Month: November 2022

Velasco, Manuel I. published the artcileA green alternative to synthetize azo compounds, COA of Formula: C10H9NO4S, the publication is Dyes and Pigments (2011), 90(3), 259-264, database is CAplus.

Different nitrates were used as sources of nitrosonium ion to obtain diazonium salts. Diverse azo compounds were synthesized in acetonitrile giving very good yields and free of byproducts in comparison with traditional synthesis. Among the tested species, the best combination for para red synthesis was nitric acid and gaseous hydrogen chloride.

Dyes and Pigments 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 C15H14O, COA of Formula: C10H9NO4S.

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

Kay, Kwang-Yol published the artcileSynthesis and electroluminescent properties of fluorene- and anthracene-derivatives containing novel tetraphenylbenzene moiety, COA of Formula: C18H10, the publication is Molecular Crystals and Liquid Crystals (2004), 167-172, database is CAplus.

2,7-Bis[(2,3,4,5-tetraphenyl)phenyl]-9,9-diethylfluorene (BTPDF) and 2,7-bis[(2,3,4,5-tetraphenyl)phenyl]-9,10-anthracene (BTPA), which consist of a diethylfluorene and an anthracene with two tetraphenylbenzene moieties, were synthesized by Diels-Alder reaction and characterized to investigate electroluminescent (EL) behavior. BTPDF and BTPA showed violet and blue photoluminescence spectra at 400 nm and 456 nm. The device of m-MTDATA (600 脜)/NPB (150 脜)/BTPDF or BTPA (300 脜)/Alq3 (300 脜)/LiF (10 脜)/Al (2000 脜) showed turn-on voltage of 9 V and 13 V and blue and green EL spectrum at 466 nm and 504 nm, resp.

Molecular Crystals and Liquid Crystals 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, COA of Formula: C18H10.

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

Singh, Jatinder published the artcileSelective and quantitative synthesis of a linear [3]catenane by two component coordination-driven self-assembly, Category: naphthyridine, the publication is Chemical Communications (Cambridge, United Kingdom) (2019), 55(48), 6866-6869, database is CAplus and MEDLINE.

Here we report the synthesis of a linear [3]catenane comprised of three interlocking rings, by coordination-driven self-assembly. Naphthalene-based acceptor A1 and triazole-based donor L1 were utilized for the self-assembly reaction, which facilitated the formation of linear [3]catenane topol. through synergistic non-covalent intercycler interactions (π-π, CH-π and CH-N).

Chemical Communications (Cambridge, United Kingdom) 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 C14H14N2O2, Category: naphthyridine.

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

Demchuk, Oleg M. published the artcileRational design of novel ligands for environmentally benign cross-coupling reactions, Formula: C22H18O2, the publication is Pure and Applied Chemistry (2011), 83(3), 633-644, database is CAplus.

Transition-metal (TM) complexes of new phosphines, readily prepared by a straightforward three-step modular synthesis, were successfully employed in difficult cross-coupling reactions conducted under mild conditions (water, “open-flask”, low temperature) that aspire to meet green chem. criteria. High yielding catalyzed by bismuth or rhodium complexes oxidative arylation of naphthoquinone gave the key 2-aryl naphthoquinone intermediates for facile bismuth triflate-catalyzed Michael addition of secondary phosphine oxides. Subsequent O-methylation and reductions of the resulting products gave access to the target air-stable phosphine ligands in good overall yields (up to 60%).

Pure and Applied 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, Formula: C22H18O2.

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

Ayyanathan, Kasirajan published the artcileCombination of sulindac and dichloroacetate kills cancer cells via oxidative damage, Formula: C20H17FO4S, the publication is PLoS One (2012), 7(7), e39949, database is CAplus and MEDLINE.

Sulindac is an FDA-approved non-steroidal anti-inflammatory drug with documented anticancer activities. Our recent studies showed that sulindac selectively enhanced the killing of cancer cells exposed to oxidizing agents via production of reactive oxygen species (ROS) resulting in mitochondrial dysfunction. This effect of sulindac and oxidative stress on cancer cells could be related to the defect in respiration in cancer cells, first described by Warburg 50 years ago, known as the Warburg effect. We postulated that sulindac might enhance the selective killing of cancer cells when combined with any compound that alters mitochondrial respiration. To test this hypothesis we have used dichloroacetate (DCA), which is known to shift pyruvate metabolism away from lactic acid formation to respiration. One might expect that DCA, since it stimulates aerobic metabolism, could stress mitochondrial respiration in cancer cells, which would result in enhanced killing in the presence of sulindac. In this study, we have shown that the combination of sulindac and DCA enhances the selective killing of A549 and SCC25 cancer cells under the conditions used. As predicted, the mechanism of killing involves ROS production, mitochondrial dysfunction, JNK signaling and death by apoptosis. Our results suggest that the sulindac-DCA drug combination may provide an effective cancer therapy.

PLoS One 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, Formula: C20H17FO4S.

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

Rice, Pamela L. published the artcileSulindac metabolites induce caspase- and proteasome-dependent degradation of β-catenin protein in human colon cancer cells, Formula: C20H17FO4S, the publication is Molecular Cancer Therapeutics (2003), 2(9), 885-892, database is CAplus.

