Month: November 2022

Prakash, G. K. Surya published the artcileCopper-mediated difluoromethylation of (hetero)aryl iodides and β-styryl Halides with tributyl(difluoromethyl)stannane, Recommanded Product: 1-(Difluoromethyl)naphthalene, the publication is Angewandte Chemie, International Edition (2012), 51(48), 12090-12094, database is CAplus and MEDLINE.

An efficient method for preparation of difluoromethyl substituted arenes, heteroarenes, and styrenes via copper-mediated difluoromethylation of aryl iodides and styrenyl halides is described. The difluoromethyl donor was synthesized from trifluoromethyl trifluoromethylsilane and trialkyltin hydrides. The reaction mechanism was explored by computational chem.

Angewandte Chemie, International Edition 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, Recommanded Product: 1-(Difluoromethyl)naphthalene.

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

Chi, Xiuling published the artcile15-Hydroxyprostaglandin dehydrogenase (15-PGDH) is up-regulated by flurbiprofen and other non-steroidal anti-inflammatory drugs in human colon cancer HT29 cells, Related Products of naphthyridine, the publication is Archives of Biochemistry and Biophysics (2009), 487(2), 139-145, database is CAplus and MEDLINE.

Non-steroidal anti-inflammatory drugs (NSAIDs) are known to inhibit prostaglandin synthetic enzyme, cyclooxygenases (COXs), as well as to exhibit anti-tumor activity although at much higher concentrations 15-Hydroxyprostaglandin dehydrogenase (15-PGDH), a key prostaglandin catabolic enzyme, was recently shown to be a tumor suppressor. Effects of NSAIDs on 15-PGDH expression were therefore examined Flurbiprofen and several other NSAIDs were found to induce 15-PGDH expression in human colon cancer HT29 cells. Flurbiprofen, the most active one, was also shown to induce 15-PGDH expression in other types of cancer cells. Induction of 15-PGDH expression appeared to occur at the stage of mRNA as levels of 15-PGDH mRNA were increased by flurbiprofen in HT29 cells. Levels of 15-PGDH were also found to be regulated at the stage of protein turnover. MEK inhibitors, PD98059 and U-0126, which inhibited ERK phosphorylation were shown to elevate 15-PGDH levels very significantly. These inhibitors did not appear to alter 15-PGDH mRNA levels but down-regulate matrix metalloproteinase-9 (MMP-9). This protease was shown to degrade and inactivate 15-PGDH suggesting that elevation of 15-PGDH levels could be due to inhibition of MMP-9 expression by these inhibitors. Similarly, flurbiprofen was also demonstrated to inhibit ERK activation and to down-regulate MMP-9 expression. Furthermore, flurbiprofen was shown to induce the expression of tissue inhibitor of metalloproteinase-1 (TIMP-1), an inhibitor of MMP-9. The turnover of 15-PGDH was found to prolong in the presence of flurbiprofen as compared to that in the absence of this drug. Taken together, these results indicate that flurbiprofen up-regulates 15-PGDH by increasing the expression and decreasing the degradation of 15-PGDH in HT29 cells.

Archives of Biochemistry and Biophysics 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

Garces, Jordi published the artcileMixed cellulose-derived benzoates bonded on allylsilica gel as HPLC chiral stationary phases: influence of the introduction of an aromatic moiety in the fixation substituent, Synthetic Route of 2960-93-2, the publication is Tetrahedron: Asymmetry (2003), 14(9), 1179-1185, database is CAplus.

Several mixed alkenoxybenzoyl/benzoates and 10-undecenoyl/benzoates of cellulose were fixed onto allylsilica gel by the radical coupling of double bonds. The introduction of an aromatic group in the fixation substituent modifies the chiral recognition ability of the resulting chiral stationary phases (CSPs) in comparison with the 10-undecenoate/benzoate cellulose derivatives Better enantioselectivity values are achieved when the electronic and geometric characteristics of both substituents, fixating and derivatizing, are similar.

Tetrahedron: Asymmetry 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, Synthetic Route of 2960-93-2.

