Month: December 2022

Sheng, Huaming published the artcileIdentification of N-Oxide and Sulfoxide Functionalities in Protonated Drug Metabolites by Using Ion-Molecule Reactions Followed by Collisionally Activated Dissociation in a Linear Quadrupole Ion Trap Mass Spectrometer, SDS of cas: 59973-80-7, the publication is Journal of Organic Chemistry (2016), 81(2), 575-586, database is CAplus and MEDLINE.

The in vivo oxidation of sulfur and nitrogen atoms in many drugs into sulfoxide and N-oxide functionalities is a common biotransformation process. Unfortunately, the unambiguous identification of these metabolites can be challenging. In the present study, ion-mol. reactions of tris(dimethylamino)borane followed by collisionally activated dissociation (CAD) in an ion trap mass spectrometer are demonstrated to allow the identification of N-oxide and sulfoxide functionalities in protonated polyfunctional drug metabolites. Only ions with N-oxide or sulfoxide functionality formed diagnostic adducts that had lost di-Me amine (DMA). This was demonstrated even for an analyte that contains a substantially more basic functionality than the functional group of interest. CAD of the diagnostic product ions (M) resulted mainly in type A (M – DMA) and B fragment ions (M – HO-B(N(CH₃)₂)₂) for N-oxides, but sulfoxides also formed diagnostic C ions (M – O=BN(CH₃)₂), thus allowing differentiation of the functionalities. Some protonated analytes yielded abundant TDMAB adducts that had lost two DMA mols. instead of just one. This provides information on the environment of the N-oxide and sulfoxide functionalities. Quantum chem. calculations were performed to explore the mechanisms of the above-mentioned reactions. The method can be implemented on HPLC for real drug anal.

Journal of Organic 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 C17H18N3NaO3S, SDS of cas: 59973-80-7.

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

Mishiba, Kentaro published the artcileDimesitylborylethynylated Arenes: Unique Electronic and Photophysical Properties Caused by Ethynediyl (CC) Spacers, Application of 9,10-Diethynylanthracene, the publication is Chemistry – A European Journal (2021), 27(17), 5432-5438, database is CAplus and MEDLINE.

Herein, the authors report the synthesis and electrochem. and photophys. properties of aromatic hydrocarbons having one or two dimesitylborylethynyl peripherals. The mono- (1) and diboryl compounds (2), readily prepared by nucleophilic substitution reaction, are fairly stable to air and moisture in the solid state. The inserted ethynediyl (CC) spacer cancels the steric hindrance between the bulky dimesitylboryl groups and aromatic rings, leading to effective π conjugation over the B-CC-Ar linkages, as revealed by cyclic voltammetry. Despite the small structural differences, the photophys. properties of the benzene, naphthalene, and anthracene derivatives are different. Virtually no emission was observed from the benzene derivatives, whereas the anthracene derivatives emitted with high quantum yields both in solution and in the solid state. Notably, the naphthalene derivatives showed aggregation-induced emission behavior. Unlike the common sterically congested triarylborane derivatives reported so far, the anthracene derivatives showed π-π^*-type absorption and emission bands, which derive from efficient intramol. orbital interactions between the B centers and anthracene moieties, as supported by DFT calculations As a result, the dimesitylborylethynyl substituents effectively lower the LUMO levels of the aromatic hydrocarbon parts, whereas the HOMO levels are almost unaffected, thereby leading to materials with controllable HOMO-LUMO gaps.

Chemistry – A European Journal published new progress about 18512-55-5. 18512-55-5 belongs to naphthyridine, auxiliary class Alkynyl,Anthracene, name is 9,10-Diethynylanthracene, and the molecular formula is C18H10, Application of 9,10-Diethynylanthracene.

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

Hamada, Yoshiki published the artcileNitrogen-containing heterocyclic compounds. XXI. Syntheses of naphthyridines by improved one step process, Recommanded Product: 2,7-Dimethyl-1,8-naphthyridine, the publication is Yakugaku Zasshi (1974), 94(10), 1328-34, database is CAplus and MEDLINE.

