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70185-52-3

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70185-52-3 Usage

Check Digit Verification of cas no

The CAS Registry Mumber 70185-52-3 includes 8 digits separated into 3 groups by hyphens. The first part of the number,starting from the left, has 5 digits, 7,0,1,8 and 5 respectively; the second part has 2 digits, 5 and 2 respectively.
Calculate Digit Verification of CAS Registry Number 70185-52:
(7*7)+(6*0)+(5*1)+(4*8)+(3*5)+(2*5)+(1*2)=113
113 % 10 = 3
So 70185-52-3 is a valid CAS Registry Number.

70185-52-3Relevant articles and documents

A new domino oxidation—rearrangement of 2,3-dihydrowogonin to negletein

Spoerlein-Guettler, Cornelia,Milius, Wolfgang,Obenauf, Johannes,Schobert, Rainer

, p. 1560 - 1562 (2018/03/29)

We report an expeditious, iodine-catalysed oxidation of 2,3-dihydrowogonin to negletein which comprises a Wessely–Moser rearrangement (WMR), associated not with an O-demethylation, as usual, but with an oxygen to oxygen methyl shift. In contrast, DDQ in 1

Activities of Wogonin Analogs and Other Flavones against Flavobacterium columnare

Tan, Cheng-Xia,Schrader, Kevin K.,Khan, Ikhlas A.,Rimando, Agnes M.

, p. 259 - 272 (2015/10/19)

In our on-going pursuit to discover natural products and natural product-based compounds to control the bacterial species Flavobacterium columnare, which causes columnaris disease in channel catfish (Ictalurus punctatus), we synthesized flavone and chalcone analogs, and evaluated these compounds, along with flavonoids from natural sources, for their antibacterial activities against two isolates of F. columnare (ALM-00-173 and BioMed) using a rapid bioassay. The flavonoids chrysin (1a), 5,7-dihydroxy-4′-methoxyflavone (11), isorhamnetin (26), luteolin (27), and biochanin A (29), and chalcone derivative 8b showed strong antibacterial activities against F. columnare ALM-00-173 based on minimum inhibition concentration (MIC) results. Flavonoids 1a, 8, 11, 13 (5,4′-dihydroxy-7-methoxyflavone), 26, and 29 exhibited strong antibacterial activities against F. columnare BioMed based upon MIC results. The 24-h 50% inhibition concentration (IC50) results revealed that 27 and 29 were the most active compounds against F. columnare ALM-00-173 (IC50 of 7.5 and 8.5 mg/l, resp.), while 26 and 29 were the most toxic compound against F. columnare BioMed (IC50 of 9.2 and 3.5 mg/l, resp.). These IC50 results were lower than those obtained for wogonin against F. columnare ALM-00-173 and F. columnare BioMed (28.4 and 5.4 mg/l, resp.). However, based on MIC results, none of the compounds evaluated in this study were as active as wogonin (MIC 0.3 mg/l for each F. columnare isolate). Further modification of the wogonin structure to enhance antibacterial is of interest.

4′-Bromo-5,6,7-trimethoxyflavone represses lipopolysaccharide-induced iNOS and COX-2 expressions by suppressing the NF-κB signaling pathway in RAW 264.7 macrophages

Kim, Dong Han,Yun, Chang Hyeon,Kim, Min Hwan,Naveen Kumar, Ch.,Yun, Bo Hee,Shin, Ji-Sun,An, Hyo Jin,Lee, Young Hun,Yun, Yong Don,Rim, Hong-Kun,Yoo, Min-Sang,Lee, Kyung-Tae,Lee, Yong Sup

, p. 700 - 705 (2012/03/26)

The regulations of the NO and PGE2 productions are research topics of interest in the field of anti-inflammatory drug development. In the present study, 5,6,7-trimethoxy- and 5,6,7-trihydroxyflavones 3a-3g were synthesized from cinnamic acid derivatives. In particular, 4′-bromo-5,6,7- trimethoxyflavone (3b) most potently inhibited the productions of NO and PGE2 in LPS-treated RAW 264.7 cells (IC50 = 14.22 ± 1.25 and 10.98 ± 6.25 μM, respectively), and these inhibitory effects were more potent than those of oroxylin A or baicalein. Consistent with these findings, 3b concentration-dependently reduced the LPS-induced expressions of iNOS and COX-2 at the protein and mRNA levels. In addition, the release of TNF-α, IL-6, and IL-1β and the mRNA expressions of these cytokines were reduced by 3b in a concentration-dependent manner. Furthermore, 3b attenuated the LPS-induced transcriptional activities of NF-κB and this was accompanied by parallel reductions in the degradation and phosphorylation of IκB-α, and consequently by a decrease in the nuclear translocation of the p65 subunit of NF-κB. Taken together, these results suggest that suppressions of the expressions of iNOS, COX-2, TNF-α, IL-6, and IL-1β via NF-κB inactivation are responsible for the anti-inflammatory effects of 3b.

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