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

Hendricker, D. G. published the artcileComplexes of 1,8-naphthyridines. VIII. Complexes of 2,7-dimethyl-1,8-naphthyridine with rare earth nitrates, Formula: C10H10N2, the publication is Journal of Inorganic and Nuclear Chemistry (1972), 34(6), 1949-54, database is CAplus.

Rare earth nitrate complexes of the type M(2,7-dmn-apy)2(NO3)3 (M = Y, La-Yb 2,7-dmnapy = 2,7-dimethyl-1,8-naphthyridine) were synthesized. The compounds were characterized by elemental analyses, molar conductances, magnetic moments, and ir (4000-200 cm-1). The molar conductance and ir spectral data show that all nitrate groups are coordinated to the metals. From this and crystallographic data of an analogous compound the complexes appear to be ten-coordinate.

Journal of Inorganic and Nuclear 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, Formula: C10H10N2.

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

Kotlyarevskii, I. L. published the artcileOxidative polycondensation of diacetylene compounds, Application In Synthesis of 18512-55-5, the publication is Izvestiya Akademii Nauk SSSR, Seriya Khimicheskaya (1961), 1905-7, database is CAplus.

cf. CA 54, 24466i.-Products of dehydrogenation of diethylbenzenes (Balandin, et al., CA 54, 8676h) brominated in CCl₄ at -15° gave a tetrabromide (I), m. 156-7°. Dehydrobromination (Deluchat, CA 28, 3062¹) gave a low yield of p-diethynylbenzene (II) m. 95°. Hydrogenation of p-Ac₂C₆H₄ over Raney Ni at normal temperature and pressure gave 86.5% 1, 4-bis(α-hydroxyethyl)benzene, m. 78.4-80°, passed over Al₂O₃ at 330° in dioxane gave crude divinylbenzene which was directly brominated to I. II in dioxane was treated with a solution of Cu₂Cl₂ and NH₄Cl in aqueous HCl and the system was shaken and blown with O until gas uptake ceased; treatment of the complex with Et₂O-H₂O gave a red-orange oligomer with repeating links of p-CCC_εH₄CC which is insoluble and explodes above 120°. Similar oxidation of II in pyridine in the presence of Cu₂Cl₂ gave a yellow oligomer free of Cl and Cu (the reddish product contained some Cl but was free of Cu). Similar oxidation of 1,4-diethynyl-1,4-dihydroxycyclohexane gave a light-colored oligomer containing 70.75% C. Similarly were prepared insoluble oligomers from 9,10-diethynyl-9,10-dihydroxy-9,10-dihydroanthracene, 9,10-diethynyl-9,10-dihydroxy-9,10-dihydrophenanthrene, and 9,10-diethynylanthracene (the latter contained some Cl). The oligomers were generally insoluble in the usual solvents.

Izvestiya Akademii Nauk SSSR, Seriya Khimicheskaya 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 In Synthesis of 18512-55-5.

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

Stepnik, Maciej published the artcileSulindac and its metabolites: Sulindac sulfide and sulindac sulfone enhance cytotoxic effects of arsenic trioxide on leukemic cell lines, HPLC of Formula: 59973-80-7, the publication is Toxicology In Vitro (2011), 25(5), 1075-1084, database is CAplus and MEDLINE.

The effects of arsenic trioxide (ATO) in combination with sulindac (SUL), sulindac sulfide (SS) or sulindac sulfone (SF) on human (Jurkat, HL-60, K562 and HPB-ALL) and mouse (EL-4) leukemic cell lines were investigated. The cells showed different sensitivity to sulindacs (2.5-200 μM) with SS being the most cytotoxic (72 h WST-1 reduction test). The cytotoxicity of ATO was enhanced by combination with sulindacs. The combination of ATO (1 μM) with SS or SF at concentrations over 50 μM induced considerable cytotoxicity in all cell lines. Normal human lymphocytes exposed for 48 h to the combinations showed smaller decrease in viability. Measurements of Jurkat, HL-60 and K562 cells exposed to ATO (1 μM) and sulindacs (100 μM or 200 μM for K562 cells) indicated apoptosis as the main cell death mechanism. The mitochondrial membrane potential measurements (JC-1 probe) indicated an active involvement of mitochondria in the process. The results did not indicate involvement of an inhibitory effect of the combinations on NF-κB activity in Jurkat, HL-60 and K562 cells.

