Month: November 2022

Romeiro, Nelilma C. published the artcileNSAIDs revisited: Putative molecular basis of their interactions with peroxisome proliferator-activated gamma receptor (PPARγ), Category: naphthyridine, the publication is European Journal of Medicinal Chemistry (2008), 43(9), 1918-1925, database is CAplus and MEDLINE.

This paper describes mol. docking studies of a series of classical NSAIDs with PPARγ receptor, which has been pointed as a new target for the design of anticancer and antiinflammatory drugs, and has been found to be responsible for some of the already established pharmacol. effects observed for marketed drugs. The results show the mol. basis of PPARγ activation by non-selective COX inhibitors.

European Journal of Medicinal Chemistry published new progress about 59973-80-7. 59973-80-7 belongs to naphthyridine, auxiliary class Immunology/Inflammation,COX, name is Sulindac sulfone, and the molecular formula is C20H17FO4S, Category: naphthyridine.

Referemce:
https://en.wikipedia.org/wiki/1,8-Naphthyridine,
1,8-Naphthyridine | C8H6N2 – PubChem

Brunell, David published the artcileStudies on the metabolism and biological activity of the epimers of Sulindac, Category: naphthyridine, the publication is Drug Metabolism and Disposition (2011), 39(6), 1014-1021, database is CAplus and MEDLINE.

Sulindac is a nonsteroidal, anti-inflammatory drug (NSAID) that was also studied for its anticancer activity. Recent studies suggest that sulindac and its metabolites act by sensitizing cancer cells to oxidizing agents and drugs that affect mitochondrial function, resulting in the production of reactive oxygen species and death by apoptosis. In contrast, normal cells are not killed under these conditions and, in some instances, are protected against oxidative stress. Sulindac has a Me sulfoxide moiety with a chiral center and was used in all of the previous studies as a mixture of the R- and S-epimers. Because epimers of a compound can have very different chem. and biol. properties, we have separated the R- and S-epimers of sulindac, studied their individual metabolism, and performed preliminary experiments on their effect on normal and lung cancer cells exposed to oxidative stress. Previous results had indicated that the reduction of (S)-sulindac to sulindac sulfide, the active NSAID, was catalyzed by methionine sulfoxide reductase (Msr) A. In the present study, we purified an enzyme that reduces (R)-sulindac and resembles MsrB in its substrate specificity. The oxidation of both epimers to sulindac sulfone is catalyzed primarily by the microsomal cytochrome P 450 (P 450) system, and the individual enzymes responsible have been identified. (S)-Sulindac increases the activity of the P 450 system better than (R)-sulindac, but both epimers increase primarily the enzymes that oxidize (R)-sulindac. Both epimers can protect normal lung cells against oxidative damage and enhance the killing of lung cancer cells exposed to oxidative stress.

Drug Metabolism and Disposition published new progress about 59973-80-7. 59973-80-7 belongs to naphthyridine, auxiliary class Immunology/Inflammation,COX, name is Sulindac sulfone, and the molecular formula is C20H17FO4S, Category: naphthyridine.

Referemce:
https://en.wikipedia.org/wiki/1,8-Naphthyridine,
1,8-Naphthyridine | C8H6N2 – PubChem

Raza, Rabia published the artcileIdentification of small molecule sulfonic acids as ecto-5′-nucleotidase inhibitors, Product Details of C10H9NO4S, the publication is Medicinal Chemistry (2012), 8(6), 1133-1139, database is CAplus and MEDLINE.

Ecto-5′-Nucleotidase inhibitors have great potential as anti-tumor agents. We have investigated biochem. properties of human and rat ecto-5′-Nucleotidases and characterized 19 small mol. sulfonic acid derivatives as potential inhibitors of ecto-5′-Nucleotidases. We identified 11 potent inhibitors of human and rat ecto-5′-Nucleotidases and checked their selectivity. Compound 10 (Sodium 2,4-dinitrobenzenesulfonate) with K_i value of 0.66 μM and 19 (N-(4-sulfamoylphenylcarbamothioyl) pivalamide) with K_i value of 0.78 μM were identified as the most potent inhibitors for human and rat ecto-5′-Nucleotidase, resp. The present compounds have low mol. weights, water solubility and equal potency as compared to the reported inhibitors.

