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Palmitoylβ-amyrin

$768

  • Brand : BIOFRON

  • Catalogue Number : BD-D0016

  • Specification : HPLC≥95%

  • CAS number : 5973-06-8

  • Formula : C17H23NO5

  • Molecular Weight : 321.37

  • PUBCHEM ID : 13915599

  • Volume : 5mg

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Catalogue Number

BD-D0016

Analysis Method

HPLC,NMR,MS

Specification

HPLC≥95%

Storage

2-8°C

Molecular Weight

321.37

Appearance

Powder

Botanical Source

Structure Type

Triterpenoids

Category

Standards;Natural Pytochemical;API

SMILES

CCCCCCCCCCCCCCCC(=O)OC1CCC2(C(C1(C)C)CCC3(C2CC=C4C3(CCC5(C4CC(CC5)(C)C)C)C)C)C

Synonyms

Hexadecanoic acid, (3β)-olean-12-en-3-yl ester/Olean-12-en-3-ol, hexadecanoate, (3β)-/β-amyrin palmitate/(3β)-Olean-12-en-3-yl palmitate/Balanophorin {Palmitate}

IUPAC Name

[(3S,4aR,6aR,6bS,8aR,12aR,14aR,14bR)-4,4,6a,6b,8a,11,11,14b-octamethyl-1,2,3,4a,5,6,7,8,9,10,12,12a,14,14a-tetradecahydropicen-3-yl] hexadecanoate

Applications

Density

1.0±0.1 g/cm3

Solubility

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

Flash Point

354.1±18.8 °C

Boiling Point

661.4±54.0 °C at 760 mmHg

Melting Point

InChl

InChI=1S/C46H80O2/c1-10-11-12-13-14-15-16-17-18-19-20-21-22-23-40(47)48-39-27-28-44(7)37(42(39,4)5)26-29-46(9)38(44)25-24-35-36-34-41(2,3)30-31-43(36,6)32-33-45(35,46)8/h24,36-39H,10-23,25-34H2,1-9H3/t36-,37-,38+,39-,43+,44-,45+,46+/m0/s1

InChl Key

VFSRKCNYYCXRGI-LAZBMHKSSA-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#:5973-06-8) 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

25609015

Abstract

Testicular germ cell tumours (TGCTs) are the most common cancer in young men. Here we perform whole-exome sequencing (WES) of 42 TGCTs to comprehensively study the cancer’s mutational profile. The mutation rate is uniformly low in all of the tumours (mean 0.5 mutations per Mb) as compared with common cancers, consistent with the embryological origin of TGCT. In addition to expected copy number gain of chromosome 12p and mutation of KIT, we identify recurrent mutations in the tumour suppressor gene CDC27 (11.9%). Copy number analysis reveals recurring amplification of the spermatocyte development gene FSIP2 (15.3%) and a 0.4 Mb region at Xq28 (15.3%). Two treatment-refractory patients are shown to harbour XRCC2 mutations, a gene strongly implicated in defining cisplatin resistance. Our findings provide further insights into genes involved in the development and progression of TGCT.

TGCTs are the most common cancer affecting young men, with a mean age at diagnosis of 36 years1,2. The main TGCT histologies are seminomas, which resemble undifferentiated primary germ cells, and non-seminomas, which show differing degrees of differentiation. Cure rates for TGCTS are generally high, due to the sensitivity of malignant testicular germ cells to platinum-based chemotherapies, however this is at the cost of an increased risk of metabolic syndrome, infertility and secondary cancer3,4,5. Furthermore, there are limited options for the patients who are platinum resistant, a group for whom the long-term survival rate is poor6.

Overall, TGCTs are markedly aneuploid with recurring gain of chromosomes 7, 8, 21, 22 and X7,8,9,10,11,12,13. In addition, gain of chromosomal material from 12p is noted in virtually all cases7,8,9, with genomic amplification and overexpression of genes in the 12p11.2-p12.1 region reported in ~10% of TGCTs14. KRAS is located in this region and has been proposed as the candidate driver14. Focused studies of TGCTs have identified somatic missense mutations and amplifications of the oncogene KIT, present in ~25% of seminomas15,16. These reported mutations are clustered in the juxta membrane and kinase encoding domains of KIT15,16. However, a study of 518 other protein kinase encoding genes failed to conclusively identify any new driver mutations17. Beyond these focused interrogations of specific genes, no systematic mutational analysis across all genes in a large series of TGCT samples has been reported to our knowledge.