Toxicology In Vitro 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 C12H25Br, HPLC of Formula: 59973-80-7.

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

Stepnik, M. published the artcileAssessment of the involvement of oxidative stress and Mitogen-Activated Protein Kinase signaling pathways in the cytotoxic effects of arsenic trioxide and its combination with sulindac or its metabolites: sulindac sulfide and sulindac sulfone on human leukemic cell lines, SDS of cas: 59973-80-7, the publication is Medical Oncology (New York, NY, United States) (2012), 29(2), 1161-1172, database is CAplus and MEDLINE.

The purpose of the study was to characterize the involvement of reactive oxygen species (ROS) in mediating the cytotoxic effects of arsenic trioxide (ATO) in combination with sulindac or its metabolites: sulfide (SS) and sulfone (SF) on human leukemic cell lines. Jurkat, HL-60, K562, and HPB-ALL cells were exposed to the drugs alone or in combinations. Cell viability was measured using WST-1 or XTT reduction tests and ROS production by dichlorodihydrofluorescein diacetate staining (flow cytometry). Modulation of (a) intracellular glutathione (GSH) level was done by using l-buthionine sulfoximine (BSO) or diethylmaleate (DEM), (b) NADPH oxidase by using diphenyleneiodonium (DPI), and (c) MAP kinases by using SB202190 (p38), SP600125 (JNK), and U0126 (ERK) inhibitors. ATO cytotoxicity (0.5 or 1 μM) was enhanced by sulindacs, with higher activity showed by the metabolites. Strong cytotoxic effects appeared at SS and SF concentrations starting from 50 μM. The induction of ROS production seemed not to be the major mechanism responsible for the cytotoxicity of the combinations. A strong potentiating effect of BSO on ATO cytotoxicity was demonstrated; DEM (10-300 μM) and DPI (0.0025-0.1 μM; 72 h) did not influence the effects of ATO. Some significant decreases in the viability of the cells exposed to ATO in the presence of MAPK inhibitors comparing with the cells exposed to ATO alone were observed; however, the effects likely resulted from a simple additive cytotoxicity of the drugs. The combinations of ATO with sulindacs offer potential therapeutic usefulness.

Medical Oncology (New York, NY, 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 C12H10FeO4, SDS of cas: 59973-80-7.

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

Liu, Suying published the artcileSulindac derivative-induced apoptosis in a human umbilical vein endothelial cell line ECV304, COA of Formula: C20H17FO4S, the publication is Chinese Medical Journal (Beijing, China, English Edition) (2002), 115(7), 1074-1077, database is CAplus and MEDLINE.

The objective was to investigate the effects of sulindac metabolites on proliferation and apoptosis in the human umbilical vein endothelial cell line ECV304 in vitro. Methods The proliferation profile of ECV304 was determined by Me thiazolyl tetrazolium (MTT) method. Cell cycle distribution, apoptosis, and the ultrastructure of ECV304 were detected by flow cytometry (FCM) and electron microscopy, resp. Results MTT assay showed that the sulfide inhibited the proliferation of ECV304 and its effect was dose-dependent; the IC₅₀ was 200 μmol/L. FCM showed that the sulfide changed cell cycle distribution. The cell cycle distribution was as follows: G₁ phase (control group 77.74%; sulfone group 75.63%; sulfide group 46.12%); S phase (control group 13.64%; sulfone group 16.40; sulfide group 27.26%); G₂-M phase (control group 8.61%; sulfone group 7.98%; sulfide group 26.62%). The apoptosis rates in the control group, sulfone group and sulfide group were 6.08, 4.81, and 51.90%, resp. Sulfide reduced the proportion of G₁ phase, increased the proportion of S phase, G₂-M phase and the apoptosis rate significantly. In the sulfide-treated cells, there were nuclear fragmentation and chromosomal condensation, shrinkage of the cell and loss of contact with neighboring cells. Apoptotic bodies were observed Sulfone showed no effect on cell proliferation, cell cycle distribution, or cell morphol. Conclusions Sulfide can significantly reduce the proliferation of ECV304, change the cell cycle distribution, and arrest cells in G₂-M phase where apoptosis may be induced. Sulfone has no such effects on this cell line.