Medicinal Chemistry published new progress about 116-63-2. 116-63-2 belongs to naphthyridine, auxiliary class Sulfonic acid,Amine,Naphthalene,Alcohol,Organic Pigment, name is 4-Amino-3-hydroxynaphthalene-1-sulfonic acid, and the molecular formula is C10H9NO4S, Product Details of C10H9NO4S.

Referemce:
https://en.wikipedia.org/wiki/1,8-Naphthyridine,
1,8-Naphthyridine | C8H6N2 – PubChem

Vidya, V. G. published the artcileSynthesis, characterization and applications of some azo dyes derived from various aromatic amines, Quality Control of 116-63-2, the publication is Asian Journal of Chemistry (2018), 30(9), 2049-2053, database is CAplus.

In this work, we report the synthesis of metal free dyes and their fastness properties. A series of monoazo dyes were obtained by diazotization of various aromatic primary amines and coupling with different components. One colored Schiff base derived from triethylenetetramine and N,N-dimethyl-4-aminobenzaldehyde was also synthesized. These colored compounds were characterized by FTIR, UV-visible, ¹H, ¹³C NMR and ESI mass spectroscopic methods. The dyeing performance of all the compounds were evaluated on cotton fabric. They were applied on bleached cotton fabric and their dyeing and fastness properties were assessed. The absorption spectra of the dyes are discussed with regard to their structure. The structure of colored dyes and Schiff base are proposed based on various spectroscopic data. The newly synthesized group of monoazo dyes gives shades ranging from yellow to reddish orange with good light fastness and excellent wash fastness.

Asian Journal of Chemistry published new progress about 116-63-2. 116-63-2 belongs to naphthyridine, auxiliary class Sulfonic acid,Amine,Naphthalene,Alcohol,Organic Pigment, name is 4-Amino-3-hydroxynaphthalene-1-sulfonic acid, and the molecular formula is C5H12O2, Quality Control of 116-63-2.

Referemce:
https://en.wikipedia.org/wiki/1,8-Naphthyridine,
1,8-Naphthyridine | C8H6N2 – PubChem

Gasparini, Laura published the artcileModulation of β-amyloid metabolism by non-steroidal anti-inflammatory drugs in neuronal cell cultures, Related Products of naphthyridine, the publication is Journal of Neurochemistry (2004), 88(2), 337-348, database is CAplus and MEDLINE.

Alzheimer disease (AD) is characterized by cerebral deposits of β-amyloid (Aβ) peptides, which are surrounded by neuroinflammatory cells. Epidemiol. studies have shown that prolonged use of non-steroidal anti-inflammatory drugs (NSAIDs) reduces the risk of developing AD. In addition, biol. data indicate that certain NSAIDs specifically lower Aβ42 levels in cultures of peripheral cells independently of cyclooxygenase (COX) activity and reduce cerebral Aβ levels in AD transgenic mice. Whether other NSAIDs, including COX-selective compounds, modulate Aβ levels in neuronal cells remains unexploited. Here, we investigated the effects of compounds from every chem. class of NSAIDs on Aβ40 and Aβ42 secretion using both Neuro-2a cells and rat primary cortical neurons. Among non-selective NSAIDs, flurbiprofen and sulindac sulfide concentration-dependently reduced the secretion not only of Aβ42 but also of Aβ40. Surprisingly, both COX-2 (celecoxib; s.c.-125) or COX-1 (s.c.-560) selective compounds significantly increased Aβ42 secretion, and either did not alter (s.c.-560; s.c.-125) or reduced (celecoxib) Aβ40 levels. The levels of βAPP C-terminal fragments and Notch cleavage were not altered by any of the NSAIDs, indicating that γ-secretase activity was not overall changed by these drugs. The present findings show that only a few non-selective NSAIDs possess Aβ-lowering properties and therefore have a profile potentially relevant to their clin. use in AD.

Journal of Neurochemistry published new progress about 59973-80-7. 59973-80-7 belongs to naphthyridine, auxiliary class Immunology/Inflammation,COX, name is Sulindac sulfone, and the molecular formula is C20H17FO4S, Related Products of naphthyridine.