Methyl-1,5-naphthyridines and methyl-1,6-naphthyridines were prepared by treating crotonaldehyde, methacrolein, or Me vinyl ketone with 3- and 4-aminopyridines in the presence of sulfo-mix, FeSO4, and H3BO3. 3-Chloro-, 3-bromo-, and 2,4-dimethyl-1,8-naphthyridines were prepared by treating glycerol with 5-chloro-, 5-bromo-, and 4,6-dimethyl-2-aminopyridines in the presence of m-O2NC6H4SO3Na, FeSO4, and H3BO3. The Hays method was also applied to 4-methyl-, 5-methyl-, 6-methyl-, and 4,6-dimethyl-2-aminopyridine, and dimethyland trimethyl-1,8-naphthyridines were obtained in a high yield. Some dimethyl- and trimethyl-1,8-naphthyridines had strong herbicidal activity.

Yakugaku Zasshi 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, Recommanded Product: 2,7-Dimethyl-1,8-naphthyridine.

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

Nobuoka, Atsushi published the artcileGlutathione-S-transferase P1-1 protects aberrant crypt foci from apoptosis induced by deoxycholic acid, Recommanded Product: Sulindac sulfone, the publication is Gastroenterology (2004), 127(2), 428-443, database is CAplus and MEDLINE.

Background & Aims: Aberrant crypt foci, precursors of colonic adenoma, are frequently pos. for glutathione-S-transferase P1-1. Because deoxycholic acid is an apoptosis-inducing xenobiotic in the colon, the authors examined the possibility that aberrant crypt foci, through the cytoprotecting function of glutathione-S-transferase P1-1, resist deoxycholic acid-induced apoptosis, thereby surviving to become adenomas and subsequently cancer. Methods: Glutathione-S-transferase P1-1 or cyclooxygenase-2 expression and the percentage of apoptotic cells in aberrant crypt foci were examined by immunohistochem. and by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling, resp. Glutathione-S-transferase P1-1 was transfected into colon cancer cells (M7609) and human lung fibroblasts, and deoxycholic acid-induced apoptosis was evaluated by a dye-uptake assay and flow cytometry. Binding of deoxycholic acid to glutathione-S-transferase P1-1 was analyzed by CD and immunoprecipitation Caspase activities were determined by colorimetric protease assay, and sulindac binding to glutathione-S-transferase P1-1 was determined by inhibition assay of glutathione-S-transferase P1-1 activity. Results: Aberrant crypt foci showed pos. immunostaining for glutathione-S-transferase P1-1 but neg. staining for cyclooxygenase-2. The percentage of apoptotic cells in aberrant crypt foci was significantly lower than in healthy epithelium, and the difference became more apparent with deoxycholic acid treatment. The impaired sensitivity of aberrant crypt foci to deoxycholic acid was restored by the glutathione-S-transferase P1-1-specific inhibitor γ-glutamyl-S-(benzyl)cysteinyl-R-phenylglycine diethylester. By transfection of glutathione-S-transferase P1-1, M7609 cells became more resistant to deoxycholic acid-induced apoptosis than mock transfectants. Direct binding of glutathione-S-transferase P1-1 to deoxycholic acid was proven by CD and by immunoprecipitation The aberrant crypt foci in adenoma patients treated with sulindac, which was shown to bind to glutathione-S-transferase P1-1, underwent apoptosis in 4 days and mostly regressed in 2-3 mo. Conclusions: Glutathione-S-transferase P1-1 protects aberrant crypt foci from deoxycholic acid-induced apoptosis and may play a pivotal role in early colon carcinogenesis.

Gastroenterology 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

Ito, Kazuaki published the artcileStudy on host-guest complexation of anions based on 2,2′-dihydroxyl-1,1′-binaphthalene derivatives, SDS of cas: 2960-93-2, the publication is Letters in Organic Chemistry (2006), 3(10), 735-740, database is CAplus.

The anion binding properties of 2,2′-dihydroxy-1,1′-binaphthalene (BINOL) derivatives were studied by ¹H NMR spectroscopy. BINOL derivatives formed complexes with anions through hydrogen bonding of the hydroxyl groups and showed a binding preference to dihydrogen phosphate (H₂PO₄^–) and acetate (AcO^–) in comparison with other anions (Cl^–, Br^–, I^–, NO₃^–, and HSO₄^–) tested.

Letters in Organic Chemistry 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 C22H18O2, SDS of cas: 2960-93-2.

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

Cho, H. published the artcileInhibition of NAD⁺-dependent 15-hydroxyprostaglandin dehydrogenase (15-PGDH) by cyclooxygenase inhibitors and chemopreventive agents, Quality Control of 59973-80-7, the publication is Prostaglandins, Leukotrienes and Essential Fatty Acids (2002), 67(6), 461-465, database is CAplus and MEDLINE.