Chinese Medical Journal (Beijing, China, English Edition) 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, COA of Formula: C20H17FO4S.

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

Wang, Wei published the artcileBorane-catalyzed metal-free hydrogenation of 2,7-disubstituted 1,8-naphthyridines, Application In Synthesis of 14903-78-7, the publication is Organic & Biomolecular Chemistry (2016), 14(28), 6683-6686, database is CAplus and MEDLINE.

Metal-free hydrogenation of 2,7-disubstituted 1,8-naphthyridines was successfully realized for the first time using in situ generated borane catalysts under mild conditions to furnish 1,2,3,4-tetrahydro-1,8-naphthyridine derivatives in 83-98% yields. Significantly, up to 74% ee was achieved for the corresponding asym. hydrogenation reactions.

Organic & Biomolecular 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 C8H11BO2, Application In Synthesis of 14903-78-7.

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

Kuzelka, Jane published the artcileModeling the Syn Disposition of Nitrogen Donors at the Active Sites of Carboxylate-Bridged Diiron Enzymes. Enforcing Dinuclearity and Kinetic Stability with a 1,2-Diethynylbenzene-Based Ligand, Formula: C10H10N2, the publication is Inorganic Chemistry (2003), 42(26), 8652-8662, database is CAplus and MEDLINE.

The syn coordination of histidine residues at the active sites of several carboxylate-rich nonheme diiron enzymes was difficult to reproduce with small mol. model compounds Ligands derived from 1,8-naphthyridine, phthalazine, and 1,2-diethynylbenzene were employed to mimic this geometric feature. The preassembled diiron(II) complex [Fe₂(μ-O₂CAr^Tol)₂(O₂CAr^Tol)₂(THF)₂] (1), where Ar^TolCO₂^– is the sterically hindered carboxylate 2,6-di(p-tolyl)benzoate, served as a convenient starting material for the preparation of Fe(II) complexes, all of which were crystallog. characterized. Use of the ligand 2,7-dimethyl-1,8-naphthyridine (Me₂-napy) afforded mononuclear [Fe(O₂CAr^Tol)₂(Me₂-napy)] (2), whereas dinuclear [Fe₂(μ-DMP)(μ-O₂CAr^Tol)₂(O₂CAr^Tol)₂(THF)] (3) resulted when 1,4-dimethylphthalazine (DMP) was employed. The dinuclear core of compound 3 is kinetically labile, as evidenced by the formation of [Fe(O₂CAr^Tol)₂(vpy)₂] (4) upon addition of 2-vinylpyridine (vpy). The diiron analog of 4, [Fe₂(μ-O₂CAr^Tol)₂(O₂CAr^Tol)₂(vpy)₂] (5), was prepared directly from 1. When the sterically more demanding ligand 2,6-di(4-tert-butylphenyl)benzoate (Ar^4-tBuPhCO₂^–) was used, mononuclear [Fe(O₂CAr^4-tBuPh)₂(THF)₂] (6) and [Fe(O₂CAr^4-tBuPh)₂(DMP)₂] (7) formed. The difficulty in stabilizing a dinuclear core with these simple (N)₂-donor ligands was circumvented by preparing a family of 1,2-diethynylbenzene-based ligands, from which were readily assembled [Fe₂(Et₂BCQEB^Et)(μ-O₂CAr^Tol)₃](OTf) (15) and [Cu₂(Et₂BCQEB^Et)(μ-I)₂] (16), where Et₂BCQEB^Et is 1,2-bis(3-ethynyl-8-carboxylatequinoline)benzene Et ester. The Et₂BCQEB^Et framework provides both structural flexibility and the desired syn N donor geometry, thus serving as a good 1st-generation ligand in this class.

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 C10H10N2, Formula: C10H10N2.

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