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Marmesinin

$1,344

  • Brand : BIOFRON

  • Catalogue Number : BD-P0726

  • Specification : 99.0%(HPLC&TLC)

  • CAS number : 495-30-7

  • Formula : C20H24O9

  • Molecular Weight : 408.4

  • PUBCHEM ID : 216283

  • Volume : 25mg

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Catalogue Number

BD-P0726

Analysis Method

HPLC,NMR,MS

Specification

99.0%(HPLC&TLC)

Storage

2-8°C

Molecular Weight

408.4

Appearance

Powder

Botanical Source

Structure Type

Coumarins

Category

SMILES

CC(C)(C1CC2=C(O1)C=C3C(=C2)C=CC(=O)O3)OC4C(C(C(C(O4)CO)O)O)O

Synonyms

(2S)-2-[2-[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxypropan-2-yl]-2,3-dihydrofuro[3,2-g]chromen-7-one

IUPAC Name

(2S)-2-[2-[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxypropan-2-yl]-2,3-dihydrofuro[3,2-g]chromen-7-one

Applications

Benzofuran glycosides and coumarins from the bark of Streblus indicus (Bur.) Corner. PUMID/DOI:DOI: 10.1016/j.phytochem.2017.01.011 Phytochemistry. 2017 Jun;138:170-177. Two pairs of rare benzofuran glucoside epimers, indicuses A and B and indicuses C and D, three biogenetically related compounds indicuses E-G, and one coumarin indicus H, as well as 11 known compounds, were isolated from the bark of Streblus indicus (Bur.) Corner. The structures of indicuses A-H were elucidated by NMR and MS data, as well as by CD. (S)-Marmesinin exhibited moderate antimicrobial activity in vitro against Bacillus subtilis and Saccharomyces cerevisiae. 7,8-Dihydroxy-3-(3-methyl-2-butenyl) coumarin, umbelliferone, and scopoletin displayed strong cytotoxic activity in vitro against human bladder carcinoma cell line EJ. The structure-activity relationships indicate that hydroxylation at C-7 in the cytotoxic compounds is crucial to their activities. Inhibition of CYP3A4 and CYP1A2 by Aegle marmelos and its constituents PUMID/DOI:DOI: 10.3109/00498254.2015.1053006 Xenobiotica. 2016;46(2):117-25. 1.Aegle marmelos (bael) is a popular tree in India and other Southeast Asian countries. The fruit is usually consumed as dried, fresh or juice, and is reported to have a high nutritional value and many perceived health benefits. Despite its edible nature and therapeutic properties, no studies are reported regarding its effects on major drug metabolizing enzymes. 2.?This study was aimed to evaluate the inhibitory potential of methanolic extract of A. marmelos fruit and its constituents (three furanocoumarins, namely marmelosin, marmesinin and 8-hydroxypsoralen, and 1 alkaloid, aegeline) towards major Cytochrome P450 enzymes (CYP3A4, 2D6, 1A2, 2C9 and 2C19) using human liver microsomes and recombinant CYPs. 3.?The methanolic extract and marmelosin was found to be competitive and time-dependant inhibitor of CYP3A4. While reversible and non-competitive inhibition was observed for CYP1A2. Time-dependent inhibition of CYP3A4 was not affected by the addition of reduced glutathione. Marmesinin showed moderate inhibition of CYP3A4 and 1A2, while aegeline was a very weak inhibitor of CYP3A4 and showed no inhibition for CYP1A2 isoform. No significant inhibition of recombinant CYP2D6, 2C9, and 2C19 was seen with the extract or its constituents. 4.?This is the first report of CYP3A4 and CYP1A2 inhibition by A. marmelos extract and one of its furanocoumarins, marmelosin. Further studies are warranted to determine if acute or prolonged use of bael fruit could affect the pharmacokinetics of drugs that are substrates of CYP3A4 or CYP1A2. A new phenolic glycoside from Cnidium monnieri fruits. PUMID/DOI:DOI: 10.1080/14786419.2013.796467 Nat Prod Res. 2013;27(21):1945-8. A new phenolic glycoside, methylpicraquassioside B (6), together with nine known glycosides, cnidioside A (1), cnidioside B (2), picraquassioside A (3), methylpicraquassioside A (4), picraquassioside B (5), xanthotoxol-8-?glucoside (7), 5-methoxy-xanthotoxol-8-?glucoside (8), 8-methoxy-xanthotoxol-5-?glucoside (9) and marmesinin (10) were isolated from n-BuOH-soluble fraction of Cnidium monnieri fruits. All the isolated compounds, however, exerted little immunomodulatory effect in RAW 264.7 cells. Antiplasmodial and cytotoxic activity of coumarin derivatives from dried roots of Angelica gigas Nakai in vitro PUMID/DOI:DOI: 10.3109/08923973.2011.559248 Immunopharmacol Immunotoxicol. 