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Eupalinolide K

$572

  • Brand : BIOFRON

  • Catalogue Number : BD-P0092

  • Specification : 98.0%(HPLC)

  • CAS number : 108657-10-9

  • Formula : C20H26O6

  • Molecular Weight : 362.4

  • PUBCHEM ID : 77985613

  • Volume : 25mg

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Quantity
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Catalogue Number

BD-P0092

Analysis Method

HPLC,NMR,MS

Specification

98.0%(HPLC)

Storage

-20℃

Molecular Weight

362.4

Appearance

Powder

Botanical Source

Structure Type

Sesquiterpenoids

Category

SMILES

CC1=CCC(C(=CC2C(C(C1)OC(=O)C(=CCO)C)C(=C)C(=O)O2)C)O

Synonyms

[(3aR,4S,6Z,9S,10E,11aR)-9-hydroxy-6,10-dimethyl-3-methylidene-2-oxo-3a,4,5,8,9,11a-hexahydrocyclodeca[b]furan-4-yl] (E)-4-hydroxy-2-methylbut-2-enoate

IUPAC Name

(9-hydroxy-6,10-dimethyl-3-methylidene-2-oxo-3a,4,5,8,9,11a-hexahydrocyclodeca[b]furan-4-yl) 4-hydroxy-2-methylbut-2-enoate

Applications

Density

1.2±0.1 g/cm3

Solubility

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

Flash Point

201.5±23.6 °C

Boiling Point

574.4±50.0 °C at 760 mmHg

Melting Point

InChl

InChI=1S/C20H26O6/c1-11-5-6-15(22)13(3)10-17-18(14(4)20(24)26-17)16(9-11)25-19(23)12(2)7-8-21/h5,7,10,15-18,21-22H,4,6,8-9H2,1-3H3/b11-5-,12-7+,13-10+/t15-,16-,17+,18+/m0/s1

InChl Key

APOGLVUGPAVNAP-OPNIFLOASA-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#:108657-10-9) 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

24752316

Abstract

The global importance of apple as a fruit crop necessitates investigations into molecular aspects of the processes that influence fruit quality and yield, including plant development, fruit ripening and disease resistance. In order to study and understand biological processes it is essential to recognise the range of molecules, which influence these processes. Small non-coding RNAs are regulatory agents involved in diverse plant activities, ranging from development to stress response. The occurrence of these molecules in apple leaves was studied by means of next-generation sequencing. 85 novel microRNA (miRNA) gene loci were predicted and characterized along with known miRNA loci. Both cis- and trans-natural antisense transcript pairs were identified. Although the trans-overlapping regions were enriched in small RNA (sRNA) production, cis-overlaps did not seem to agree. More than 150 phased regions were also identified, and for a small subset of these, potential miRNAs that could initiate phasing, were revealed. Repeat-associated siRNAs, which are generated from repetitive genomic regions such as transposons, were also analysed. For this group almost all available repeat sequences, associated with the apple genome and present in Repbase, were found to produce siRNAs. Results from this study extend our current knowledge on apple sRNAs and their precursors significantly. A rich molecular resource has been created and is available to the research community to serve as a baseline for future studies.

Title

Extending the sRNAome of Apple by Next-Generation Sequencing

Author

Marike Visser, 1 , 2 Anelda P. van der Walt, 3 Hans J. Maree, 2 , 4 D. Jasper G. Rees, 1 and Johan T. Burger 2 , *

Publish date

2014;

PMID

30004572

Abstract

Background
Antiphospholipid syndrome (APS) is an autoimmune disease characterised by the presence of antiphospholipid (aPL) antibodies that have prothrombotic activity. Antiphospholipid antibodies are associated with an increased risk of pregnancy complications (recurrent miscarriage, premature birth, intrauterine growth retardation) and thrombotic events (both arterial and venous). The most common thrombotic events include brain ischaemia (stroke or transient ischaemic attack) and deep vein thrombosis. To diagnose APS, the presence of aPL antibodies in two measurements and at least one thrombotic event or pregnancy complication are required. It is unclear if people with positive aPL antibodies but without any previous thrombotic events should receive primary antithrombotic prophylaxis.

Objectives
To assess the effects of antiplatelet or anticoagulant agents versus placebo or no intervention or other intervention on the development of thrombosis in people with aPL antibodies who have not had a thrombotic event. We did not address obstetric outcomes in this review as these have been thoroughly addressed by other Cochrane Reviews.

Search methods
We searched the Cochrane Vascular Specialised Register (4 December 2017), the Cochrane Central Register of Controlled Trials (CENTRAL) (last search 29 November 2017), MEDLINE Ovid, Embase Ovid, CINAHL, and AMED (searched 4 December 2017), and trials registries (searched 29 November 2017). We also checked reference lists of included studies, systematic reviews, and practice guidelines, and contacted experts in the field.

Selection criteria
We included randomised controlled trials (RCTs) that compared any antiplatelet or anticoagulant agents, or their combinations, at any dose and mode of delivery with placebo, no intervention, or other intervention. We also included RCTs that compared antiplatelet or anticoagulant agents with each other or that compared two different doses of the same drug. We included studies performed in people of any age and with no history of thrombosis (as defined by APS Sapporo classification criteria or updated Sydney classification criteria), but with aPL antibodies confirmed on at last two separate measurements. The studies included both pregnant women who tested positive for aPL antibodies and had a history of recurrent obstetric complications, as well as non‐pregnancy related cases with positive screening for antibodies, in accordance with the criteria mentioned above.

