of several cell lines of E. coli when present during irradiation in oxia [4].

High impact information on Phenylanthranilic acid

• We investigated the permeation pathway of human CFTR with measurements on conduction and open-channel blockade by diphenylamine-2-carboxylic acid (DPC) [5].
• The effects of ACh were blocked by 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS), 5-nitro2-(3-phenylpropylamino)benzoic acid (NPPB), or diphenylamine-2-carboxylic acid (DPC), and the effects of secretin were inhibited by NPPB or DPC and unaffected by DIDS [6].
• Derivatization of the carboxylate moiety in moderately selective COX-1 inhibitors, such as 5,8,11,14-eicosatetraynoic acid (ETYA) and arylacetic and fenamic acid NSAIDs, exemplified by indomethacin and meclofenamic acid, respectively, generated potent and selective COX-2 inhibitors [7].
• The activity of SLC26A7 was inhibited by all inhibitors of anion transporters tested, 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid, diphenylamine-2-carboxylic acid, and glybenclamide [8].
• Diphenylamine and N-phenylanthranilic acid neither affected COX activity in platelets nor modified the activation state of neutrophils [9].

Biological context of Phenylanthranilic acid

• N-phenylanthranilic acid (NPAA), ouabain, BaCl(2) and bumetanide were used to determine the role of basolateral Na,K-ATPase, apical Cl(-)-channel, and basolateral K(+)-channel and Na(+)(K(+))2Cl(-)-cotransporter activities, respectively, in active ion transport across RCrECL [10].
• 1H-Nuclear magnetic resonance pattern recognition studies with N-phenylanthranilic acid in the rat: time- and dose-related metabolic effects [11].
• Protein biomarkers of nephrotoxicity; a review and findings with cyclosporin A, a signal transduction kinase inhibitor and N-phenylanthranilic acid [12].

Anatomical context of Phenylanthranilic acid

• Furthermore, a temperature labile factor secreted by submucosal glands appears to alter the baseline activation of 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid and/or diphenylamine-2-carboxylic acid-sensitive chloride channels in the surface airway epithelium [13].
• The remaining amiloride-insensitive I(sc) component in epididymis and vas deferens cells was partially inhibited by apical application of the Cl(-) channel blocker diphenylamine-2-carboxylic acid (1 mM) [14].
• Diphenylamine-2-carboxylic acid (DPC), Usually an inhibitor of Cl- and non-selective cation channels, inhibits Cl-/HCO3- exchange and opens Cl- and cation conductances in rabbit gallbladder epithelium [15].
• This, and the observation that N-phenylanthranilic acid did not affect the ultrastructure of the cells, suggested that plasma membrane chloride channels are involved in the initial signaling cascade triggered when lymphatic endothelial cells begin to adhere to a substrate [16].
• Diphenylamine-2-carboxylic acid potentiates the cyclic nucleotides-mediated relaxation of porcine coronary artery: possible involvement of the inhibitory effect on the efflux of cyclic nucleotides [17].

Associations of Phenylanthranilic acid with other chemical compounds

• The presence of a carboxylic acid group in the diphenylamine (N-phenylanthranilic acid) highly increased its ability to reduce the L-selectin surface expression in neutrophils [9].
• We report a structural series of N-phenylanthranilic acid derivatives and steroid carboxylates that selectively inhibit recombinant AKR1C isoforms but do not inhibit recombinant COX-1 or COX-2 [18].
• Chloride channel blockers, 5-nitro-2-(3-phenylpropylamino) benzoic acid (NPPB) and N-phenylanthranilic acid (DPC), practically abolished taurine release [19].
• The whole-cell Cl- current was only partially blocked by both 5-nitro-2-(3-phenylpropylamino) benzoic acid (NPPB, 0.5 mM) and diphenylamine-2-carboxylic acid (DPC, 1.0 mM), but 4-acetamido-4'-isothiocyanato-stilbene-2,2'-disulfonic acid (SITS, 0.5 mM) was without effect [20].
• Stilbene disulfonate and phenylanthranilic acid derivatives block Cl- transport and ACTH secretion from mouse AtT-20 clonal corticotrophs [21].

Gene context of Phenylanthranilic acid

• In addition, the Cl channel blockers 5-nitro-2-(3-phenylpropylamino)benzoate (NPPB; 50 microM) and diphenylamine-2-carboxylic acid (DPC; 3 mM) reduced the cAMP-evoked currents by only approximately 10% [22].
• Other chloride channel inhibitors, 4,4'-diisothiocyanatostilbene-2-2'-disulfonic acid and diphenylamine-2-carboxylic acid, also inhibited FITC-albumin uptake [23].
• Lead compounds, 4-chloro-N-phenylanthranilic acid and 4-benzoyl-benzoic acid for the N-phenylanthranilic acid analogs and most steroid carboxylates, exhibited IC(50) values that had greater than 500-fold selectivity for AKR1C isozymes compared with COX-1 and COX-2 [18].
• Taken together, our results indicate that RSMT-A5 cells possess a beta-adrenergic receptor system which controls intracellular volume and chloride content by modulating transport processes that are 1) cAMP-responsive and 2) inhibitable by the putative chloride channel blocker N-phenylanthranilic acid [24].

Analytical, diagnostic and therapeutic context of Phenylanthranilic acid

• The oral administration of a suspension of N-phenylanthranilic acid (N-PAA), over the range of 0.5 to 2 mmol/kg for 14 consecutive days, caused a dose-related renal papillary necrosis (RPN), which involved no more than 30% of the medullary apex [25].

References