2011 Dec;33(4):663-6. The butanol-soluble fraction of the dried root of Angelica gigas exhibited significant protection against chloroquine-sensitive strains of Plasmodium falciparum using the parasite lactate dehydrogenase assay method. Using antiplasmodial activity-guided fractionation, five coumarins, marmesinin (1), nodakenin (2), skimmin (3), apiosylskimmin (4), and magnolioside (5), were isolated and evaluated for in vitro antiplasmodial activity, as well as for their cytotoxic potential on SK-OV-3 cancer cell lines. Compounds 1 and 5 showed notable growth inhibitory activity against chloroquine-sensitive strains of P. falciparum with IC(50) values of 5.3 and 8.2 mu M. The compounds showed no significant cytotoxicity (IC(50) > 100 mu M) toward the SK-OV-3 cancer cell line. This is the first report on the antiplasmodial activity of these coumarin derivatives from the dried root of A. gigas. Neuroprotective Coumarins from the Root of Angelica gigas: Structure-Activity Relationships PUMID/DOI: Arch Pharm Res. 2007 Nov;30(11):1368-73. An n-butanol-soluble fraction of the root of Angelica gigas Nakai (Umbelliferae) exhibited significantprotection against glutamate-induced toxicity in primary cultured rat cortical cells. Usingneuroprotective activity-guided fractionation, nine coumarins; marmesinin (1), nodakenin (2),columbianetin-O-β-D-glucopyranoside (3), (S)-peucedanol-7-O-β-D-glucopyranoside (4), (S)-peucedanol-3'-O-β-D-glucopyranoside (5), skimmin (6), apiosylskimmin (7), isoapiosylskimmin(8) and magnolioside (9), were isolated from the n-butanol fraction. Of these nine coumarins,three dihydrofuranocoumarins; 1, 2 and 3, exhibited significant neuroprotective activitiesagainst glutamate-induced toxicity, exhibiting cell viabilities of about 50% at concentrationsranging from 0.1 to 10 µM. To explore the structure-activity relationships of coumarins, sixteenpreviously isolated compounds; 10-25, were simultaneously evaluated in the same system.Our results revealed that cyclization of the isoprenyl group, such as dihydropyran or dihydrofuran,or the furan ring at the C-6 position of coumarin, as well as lipophilicity played an importantrole in the neuroprotective activity of coumarins. Linear furanocoumarin protects rat myocardium against lipidperoxidation and membrane damage during experimental myocardial injury PUMID/DOI:DOI: 10.1016/j.biopha.2003.12.007 Biomed Pharmacother. 2004 Jul-Aug;58(6-7):393-400. The antioxidant activity and the membrane effects of linear furanocoumarin marmesinin isolated from Aegle marmelose was evaluated during experimental myocardial injury. Isoproterenol (150 mg kg(-1) intraperitonially twice at an interval of 24 h) caused increase in the levels of serum marker enzymes via creatinekinase (CK), creatinekinase-MB (CK-MB) isoenzyme, lactatedehydrogenase (LDH) and lactatedehydrogenase isoenzyme (LDH,). It also produced electrocardiographic changes such as increased heart rate, reduced R amplitude and ST elevation. Marmesinin at a dose of 200 mg kg(-1), when administered orally, demonstrated a decrease in serum enzyme levels and restored the electrocardiographic changes towards normalcy. Myocardial injury was accompanied by the disintegration of lipidperoxides and the impairment of natural scavengers. Marmesinin oral treatment for 2 days before and during isoproterenol administration decreased the effect of lipidperoxidation. It was also shown to have a membrane stabilizing action by inhibiting the release of beta-glucuronidase from the subcellular fractions. Thus, linear furanocoumarin marmesinin could have the protective effect against the damage caused by experimental myocardial injury. (C) 2004 Elsevier SAS. All rights reserved.

