Month: November 2022

Nixon, J. B. published the artcileEvaluation of eicosanoids and NSAIDs as PPARγ ligands in colorectal carcinoma cells, Related Products of naphthyridine, the publication is Prostaglandins, Leukotrienes and Essential Fatty Acids (2003), 68(5), 323-330, database is CAplus and MEDLINE.

The activation of peroxisome proliferator activated receptor γ (PPARγ) may play a role in the control of colorectal carcinogenesis. The expression of PPARγ was examined by Western blotting in human colorectal tumors and matched normal adjacent tissues, as well as in various colorectal carcinoma cell lines. In the tissues, the expression of PPARγ was elevated in tumors relative to the adjacent normal tissues. Each colorectal carcinoma cell line expressed PPARγ. The ability of various eicosanoids to bind PPARγ in colorectal carcinoma cells was investigated using luciferase reporter assays. The well-known PPARγ ligands, troglitazone and 15-deoxy-Δ^12,14-prostaglandin J₂ strongly induced PPARγ binding activity. Products of lipoxygenases displayed moderate binding activity, while other prostaglandins and fatty acids displayed little or no reporter activation. The activation of PPARγ by 13(S)-HODE, the major metabolite of 15-lipoxygenase-1 from linoleic acid, was concentration dependent reaching maximum at 10 μM (35-fold activation). The endogenous production of 13(S)-HODE by expression of 15-LO-1 did not activate PPARγ. The ability of various nonsteroidal anti-inflammatory drugs (NSAIDs) to induce PPARγ activation was also evaluated. The conventional NSAIDs that inhibit both cyclooxygenases (COX-1 and COX-2) also induced PPARγ binding activity. In general, however, neither COX-1- nor COX-2-specific inhibitors induced the activation of PPARγ. Taken together, the metabolites of 15-lipoxygenase and the conventional NSAIDs were confirmed as exogenous ligands for PPARγ in colorectal carcinoma cells.

Prostaglandins, Leukotrienes and Essential Fatty Acids 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

Santiesteban, Oscar J. published the artcileIdentification of toxin inhibitors using a magnetic nanosensor-based assay, Safety of Sulindac sulfone, the publication is Small (2014), 10(6), 1202-1211, database is CAplus and MEDLINE.

A magnetic nanosensor-based method is described to screen a library of drugs for potential binding to toxins. Screening is performed by measuring changes in the magnetic relaxation signal of the nanosensors (bMR nanosensors) in aqueous suspension upon addition of the toxin. The Anthrax lethal factor (ALF) is selected as a model toxin to test the ability of our bMR nanosensor-based screening method to identify potential inhibitors of the toxin. Out of 30 mols. screened, sulindac, naproxen and fusaric acid are found to bind LF, with dissociation constants in the low micromolar range. Further biol. anal. of the free mols. in solution indicate that sulindac and its metabolic products inhibited LF cytotoxicity to macrophages with IC₅₀ values in the micromolar range. Meanwhile, fusaric acid is found to be less effective at inhibiting LF cytotoxicity, while naproxen does not inhibit LF toxicity. Most importantly, when the sulindac and fusaric acid-bMR nanosensors themselves are tested as LF inhibitors, as opposed to the corresponding free mols., they are stronger inhibitors of LF with IC₅₀ values in the nanomolar range. Taken together, these studies show that a bMR nanosensors-based assay can be used to screen known drugs and other small mols. for inhibitor of toxins. The method can be easily modified to screen for inhibitors of other mol. interactions and not only the selected free mol. can be study as potential inhibitors but also the bMR nanosensors themselves achieving greater inhibitory potential.

Small 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, Safety of Sulindac sulfone.

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

Jo, Tae Geun published the artcileA single fluorescent chemosensor for multiple targets of Cu²⁺, Fe^2+/3+ and Al³⁺ in living cells and a near-perfect aqueous solution, SDS of cas: 116-63-2, the publication is RSC Advances (2017), 7(46), 28723-28732, database is CAplus.

A sulfonate-based chemosensor 1 was designed and synthesized for sensing various analytes: Cu²⁺, Fe^2+/3+ and Al³⁺. Sensor 1 showed a high selectivity and sensitivity for the analytes in a near-perfect aqueous medium. Cu²⁺ and Fe^2+/3+ could be monitored by fluorescence quenching of 1. It had sufficiently low detection limits (1.25 μM for Cu²⁺ and 3.96 μM for Fe³⁺), which were below the recommended levels of the World Health Organization for Cu²⁺ (31.5 μM) and the Environmental Protection Agency for Fe³⁺ (5.37 μM). 1 showed the high preferential selectivity for Cu²⁺ and Fe³⁺ in the presence of competitive metal ions without any interference. Importantly, pyrophosphate could be used to distinguish Fe³⁺ from Cu²⁺. In addition, this sensor could monitor Al³⁺ through fluorescence emission change. Moreover, 1 was successfully applied to quantify and image Al³⁺ in water samples and living cells. Based on photophys. studies and theor. calculations, the sensing mechanisms of 1 for Cu²⁺ and Al³⁺ were explained, resp.