Data collection and analysis
Pairs of authors independently selected studies for inclusion, extracted data, and assessed the risk of bias for the included studies and quality of evidence using GRADE. Any discrepancies were resolved through discussion or by consulting a third review author when necessary. In addition, one review author checked all the extracted numerical data.

Main results
We included nine studies involving 1044 randomised participants. The studies took place in several countries and had different funding sources. No study was at low risk of bias in all domains. We classified all included studies as at unclear or high risk of bias in two or more domains. Seven included studies focused mainly on obstetric outcomes. One study included non‐pregnancy‐related cases, and one study included both pregnancy‐related cases and other patients with positive results for aPL antibodies. The remaining studies concerned women with aPL antibodies and a history of pregnancy failure. Four studies compared anticoagulant with or without acetylsalicylic acid (ASA) versus ASA only and observed no clear difference in thrombosis risk (risk ratio (RR) 0.98, 95% confidence interval (CI) 0.25 to 3.77; 4 studies; 493 participants; low‐quality evidence). No major bleeding was reported, but minor bleeding risk (nasal bleeding, menorrhagia) was higher in the anticoagulant with ASA group as compared with ASA alone in one study (RR 22.45, 95% CI 1.34 to 374.81; 1 study; 164 participants; low‐quality evidence). In one study ASA was compared with placebo, and there were no clear differences in thrombosis (RR 5.21, 95% CI 0.63 to 42.97; 1 study; 98 participants; low‐quality evidence) or minor bleeding risk between the groups (RR 3.13, 95% CI 0.34 to 29.01; 1 study; 98 participants; low‐quality evidence), and no major bleeding was observed. Two studies compared ASA with low molecular weight heparin (LMWH) versus placebo or intravenous immunoglobulin (IVIG), and no thrombotic events were observed in any of the groups. Moreover, there were no clear differences in the risk of bleeding requiring transfusion (RR 9.0, 95% CI 0.49 to 164.76; 1 study; 180 participants; moderate‐quality evidence) or postpartum bleeding (RR 1.30, 95% CI 0.60 to 2.81; 1 study; 180 participants; moderate‐quality evidence) between the groups. Two studies compared ASA with high‐dose LMWH versus ASA with low‐dose LMWF or unfractionated heparin (UFH); no thrombotic events or major bleeding was reported. Mortality and quality of life data were not reported for any of the comparisons.

Authors’ conclusions
There is insufficient evidence to demonstrate benefit or harm of using anticoagulants with or without ASA versus ASA alone in people with aPL antibodies and a history of recurrent pregnancy loss and with no such history; ASA versus placebo in people with aPL antibodies; and ASA with LMWH versus placebo or IVIG, and ASA with high‐dose LMWH versus ASA with low‐dose LMWH or UFH, in women with aPL antibodies and a history of recurrent pregnancy loss, for the primary prevention of thrombotic events. In a mixed population of people with a history of previous pregnancy loss and without such a history treated with anticoagulant combined with ASA, the incidence of minor bleeding (nasal bleeding, menorrhagia) was increased when compared with ASA alone. Studies that are adequately powered and that focus mainly on thrombotic events are needed to draw any firm conclusions on the primary prevention of thrombotic events in people with antiphospholipid antibodies

KEYWORDS

Humans, Antibodies, Antiphospholipid, Primary Prevention, Anticoagulants, Anticoagulants/therapeutic use, Antiphospholipid Syndrome, Antiphospholipid Syndrome/complications, Platelet Aggregation Inhibitors, Platelet Aggregation Inhibitors/therapeutic use, Randomized Controlled Trials as Topic, Thrombosis, Thrombosis/prevention & control

Title

Antiplatelet and anticoagulant agents for primary prevention of thrombosis in individuals with antiphospholipid antibodies

Author

Malgorzata M Bala,corresponding author Elżbieta Paszek, Wiktoria Lesniak, Dorota Wloch‐Kopec, Katarzyna Jasinska, and Anetta Undas

Publish date

2018 Jul

PMID

17255337

Abstract

The claudins constitute a 24-member family of proteins that are critical for the function and formation of tight junctions. Here, we examine the expression of claudin-7 in squamous cell carcinoma (SCC) of the esophagus and its possible role in tumor progression. In the normal esophagus, expression of claudin-7 was confined to the cell membrane of differentiated keratinocytes. However, in the tumor samples, claudin-7 expression is often lost or localized to the cytoplasm. Assaying esophageal SCC lines revealed variable expression of claudin-7, with some lacking expression completely. Knockdown of claudin-7 in SCC cell lines using a small interfering RNA approach led to decreased E-cadherin expression, increased cell growth, and enhanced invasion into a three-dimensional matrix. The opposite was observed when claudin-7 was overexpressed in esophageal SCC cells lacking both claudin-7 and E-cadherin. In this context, the claudin-7-overexpressing cells became more adhesive and less invasive associated with increased E-cadherin expression. In summary, we demonstrate that claudin-7 is mislocalized during the malignant transformation of esophageal keratinocytes. We also demonstrate a critical role for claudin-7 expression in the regulation of E-cadherin in these cells, suggesting this may be one mechanism for the loss of epithelial architecture and invasion observed in esophageal SCC.

Title

Dysregulation of Claudin-7 Leads to Loss of E-Cadherin Expression and the Increased Invasion of Esophageal Squamous Cell Carcinoma Cells

Author

Mercedes Lioni,* Patricia Brafford,* Claudia Andl,† Anil Rustgi,† Wafik El-Deiry,‡ Meenhard Herlyn,* and Keiran S.M. Smalley*

Publish date

2007 Feb;