Density

Solubility

Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.

Flash Point

Boiling Point

Melting Point

InChl

InChI=1S/C20H24O9/c1-20(2,29-19-18(25)17(24)16(23)13(8-21)28-19)14-6-10-5-9-3-4-15(22)27-11(9)7-12(10)26-14/h3-5,7,13-14,16-19,21,23-25H,6,8H2,1-2H3/t13-,14+,16-,17+,18-,19+/m1/s1

InChl Key

HXCGUCZXPFBNRD-NEDVQNLSSA-N

WGK Germany

RID/ADR

HS Code Reference

2933990000

Personal Projective Equipment

Correct Usage

For Reference Standard and R&D, Not for Human Use Directly.

Meta Tag

provides coniferyl ferulate(CAS#:495-30-7) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

No Technical Documents Available For This Product.

PMID

32450789

Abstract

MicroRNAs (miRNAs) play crucial roles in regulating eukaryotic gene expression. Recent studies indicated that aberrantly expressed miRNAs are involved in the pathogenesis of ankylosing spondylitis (AS). Indeed, hsa-miR-495-3p (miR-495) has been reported as an anti-oncogene in different cancers. However, the role of miR-495 in AS is still unknown.

Methods
In this study, quantitative real-time polymerase chain reaction (PCR) was used to detect the expression of miR-495 in the peripheral blood mononuclear cells (PBMCs), whole blood, and serum of patients with AS. Bisulfite-specific PCR sequencing and methylated DNA immunoprecipitation were used to detect the methylation in the promoter region of miR-495. To determine the influence of miR-495 expression on the target gene, programmed cell death 10 (PDCD10), dual luciferase reporter assays together with an adenoviral vector containing the miR-495 locus were used. Receiver operating characteristic (ROC) curves were used to evaluate the efficacy of miR-495 as a diagnostic biomarker of AS. Gene Ontology, Kyoto Encyclopedia of Genes and Genomes pathway analysis, and western blotting were used to explore the potential role of miR-495 in AS pathogenesis and the mechanism by which it facilitates AS pathogenesis.

Results
miR-495 is down-regulated and the promoter region of miR-495 is highly methylated in AS. The expression of miR-495 is negatively associated with PDCD10 expression in both patients with AS and healthy controls. Further experiments showed that PDCD10 can be targeted by miR-495. The ROC curves of miR-495 suggested that it is a very specific and sensitive biomarker for AS diagnosis. Bioinformatics analysis and signal pathway studies indicated that miR-495 can down-regulate β-catenin and transforming growth factor-β1.

Conclusions
Our studies indicated that down-regulation of miR-495 can be used as a potential molecular marker for the diagnosis and treatment of AS, thus providing new insights into the role of miRNAs in AS pathology.

KEYWORDS

MiR-495, Methylation, PDCD10, Biomarker, Target, Ankylosing spondylitis

Title

Down-regulated miR-495 can target programmed cell death 10 in ankylosing spondylitis

Author

Wen-Juan Ni1,2 and Xiao-Min Lengcorresponding author1,2

Publish date

2020

PMID

30146342

Abstract

Cisplatin (DDP) resistance has become the leading cause of mortality in non-small cell lung cancer (NSCLC). miRNA dysregulation significantly contributes to tumor progression. In this study, we found that miR-495 was significantly downregulated in lung cancer tissue specimens. This study aimed to elucidate the functions, direct target genes, and molecular mechanisms of miR-495 in lung cancer. miR-495 downregulated its substrate UBE2C through direct interaction with UBE2C 3′- untranslated region. UBE2C is a proto-oncogene activated in lung cancer; however, its role in chemotherapeutic resistance is unclear. Herein, UBE2C expression levels were higher in DDP-resistant NSCLC cells; this was associated with the proliferation, invasion, and DDP resistance in induced cisplatin-resistant NSCLC cells. Furthermore, epithelial-mesenchymal transitions (EMT) contributed to DDP resistance. Moreover, UBE2C knockdown downregulated vimentin. In contrast, E-cadherin was upregulated. Importantly, miR-495 and UBE2C were associated with cisplatin resistance. We attempted to evaluate their effects on cell proliferation and cisplatin resistance. We also performed EMT, cell migration, and invasion assays in DDP-resistant NSCLC cells overexpressing miR-495 and under-expressing UBE2C. Furthermore, in silico assays coupled with western blotting and luciferase assays revealed that UBE2C directly binds to the 5′-UTR of the drug-resistance genes ABCG2 and ERCC1. Furthermore, miR-495 downregulated ABCG2 and ERCC1 via regulation of UBE2C. Together, the present results indicate that the miR495-UBE2C-ABCG2/ERCC1 axis reverses DDP resistance via downregulation of anti-drug genes and reducing EMT in DDP-resistant NSCLC cells.

