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ent-13,16β,17-Trihydroxykauran-19-oic acid

$1,248

  • Brand : BIOFRON

  • Catalogue Number : BN-O0961

  • Specification : 98%(HPLC)

  • CAS number : 142543-30-4

  • Formula : C20H32O5

  • Molecular Weight : 352.47

  • Volume : 5mg

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Catalogue Number

BN-O0961

Analysis Method

HPLC,NMR,MS

Specification

98%(HPLC)

Storage

2-8°C

Molecular Weight

352.47

Appearance

Botanical Source

Structure Type

Category

Standards;Natural Pytochemical;API

SMILES

Synonyms

IUPAC Name

Density

Solubility

Flash Point

Boiling Point

Melting Point

InChl

InChI=1S/C18H16O6/c1-2-14(21)24-18-16(22)15-12(20)8-11(19)9-13(15)23-17(18)10-6-4-3-5-7-10/h3-9,17-20H,2H2,1H3/t17-,18+/m1/s1

InChl Key

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#:142543-30-4) 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

28893626

Abstract

Low-density lipoprotein nanoparticles reconstituted with the natural omega-3 fatty acid, docosahexaenoic acid (LDL-DHA), have been reported to selectively kill hepatoma cells and reduce the growth of orthotopic liver tumors in the rat. To date, little is known about the cell death pathways by which LDL-DHA nanoparticles kill tumor cells. Here we show that the LDL-DHA nanoparticles are cytotoxic to both rat hepatoma and human hepatocellular carcinoma (HCC) cell lines. Following LDL-DHA treatment both rat and human HCC cells experience pronounced lipid peroxidation, depletion of glutathione and inactivation of the lipid antioxidant glutathione peroxidase-4 (GPX4) prior to cell death. Inhibitor studies revealed that the treated HCC cells die independent of apoptotic, necroptotic or autophagic pathways, but require the presence of cellular iron. These hallmark features are consistent and were later confirmed to reflect ferroptosis, a novel form of nonapoptotic iron-dependent cell death. In keeping with the mechanisms of ferroptosis cell death, GPX4 was also found to be a central regulator of LDL-DHA induced tumor cell killing. We also investigated the effects of LDL-DHA treatments in mice bearing human HCC tumor xenografts. Intratumoral injections of LDL-DHA severely inhibited the growth of HCC xenografts long term. Consistent with our in vitro findings, the LDL-DHA treated HCC tumors experienced ferroptotic cell death characterized by increased levels of tissue lipid hydroperoxides and suppression of GPX4 expression. Conclusion: LDL-DHA induces cell death in HCC cells through the ferroptosis pathway, this represents a novel molecular mechanism of anticancer activity for LDL-DHA nanoparticles.

KEYWORDS

Nanoparticle, low-density lipoprotein, hepatocellular carcinoma, docosahexaenoic acid, ferroptosis, glutathione peroxidase

Title

Low-Density Lipoprotein Docosahexaenoic Acid Nanoparticles Induce Ferroptotic Cell Death in Hepatocellular Carcinoma

Author

Weijun Ou, Rohit S. Mulik, Arnida Anwar, Jeffrey G McDonald, Xiaoshun He, Ian R. Corbin

Publish date

2018 Nov 1.

PMID

27477280

Abstract

KRAS is one of the most commonly mutated oncogenes in human cancer. Mutant KRAS aberrantly regulates metabolic networks. However, the contribution of cellular metabolism to mutant KRAS tumorigenesis is not completely understood. We report that mutant KRAS regulates intracellular fatty acid metabolism through Acyl-coenzyme A (CoA) synthetase long-chain family member 3 (ACSL3), which converts fatty acids into fatty Acyl-CoA esters, the substrates for lipid synthesis and β-oxidation. ACSL3 suppression is associated with depletion of cellular ATP and causes the death of lung cancer cells. Furthermore, mutant KRAS promotes the cellular uptake, retention, accumulation, and β-oxidation of fatty acids in lung cancer cells in an ACSL3-dependent manner. Finally, ACSL3 is essential for mutant KRAS lung cancer tumorigenesis in vivo and is highly expressed in human lung cancer. Our data demonstrate that mutant KRAS reprograms lipid homeostasis, establishing a metabolic requirement that could be exploited for therapeutic gain.

Title

Fatty Acid Oxidation Mediated by Acyl-CoA Synthetase Long Chain 3 Is Required for Mutant KRAS Lung Tumorigenesis

Author

Mahesh S. Padanad, Georgia Konstantinidou, Niranjan Venkateswaran, Margherita Melegari, Smita Rindhe, Matthew Mitsche, Chendong Yang, Kimberly Batten, Kenneth E. Huffman, Jingwen Liu, Ximing Tang, Jaime Rodriguez-Canales, Neda Kalhor, Jerry W. Shay, John D. Minna, Jeffrey McDonald, Ignacio I. Wistuba, Ralph J. DeBerardinis, Pier Paolo Scaglioni

Publish date

2016 Aug 31.

PMID

25172021

Abstract

Alternative splicing affects ~95% of eukaryotic genes, greatly expanding the coding capacity of complex genomes. Although our understanding of alternative splicing has increased rapidly, current knowledge of splicing regulation has largely been derived from studies of highly expressed mRNAs. Telomerase is a key example of a protein that is alternatively spliced, but it is expressed at very low levels, and although it is known that misregulation of telomerase splicing is a hallmark of nearly all cancers, the details of this process are unclear. Here we review work showing that hTERT expression is in part regulated by atypical alternative splicing, perhaps due to its exceptionally low expression level. We propose these differential regulatory mechanisms may be widely applicable to other genes and may provide new opportunities for development of cancer therapeutics.

KEYWORDS

RNA splicing, regulation, low-abundance transcript, telomere, cancer therapy

Title

Alternative Splicing Regulation of Telomerase: A New Paradigm

Author

Mandy S. Wong, Woodring E. Wright, Jerry W. Shay

Publish date

2015 Oct 1.


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