Here we perform WES of a series of 42 TGCTs to characterize the mutational signature of these tumours and to search for additional driver mutations and pathways disrupted. Our analyses demonstrate these tumours to be relatively homogeneous in profile with a markedly low rate of non-synonymous mutations and provide some novel insights into the genomic architecture of this biologically interesting tumour type.

Title

Whole-exome sequencing reveals the mutational spectrum of testicular germ cell tumours

Author

Kevin Litchfield,1 Brenda Summersgill,2 Shawn Yost,1 Razvan Sultana,1 Karim Labreche,1,3 Darshna Dudakia,1 Anthony Renwick,1 Sheila Seal,1 Reem Al-Saadi,2 Peter Broderick,1 Nicholas C. Turner,4 Richard S. Houlston,1 Robert Huddart,5 Janet Shipley,2 and Clare Turnbulla,1,6

Publish date

2015;

PMID

2771637

Abstract

Oligodeoxynucleotides containing phosphoramidate internucleotide links 3′-OP(O)NH-5′ have been prepared using standard solid phase phosphoramidite techniques. For the incorporation of the phosphoramidate linkages we have used monomer as well as dimer building blocks. With the monomer 3′-phosphoramidite building blocks, which are derived from 5′-amino-2′,5′-dideoxynucleosides, it is possible to incorporate phosphoramidate links into specific positions within an oligodeoxynucleotide. Furthermore the synthesis of several dinucleoside phosphate derivatives which are linked by phosphoramidate bonds are described. The internucleotide phosphoramidate linkage was performed using the Staudinger reaction followed by a Michaelis-Arbuzov type transformation. After 3′-phosphitylation these dinucleosides are compatible with the current phosphoramidite methodology of oligodeoxynucleotide synthesis.

Title

Synthesis and selective cleavage of oligodeoxyribonucleotides containing non-chiral internucleotide phosphoramidate linkages.

Author

M Mag and J W Engels

Publish date

1989 Aug 11

PMID

25196520

Abstract

The rapidly activating delayed rectifier potassium current (IKr) plays a critical role in cardiac repolarization. Although IKr is known to be regulated by both α1- and β1-adrenergic receptors (ARs), the cross-talk and feedback mechanisms that dictate its response to α1- and β1-AR activation are not known. In the present study, IKr was recorded using the whole-cell patch-clamp technique. IKr amplitude was measured before and after the sequential application of selective adrenergic agonists targeting α1- and β1-ARs. Stimulation of either receptor alone (α1-ARs using 1 μM phenylephrine (PE) or β1-ARs using 10 μM xamoterol (Xamo)) reduced IKr by 0.22 ± 0.03 and 0.28 ± 0.01, respectively. The voltage-dependent activation curve of IKr shifted in the negative direction. The half-maximal activation voltage (V0.5) was altered by −6.35 ± 1.53 and −1.95 ± 2.22 mV, respectively, with no major change in the slope factor (k). When myocytes were pretreated with Xamo, PE-induced reduction in IKr was markedly blunted and the corresponding change in V0.5 was significantly altered. Similarly, when cells were pretreated with PE, Xamo-induced reduction of IKr was significantly attenuated. The present results demonstrate that functional cross-talk between α1- and β1-AR signaling regulates IKr. Such non-linear regulation may form a protective mechanism under excessive adrenergic stimulation.

KEYWORDS

adrenergic receptors, potassium current, cross-talk, arrhythmia

Title

Functional Cross-Talk between the α1- and β1-Adrenergic Receptors Modulates the Rapidly Activating Delayed Rectifier Potassium Current in Guinea Pig Ventricular Myocytes

Author

Di Xu,* Sen Wang,† Ting-Ting Wu,† Xiao-Yan Wang, Jin Qian, and Yan Guo

Publish date

2014 Aug;