15-Hydroxyprostaglandin dehydrogenase (15-PGDH) catalyzes NAD⁺-dependent oxidation of 15(S)-hydroxyl group of prostaglandins and has been considered a key enzyme involved in biol. inactivation of prostaglandins. This enzyme is markedly induced by androgens in hormone-sensitive human prostate cancer cells and may be involved in tumorigenesis. Inhibition of this enzyme may be of value in anticancer therapy. Non-steroidal anti-inflammatory drugs (NSAIDs) which inhibit cyclooxygenases (COXs) have been shown to be chemopreventive in epidemiol. and animal-model studies. However, chemoprevention by these drugs may not be directly related to their inhibition of COXs. Other targets may be also involved in their chemopreventive activity. The authors have examined a variety of NSAIDs including COX-2 selective inhibitors, peroxisome proliferator-activated receptor (PPAR) γ agonists and phytophenolic compounds which have been shown to be chemopreventive for their effect on 15-PGDH. It was found that most of these compounds were potent inhibitors of 15-PGDH. Among these compounds, ciglitazone appeared to be the most powerful inhibitor (IC₅₀=2.7 μM). Inhibition by ciglitazone was non-competitive with respect to NAD⁺ and uncompetitive with respect to PGE₂.

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, Quality Control of 59973-80-7.

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

Skopinski, Piotr published the artcileSuppression of angiogenic activity of sera from diabetic patients with non-proliferative retinopathy by compounds of herbal origin and sulindac sulfone, Quality Control of 59973-80-7, the publication is International Journal of Molecular Medicine (2004), 14(4), 707-711, database is CAplus and MEDLINE.

Angiogenesis, the process of new blood vessel formation, is the key event in the mechanism of several pathol. processes including diabetic retinopathy. The physiol. control of angiogenesis depends on the balance between stimulatory and inhibitory factors. Therefore, a number of anti-angiogenic approaches has been developed, many of them based on the inhibition of the functional activity of pro-angiogenic factors. The aim of the present study was to compare the anti-angiogenic effectiveness of sulindac sulfone and some herbal compounds in the serum-induced angiogenesis test performed in Balb/c mice. Pooled sera from 35 patients with diabetes type 2 and retinopathy were used as pro-angiogenic stimuli. The strongest inhibitory effect was observed for the sulindac sulfone and ursolic acid in the highest concentration of 200 μg/mL, as well as for the low-dosage concomitant treatment with 2 μg/mL of epigallocatechin gallate (EGCG, green tea flavanol), ursolic acid (plant-derived triterpenoid), sulindac sulfone and convalamaroside (steroidal saponin). Combination treatment was significantly more effective than monotherapy with medium (20 μg/mL) or lowest doses of tested compounds The present study is the first to demonstrate the potent anti-angiogenic effect of the combination therapy comprising of plant-derived extracts and sulindac sulfone, as tested in the in vivo angiogenesis exptl. model with sera of non-proliferative diabetic retinopathy patients used as the pro-angiogenic stimuli. We think that it might be the first step toward application of some of these compounds, in the future, in preventive antiangiogenic therapy of these patients, as well, as in the treatment of later, proliferative stage of this disease.

International Journal of Molecular Medicine 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 C15H14O3, Quality Control of 59973-80-7.

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

Staniewicz, Robert J. published the artcilePreparation and investigation of the spectral and electrochemical properties of mixed-ligand ruthenium(II) complexes containing 1,8-naphthyridines, Application In Synthesis of 14903-78-7, the publication is Inorganic Chemistry (1977), 16(9), 2166-71, database is CAplus.

Mixed-ligand complexes of the form Ru(bpy)2L2+ and Ru(phen)2L2+, L = 1,8-naphthyridine (napy), 2,7-dimethyl-1,3-naphthyridine, 2-methyl-1,8-naphthyridine, and pyrido[2,3-b]pyrazine, and bpy is 2,2′-bipyridine and phen is 1,10-phenanetroline were prepared and isolated as their PF6- salts. The formulations were confirmed by elemental and anal. and conductivity measurements while the purity of the compounds was judged by the single maximum observed in the a.c. polarograms. The solution spectra of the mixed-ligand complexes are characterized by a high-intensity (ε ∼104) metal-to-ligand charge-transfer band at ∼450 nm and π → π* intraligand UV transitions. The energies and intensities of these absorptions are compared with previously reported Ru(byp)2X22+ complexes. The reduction potentials (Ru3+/Ru2+) for the napy mixed-ligand complexes were determined using both cyclic voltammetry and a.c. polarog. and the reversibility of the electrochem. couples was established. The E1/2 values do not vary greatly from those observed for the (phen)3- and (bpy)3Ru(II) complexes thus indicating that the stability of the Ru(II) state has not been significantly altered by the replacement of a phen or bpy with a napy type ligand.