Colorectal cancer (CRC) is the second leading cause of cancer death in the USA. Accumulation of β-catenin protein is nearly ubiquitous in colon adenomas and cancers, presumably due to mutations in the APC or β-catenin genes that inhibit proteasome-dependent degradation of β-catenin protein. Substantial clin., epidemiol., and animal evidence indicate that sulindac and other non-steroidal anti-inflammatory drugs (NSAIDs) prevent the development of CRC. The mechanisms by which sulindac exerts its potent growth inhibitory effects against colon tumor cells are incompletely understood, but down-regulation of β-catenin was suggested as one potential mechanism. The goal of this study was to determine the mechanism of β-catenin protein down-regulation by sulindac metabolites. Treatment of human colon cancer cell lines with apoptotic concentrations of sulindac metabolites (sulindac sulfide, sulindac sulfone) induced a dose- and time-dependent inhibition of β-catenin protein expression. Inhibition of proteasome activity with MG-132 partially blocked the ability of sulindac sulfide and sulindac sulfone to inhibit β-catenin protein expression. Pretreatment with the caspase inhibitor z-VAD-fmk blocked morphol. signs of apoptosis as well as caspase cleavage, and also partially prevented β-catenin degradation by sulindac metabolites. These effects occurred in cells with bi-allelic APC mutation (SW480), with wild-type APC but mono-allelic β-catenin mutation (HCT116) and in cells that lack expression of either COX-1 or -2 (HCT15). These results indicate that loss of β-catenin protein induced by sulindac metabolites is COX independent and at least partially due to reactivation of β-catenin proteasome degradation and partially a result of caspase activation during the process of apoptosis.

Molecular Cancer Therapeutics 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, Formula: C20H17FO4S.

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

Briza, Tomas published the artcileChromophoric Binaphthyl Derivatives, Application of 2,2′-Dimethoxy-1,1′-binaphthalene, the publication is Organic Letters (2005), 7(17), 3661-3664, database is CAplus and MEDLINE.

A short synthetic route is outlined, starting from bromobinaphthyl derivatives, via halogen lithium exchange, subsequent Michael reaction with dimethylaminoacrolein, hydrolysis to the corresponding aldehyde, and final condensation with a benzothiazolium unit to produce a binaphthyl-pentamethinium system, which absorbs in the visible range around 450 nm. Enantiopure ligands show a good Cotton effect in the CD spectrum. Preliminary data show potential of these compounds in the area of supramol. chem. (enantioselective recognition) and also for medicinal application (induction of apoptosis).

Organic Letters 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, Application of 2,2′-Dimethoxy-1,1′-binaphthalene.

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

Piazza, Gary A. published the artcileA novel sulindac derivative that does not inhibit cyclooxygenases but potently inhibits colon tumor cell growth and induces apoptosis with antitumor activity, Name: Sulindac sulfone, the publication is Cancer Prevention Research (2009), 2(6), 572-580, database is CAplus and MEDLINE.

Nonsteroidal anti-inflammatory drugs such as sulindac have shown promising antineoplastic activity, although toxicity from cyclooxygenase (COX) inhibition and the suppression of prostaglandin synthesis limits their use for chemoprevention. Previous studies have concluded that the mechanism responsible for their antineoplastic activity may be COX independent. To selectively design out the COX inhibitory activity of sulindac sulfide (SS), in silico modeling studies were done that revealed the crucial role of the carboxylate moiety for COX-1 and COX-2 binding. These studies prompted the synthesis of a series of SS derivatives with carboxylate modifications that were screened for tumor cell growth and COX inhibitory activity. A SS amide (SSA) with a N,N-dimethylethyl amine substitution was found to lack COX-1 and COX-2 inhibitory activity, yet potently inhibit the growth of human colon tumor cell lines, HT-29, SW480, and HCT116 with IC₅₀ values of 2 to 5 μmol/L compared with 73 to 85 μmol/L for SS. The mechanism of growth inhibition involved the suppression of DNA synthesis and apoptosis induction. Oral administration of SSA was well-tolerated in mice and generated plasma levels that exceeded its in vitro IC₅₀ for tumor growth inhibition. In the human HT-29 colon tumor xenograft mouse model, SSA significantly inhibited tumor growth at a dosage of 250 mg/kg. Combined treatment of SSA with the chemotherapeutic drug, Camptosar, caused a more sustained suppression of tumor growth compared with Camptosar treatment alone. These results indicate that SSA has potential safety and efficacy advantages for colon cancer chemoprevention as well as utility for treating malignant disease if combined with chemotherapy.

Cancer Prevention 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, Name: Sulindac sulfone.

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

Giladi, Nis published the artcileCurcumin potentiates the pro-apoptotic effects of sulindac sulfone in colorectal cancer, Related Products of naphthyridine, the publication is Expert Opinion on Investigational Drugs (2010), 19(S1), S117-S124, database is CAplus and MEDLINE.

Objective: The use of sulindac sulfone (SFN) for colorectal cancer (CRC) therapy is limited due to its toxicity. The present study was carried out to examine whether curcumin, a novel chemopreventive agent, can potentiate the effects of low dosages of SFN in CRC treatment. Methods: HT-29 CRC cells were exposed to SFN (200 – 400 microM), curcumin (5 – 10 microM) or their combination. The cytotoxic effects of the drugs were evaluated using growth inhibition assays. Annexin V/PI and cell cycle anal. were employed to study the mechanism of action of the drugs. The therapeutic efficacy of the drugs in vivo was examined using the aberrant crypt foci (ACF) model. The treatment groups included eight rats/group. Results: Treatment of cells with curcumin and SFN resulted in a synergistic inhibitory effect of 50 – 90% (p < 0.005) on cell growth. Growth inhibition was associated with inhibition of proliferation, G2/M arrest and induction of apoptosis. Administration of curcumin (0.6%) and SFN (0.06%) to 1, 2-dimethylhydrazine treated rats significantly reduced (by 75%, p < 0.01) the number of ACF. Conclusions: Curcumin augments the therapeutic effects of SFN. This may be clin. important since the addition of curcumin to low dosages of SFN may encourage a safer and potent combinatorial treatment regimen for CRC.

Expert Opinion on Investigational Drugs 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