RSC Advances 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, SDS of cas: 116-63-2.

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

Matheis, Christian published the artcileSandmeyer Difluoromethylation of (Hetero-)Arenediazonium Salts, Application of 1-(Difluoromethyl)naphthalene, the publication is Organic Letters (2014), 16(22), 5984-5987, database is CAplus and MEDLINE.

A Sandmeyer-type difluoromethylation process has been developed that allows the straightforward conversion of (hetero)arenediazonium salts into the corresponding difluoromethyl (hetero)arenes under mild conditions. The actual difluoromethylating reagent, a difluoromethyl-copper complex, is formed in situ from copper thiocyanate and TMS-CF₂H. The diazonium salts are either preformed or generated in situ from broadly available aromatic amines.

Organic Letters published new progress about 53731-26-3. 53731-26-3 belongs to naphthyridine, auxiliary class Difluoromethyl,Fluoride,Naphthalene, name is 1-(Difluoromethyl)naphthalene, and the molecular formula is C11H8F2, Application of 1-(Difluoromethyl)naphthalene.

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

Chen, Yen-Ling published the artcileCapillary electrophoresis combining field-amplified sample stacking and electroosmotic flow suppressant for analysis of sulindac and its two metabolites in plasma, Quality Control of 59973-80-7, the publication is Journal of Chromatography A (2006), 1119(1-2), 176-182, database is CAplus and MEDLINE.

Field-amplified sample stacking with electroosmotic flow (EOF) suppressant in capillary electrophoresis was used to determine the concentration of sulindac (SU) and its two active metabolites, sulindac sulfide (SI) and sulindac sulfone (SO), in human plasma. After acidification, the analytes were extracted from the plasma with dichloromethane. Before sample loading, a water plug (0.5 psi, 3 s) was injected to contain sample anions and to permit field-amplified stacking. Electrokinetic injection at a reversed voltage (-6 kV, 99.9 s) was then used to introduce anions. Separation was performed using phosphate buffer (80 mM, pH 6.0) containing 2,6-di-O-methyl-β-cyclodextrin (0.75 mM), and poly(ethylene oxide) (0.01%) as an EOF suppressant. The separation was performed at -30 kV and 200 nm. During method validation, calibration plots were linear (r > 0.994) over a range of 0.3-30.0 μM for SU and SO, and 0.5-30.0 μM for SI. During intra- and inter-day anal., relative standard deviations (RSD) and relative errors (RE) were all less than 16%. The limits of detection were 0.1 μM for SU and SO, and 0.3 μM for SI (S/N = 4, sampling 99.9 s at -6 kV). This method was feasible for determining SU and its metabolites in plasma. One female volunteer (27 years, 42 kg) was orally administered one SU tablet (Clinoril, 200 mg/tab), and blood samples were drawn at regular intervals over an 8 h period. After pretreatment and anal., the plasma levels of SU, SI and SO were monitored. The pharmacokinetic profile of SU was also investigated.

Journal of Chromatography A 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, Quality Control of 59973-80-7.

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

Lim, Jin T. E. published the artcileSulindac Sulfide and Exisulind Inhibit Expression of the Estrogen and Progesterone Receptors in Human Breast Cancer Cells, SDS of cas: 59973-80-7, the publication is Clinical Cancer Research (2006), 12(11), 3478-3484, database is CAplus and MEDLINE.

In previous studies, we found that sulindac sulfide and exisulind (sulindac sulfone, Aptosyn) cause growth inhibition, arrest cells in the G₁ phase of the cell cycle, and induce apoptosis in human breast cancer cell lines. These effects were associated with decreased expression of cyclin D1. The present study focuses on the effects of sulindac sulfide and exisulind on hormone signaling components in breast cancer cells. We found that estrogen receptor (ER)-pos. and progesterone receptor (PR)-pos. T47D breast cancer cells were somewhat more sensitive to growth inhibition by sulindac sulfide or exisulind than ER-neg. PR-neg. MB-MDA-468 breast cancer cells. Further studies indicated that sulindac sulfide and exisulind caused marked down-regulation of expression of the ER and PR-A and PR-B in T47D cells. However, neither compound caused a major change in expression of the retinoic acid receptor α (RARα), RAR{szligbeta}, or RARα in T47D cells. Sulindac sulfide and exisulind also caused a decrease in expression of the ER in estrogen-responsive MCF-7 breast cancer cells. Both compounds also markedly inhibited estrogen-stimulated activation of an estrogen-responsive promoter in transient transfection reporter assays. Treatment of T47D cells with specific protein kinase G (PKG) activators did not cause a decrease in ER or PR expression. Therefore, although sulindac sulfide and exisulind can cause activation of PKG, the inhibitory effects of these two compounds on ER and PR expression does not seem to be mediated by PKG. Our findings suggest that the growth inhibition by sulindac sulfide and exisulind in ER-pos. and PR-pos. human breast cancer cells may be mediated, in part, by inhibition of ER and PR signaling. Thus, these and related compounds may provide a novel approach to the prevention and treatment of human breast cancers, especially those that are ER pos.

Clinical Cancer Research 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, SDS of cas: 59973-80-7.

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