KEYWORDS

MicroRNA-495, UBE2C, ABCG2, ERCC1, EMT, Cisplatin resistant

Title

The miR 495-UBE2C-ABCG2/ERCC1 axis reverses cisplatin resistance by downregulating drug resistance genes in cisplatin-resistant non-small cell lung cancer cells

Author

Jiwei Guo,a,⁎,1 Dan Jin,b,1 Yan Wu,a Lijuan Yang,a Jing Du,a Kaikai Gong,a Weiwei Chen,a Juanjuan Dai,a Shuang Miao,a and Sichuan Xia

Publish date

2018 Sep;

PMID

32625491

Abstract

The Panel on Food Additives and Nutrient Sources added to Food (ANS) provides a scientific opinion re‐evaluating the safety of sorbitan monostearate (E 491), sorbitan tristearate (E 492), sorbitan monolaurate (E 493), sorbitan monooleate (E 494) and sorbitan monopalmitate (E 495) when used as food additives. The Scientific Committee on Food (SCF) allocated an acceptable daily intake (ADI) of 25 mg/kg body weight (bw) per day for E 491, E 492 and E 495 singly or in combination; and a separate group ADI for E 493 and E 494 singly or in combination of 5 mg/kg bw per day calculated as sorbitan monolaurate in 1974. The Panel noted that after oral administration sorbitan monostearate can be either hydrolysed to its fatty acid moiety and the corresponding anhydrides of sorbitol and excreted via urine or exhaled as CO 2 or excreted intact in the faeces. The Panel considered that sorbitan esters did not raise concern for genotoxicity. Based on the no observed adverse effect level (NOAEL) of 2,600 mg sorbitan monostearate/kg bw per day, taking into account the ratio between the molecular weight of sorbitan monostearate (430.62 g/mol) and sorbitan (164.16 g/mol), and applying an uncertainty factor of 100, the Panel derived a group ADI of 10 mg/kg bw per day expressed as sorbitan for sorbitan esters (E 491-495) singly or in combination. This group ADI of 10 mg sorbitan/kg bw per day is equivalent to 26 mg sorbitan monostearate/kg bw per day. The Panel concluded that the exposure at the mean and the 95th percentile level, using non‐brand‐loyal scenario, did not exceed the ADI in any of the population groups. The Panel on the request for an amendment of specifications regarding the removal of ‘congealing range’ concluded that it could be eventually replaced by another identification parameter such as melting point.

KEYWORDS

food additive, sorbitan monostearate, sorbitan tristearate, sorbitan monolaurate, sorbitan monooleate and sorbitan monopalmitate, sorbitan esters

Title

Re‐evaluation of sorbitan monostearate (E 491), sorbitan tristearate (E 492), sorbitan monolaurate (E 493), sorbitan monooleate (E 494) and sorbitan monopalmitate (E 495) when used as food additives

Author

EFSA Panel on Food Additives and Nutrient Sources added to Food (ANS), Alicja Mortensen, Fernando Aguilar, Riccardo Crebelli, Alessandro Di Domenico, Birgit Dusemund, Maria Jose Frutos, Pierre Galtier, David Gott, Ursula Gundert‐Remy, Jean‐Charles Leblanc, Oliver Lindtner, Peter Moldeus, Pasquale Mosesso, Dominique Parent‐Massin, Agneta Oskarsson, Ivan Stankovic, Ine Waalkens‐Berendsen, Rudolf Antonius Woutersen, Matthew Wright, Maged Younes, Polly Boon, Dimitrios Chrysafidis, Rainer Gurtler, Paul Tobback, Andrea Altieri, Ana Maria Rincon, and Claude Lambre

Publish date

2017 May