Inorganic 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 C26H41N5O7S, Application In Synthesis of 14903-78-7.

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

Sebastian, S. published the artcileVibrational spectra, molecular structure, natural bond orbital, first order hyperpolarizability, TD-DFT and thermodynamic analysis of 4-amino-3-hydroxy-1-naphthalenesulfonic acid by DFT approach, Category: naphthyridine, the publication is Spectrochimica Acta, Part A: Molecular and Biomolecular Spectroscopy (2013), 167-178, database is CAplus and MEDLINE.

Vibrational spectral anal. of 4-amino-3-hydroxy-1-naphthalenesulfonicacid (4A3HNSA) mol. were carried out using FTIR and FT-Raman spectroscopic techniques. The equilibrium geometry, harmonic vibrational wavenumbers, various bonding features were computed using d. functional B3LYP method with 6-31G(d,p) as basis set. The Non-Linear Optical (NLO) behavior of 4A3HNSA was studied by determination of the elec. dipole moment (μ) and hyperpolarizability β using HF/6-31G(d,p) method. Stability of the mol. arising from hyperconjugative interactions, charge delocalization were analyzed using natural bond orbital (NBO) anal. Charge in electron d. (ED) in σ^* and π^* antibonding orbitals and second order delocalization energies (E2) confirms the occurrence of Intramol. Charge Transfer (ICT) within the mol. The energy and oscillator strength calculated by Time-Dependent D. Functional Theory (TD-DFT) complements with the exptl. findings. The simulated spectra satisfactorily coincide with the exptl. spectra.

Spectrochimica Acta, Part A: Molecular and Biomolecular Spectroscopy 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, Category: naphthyridine.

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

Curiel-Lewandrowski, Clara published the artcileRandomized, double-blind, placebo-controlled trial of sulindac in individuals at risk for melanoma Evaluation of potential chemopreventive activity, Quality Control of 59973-80-7, the publication is Cancer (Hoboken, NJ, United States) (2012), 118(23), 5848-5856, database is CAplus and MEDLINE.

BACKGROUND: : Reduced melanoma risk has been reported with regular use of nonsteroidal anti-inflammatory drugs (NSAIDs). However, the ability of NSAIDs to reach melanocytes in vivo and modulate key biomarkers in preneoplastic lesions such as atypical nevi has not been evaluated. METHODS: : This randomized, double-blind, placebo-controlled trial of sulindac was conducted in individuals with atypical nevi (AN) to determine bioavailability of sulindac and metabolites in nevi and effect on apoptosis and vascular endothelial growth factor A (VEGFA) expression in AN. Fifty subjects with AN ≥4 mm in size and 1 benign nevus (BN) were randomized to sulindac (150 mg twice a day) or placebo for 8 wk. Two AN were randomized for baseline excision, and 2 AN and BN were excised after intervention. RESULTS: : Postintervention sulindac, sulindac sulfone, and sulindac sulfide concentrations were 0.31 ± 0.36, 1.56 ± 1.35, and 2.25 ± 2.24 μg/mL in plasma, and 0.51 ± 1.05, 1.38 ± 2.86, and 0.12 ± 0.12 μg/g in BN, resp. Sulindac intervention did not significantly change VEGFA expression but did increase expression of the apoptotic marker cleaved caspase-3 in AN (increase of 3 ± 33 in sulindac vs decrease of 25 ± 45 in the placebo arm, P = .0056), although significance was attenuated (P = .1103) after adjusting for baseline expression. CONCLUSIONS: : Eight weeks of sulindac intervention resulted in high concentrations of sulindac sulfone, a proapoptotic metabolite, in BN but did not effectively modulate VEGFA and cleaved caspase-3 expression. Study limitations included limited exposure time to sulindac and the need to optimize a panel of biomarkers for NSAID intervention studies.

Cancer (Hoboken, NJ, United States) 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