Referemce:
https://en.wikipedia.org/wiki/1,8-Naphthyridine,
1,8-Naphthyridine | C8H6N2 – PubChem

Mastalarz, H. published the artcileThe synthesis of some 2,7-disubstituted 1,8-naphthyridines, Synthetic Route of 14903-78-7, the publication is Polish Journal of Chemistry (1994), 68(3), 459-65, database is CAplus.

The reaction of 2,7-dichloro-1,8-naphthyridine (I) with the Na salts of some active methylene compounds is described. The resulting 7-chloro-2-substituted and 2,7-disubstituted 1,8-naphthyridine derivatives exist in 2(1H)-naphthryidine form. The reactions of 2,7-dichloro-1,8-naphthyridine with diethanolamine, hydrolysis and acid-catalyzed decomposition for some of the obtained compounds were also reported.

Polish Journal of Chemistry published new progress about 14903-78-7. 14903-78-7 belongs to naphthyridine, auxiliary class 6.6_Aromatics,Naphthyridines, name is 2,7-Dimethyl-1,8-naphthyridine, and the molecular formula is C10H10N2, Synthetic Route of 14903-78-7.

Referemce:
https://en.wikipedia.org/wiki/1,8-Naphthyridine,
1,8-Naphthyridine | C8H6N2 – PubChem

Cousido-Siah, Alexandra published the artcileStructural analysis of sulindac as an inhibitor of aldose reductase and AKR1B10, Product Details of C20H17FO4S, the publication is Chemico-Biological Interactions (2015), 290-296, database is CAplus and MEDLINE.

Aldose reductase (AR, AKR1B1) and AKR1B10 are enzymes implicated in important pathologies (diabetes and cancer) and therefore they have been proposed as suitable targets for drug development. Sulindac is the metabolic precursor of the potent non-steroidal anti-inflammatory drug (NSAID) sulindac sulfide, which suppresses prostaglandin production by inhibition of cyclooxygenases (COX). In addition, sulindac has been found to be one of the NSAIDs with higher antitumoral activity, presumably through COX inhibition. However, sulindac anticancer activity could be partially mediated through COX-independent mechanisms, including the participation of AR and AKR1B10. Previously, it had been shown that sulindac and sulindac sulfone were good AR inhibitors and the structure of the ternary complex with NADP⁺ and sulindac was described (PDB ID 3U2C). In this work, we determined the three-dimensional structure of AKR1B10 with sulindac and established structure-activity relationships (SAR) of sulindac and their derivatives with AR and AKR1B10. The difference in the IC₅₀ values for sulindac between AR (0.36 μM) and AKR1B10 (2.7 μM) might be explained by the different positioning and stacking interaction given by Phe122/Phe123, and by the presence of two buried and ordered water mols. in AKR1B10 but not in AR. Moreover, SAR anal. shows that the substitution of the sulfinyl group is structurally allowed in sulindac derivatives Hence, sulindac and its derivatives emerge as lead compounds for the design of more potent and selective AR and AKR1B10 inhibitors.

Chemico-Biological Interactions published new progress about 59973-80-7. 59973-80-7 belongs to naphthyridine, auxiliary class Immunology/Inflammation,COX, name is Sulindac sulfone, and the molecular formula is C20H17FO4S, Product Details of C20H17FO4S.

Referemce:
https://en.wikipedia.org/wiki/1,8-Naphthyridine,
1,8-Naphthyridine | C8H6N2 – PubChem

Wang, Huiwen published the artcileMonitoring of Parathion-Methyl Based on PtNPs Combined with 4-Amino-3-Hydroxy-1-Naphthalenesulfonic Acid Fluorescent Probe and Enzyme Inhibition, SDS of cas: 116-63-2, the publication is Chemistry Africa (2022), 5(1), 99-105, database is CAplus.

In this paper, a new fluorescence anal. method was proposed to detect parathion-Me (PM) based on platinum nanoparticles (PtNPs) and 4-amino-3-hydroxy-1-naphthalenesulfonic acid (AHNSA) as fluorescent probe. AHNSA with high fluorescence could combine with PtNPs by electrostatic attraction, bringing out fluorescence quenching of AHNSA. Acetylthiocholine (ATCh) was hydrolyzed by acetylcholinesterase (AChE) to produce thiocholine, which could induce the aggregation of PtNPs by electrostatic attraction and restore the fluorescence intensity of AHNSA. However, in the presence of PM, the catalytic activity of AChE is inhibited, leading to the quenching of fluorescence of AHNSA again. Under the optimal conditions, the linear range of parathion-Me (PM) detection was 0.26-53.3 ng/mL (R2 = 0.994), and the limit of detection was 0.17 ng/mL (S/N = 3). In addition, this method has been successfully used for the determination of PM in water and food samples.

Chemistry Africa published new progress about 116-63-2. 116-63-2 belongs to naphthyridine, auxiliary class Sulfonic acid,Amine,Naphthalene,Alcohol,Organic Pigment, name is 4-Amino-3-hydroxynaphthalene-1-sulfonic acid, and the molecular formula is C7H13NO2, SDS of cas: 116-63-2.

Referemce:
https://en.wikipedia.org/wiki/1,8-Naphthyridine,
1,8-Naphthyridine | C8H6N2 – PubChem

Svejstrup, Thomas D. published the artcileSynthesis of Arylamines via Aminium Radicals, Name: 2,2′-Dimethoxy-1,1′-binaphthalene, the publication is Angewandte Chemie, International Edition (2017), 56(47), 14948-14952, database is CAplus and MEDLINE.

Arylamines constitute the core structure of many therapeutic agents, agrochems., and organic materials. The development of methods for the efficient and selective construction of these structural motifs from simple building blocks is desirable but still challenging. We demonstrate that protonated electron-poor O-aryl hydroxylamines give aminium radicals in the presence of Ru(bpy)₃Cl₂. These highly electrophilic species undergo polarized radical addition to aromatic compounds in high yield and selectivity. We successfully applied this method to the late-stage modification of chiral catalyst templates, therapeutic agents, and natural products.

Angewandte Chemie, International Edition published new progress about 2960-93-2. 2960-93-2 belongs to naphthyridine, auxiliary class Naphthalene,Ether,Other MOF ligands,Organic ligands for MOF materials, name is 2,2′-Dimethoxy-1,1′-binaphthalene, and the molecular formula is C13H10O3, Name: 2,2′-Dimethoxy-1,1′-binaphthalene.

Referemce:
https://en.wikipedia.org/wiki/1,8-Naphthyridine,
1,8-Naphthyridine | C8H6N2 – PubChem

Bravi, Luca published the artcileSulindac metabolites decrease cerebrovascular malformations in CCM3-knockout mice, Recommanded Product: Sulindac sulfone, the publication is Proceedings of the National Academy of Sciences of the United States of America (2015), 112(27), 8421-8426, database is CAplus and MEDLINE.

Cerebral cavernous malformation (CCM) is a disease of the central nervous system causing hemorrhage-prone multiple lumen vascular malformations and very severe neurol. consequences. At present, the only recommended treatment of CCM is surgical. Because surgery is often not applicable, pharmacol. treatment would be highly desirable. We describe here a murine model of the disease that develops after endothelial-cell-selective ablation of the CCM3 gene. We report an early, cell-autonomous, Wnt-receptor-independent stimulation of β-catenin transcription activity in CCM3-deficient endothelial cells both in vitro and in vivo and a triggering of a β-catenin-driven transcription program that leads to endothelial-to-mesenchymal transition. TGF-β/BMP signaling is then required for the progression of the disease. We also found that the anti-inflammatory drugs sulindac sulfide and sulindac sulfone, which attenuate β-catenin transcription activity, reduce vascular malformations in endothelial CCM3-deficient mice. This study opens previously unidentified perspectives for an effective pharmacol. therapy of intracranial vascular cavernomas.

Proceedings of the National Academy of Sciences of the United States of America published new progress about 59973-80-7. 59973-80-7 belongs to naphthyridine, auxiliary class Immunology/Inflammation,COX, name is Sulindac sulfone, and the molecular formula is C20H17FO4S, Recommanded Product: Sulindac sulfone.

Referemce:
https://en.wikipedia.org/wiki/1,8-Naphthyridine,
1,8-Naphthyridine | C8H6N2 – PubChem