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Sennidin B

$2,304

  • Brand : BIOFRON

  • Catalogue Number : BD-H0064

  • Specification : 98%

  • CAS number : 517-44-2

  • Formula : C30H18O10

  • Molecular Weight : 538.47

  • PUBCHEM ID : 10459879

  • Volume : 20mg

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Catalogue Number

BD-H0064

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

-20℃

Molecular Weight

538.47

Appearance

Yellow powder

Botanical Source

Sennae Folium

Structure Type

Anthraquinones

Category

Standards;Natural Pytochemical;API

SMILES

C1=CC2=C(C(=C1)O)C(=O)C3=C(C2C4C5=C(C(=CC=C5)O)C(=O)C6=C4C=C(C=C6O)C(=O)O)C=C(C=C3O)C(=O)O

Synonyms

(9R,9'S)-4,4',5,5'-Tetrahydroxy-10,10'-dioxo-9,9',10,10'-tetrahydro-9,9'-bianthracene-2,2'-dicarboxylic acid/1,4-Dichlorobutane-2,3-acetonide/meso-4,5-Bis-chlormethyl-2,2-dimethyl-dioxolan/Sennidin B/[9,9'-Bianthracene]-2,2'-dicarboxylic acid, 9,9',10,10'-tetrahydro-4,4',5,5'-tetrahydroxy-10,10'-dioxo-, (9R,9'S)-

IUPAC Name

(9S)-9-[(9R)-2-carboxy-4,5-dihydroxy-10-oxo-9H-anthracen-9-yl]-4,5-dihydroxy-10-oxo-9H-anthracene-2-carboxylic acid

Density

1.7±0.1 g/cm3

Solubility

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

Flash Point

452.6±30.8 °C

Boiling Point

801.8±65.0 °C at 760 mmHg

Melting Point

InChl

InChI=1S/C30H18O10/c31-17-5-1-3-13-21(15-7-11(29(37)38)9-19(33)25(15)27(35)23(13)17)22-14-4-2-6-18(32)24(14)28(36)26-16(22)8-12(30(39)40)10-20(26)34/h1-10,21-22,31-34H,(H,37,38)(H,39,40)/t21-,22+

InChl Key

JPMRHWLJLNKRTJ-SZPZYZBQSA-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#:517-44-2) 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

26302863

Abstract

Non-invasive “hot spot imaging” and localization of necrotic tissue may be helpful for definitive diagnosis of myocardial viability, which is essential for clinical management of ischemic heart disease. We labeled Sennidin A (SA), a naturally occurring median dianthrone compound, with (131)I and evaluated (131)I SA as a potential necrosis-avid diagnostic tracer agent in rat model of reperfused myocardial infarction. Magnetic resonance imaging (MRI) was performed to determine the location and dimension of infarction. (131)I-SA was evaluated in rat model of 24-hour old reperfused myocardial infarction using single-photon emission computed tomography/computed tomography (SPECT/CT), biodistribution, triphenyltetrazolium chloride (TTC) histochemical staining, serial sectional autoradiography and microscopy. Gamma counting revealed high uptake and prolonged retention of (131)I SA in necrotic myocardium and fast clearance from non-targeted tissues. On SPECT/CT images, myocardial infarction was persistently visualized as well-defined hotspots over 24h, which was confirmed by perfect matches of images from post-mortem TTC staining and autoradiography. Radioactivity concentration in infarcted myocardium was over 9 times higher than that of the normal myocardium at 24h. With favorable hydrophilicity and stability, radioiodinated SA may serve as a necrosis-avid diagnostic agent for assessment of myocardial viability.

Copyright © 2015 Elsevier B.V. All rights reserved.

KEYWORDS

Biodistribution; Hypericin (PubChem CID: 5281051); Necrosis avidity; Radioiodinated Sennidin A; Reperfused myocardial infarction; SPECT; Sennidin A (PubChem CID: 122839)

Title

Exploring diagnostic potentials of radioiodinated sennidin A in rat model of reperfused myocardial infarction.

Author

Jiang C1, Gao M1, Li Y1, Huang D1, Yao N1, Ji Y2, Liu X1, Zhang D1, Wang X1, Yin Z3, Jing S4, Ni Y5, Zhang J6.

Publish date

2015 Nov 10;

PMID

26262613

Abstract

Hepatitis C virus (HCV) is an important etiological agent of severe liver diseases, including cirrhosis and hepatocellular carcinoma. The HCV genome encodes nonstructural protein 3 (NS3) helicase, which is a potential anti-HCV drug target because its enzymatic activity is essential for viral replication. Some anthracyclines are known to be NS3 helicase inhibitors and have a hydroxyanthraquinone moiety in their structures; mitoxantrone, a hydroxyanthraquinone analogue, is also known to inhibit NS3 helicase. Therefore, we hypothesized that the hydroxyanthraquinone moiety alone could also inhibit NS3 helicase. Here, we performed a structure-activity relationship study on a series of hydroxyanthraquinones by using a fluorescence-based helicase assay. Hydroxyanthraquinones inhibited NS3 helicase with IC50 values in the micromolar range. The inhibitory activity varied depending on the number and position of the phenolic hydroxyl groups, and among different hydroxyanthraquinones examined, 1,4,5,8-tetrahydroxyanthraquinone strongly inhibited NS3 helicase with an IC50 value of 6 µM. Furthermore, hypericin and sennidin A, which both have two hydroxyanthraquinone-like moieties, were found to exert even stronger inhibition with IC50 values of 3 and 0.8 µM, respectively. These results indicate that the hydroxyanthraquinone moiety can inhibit NS3 helicase and suggest that several key chemical structures are important for the inhibition.

KEYWORDS

NS3 helicase; fluorescence resonance energy transfer; hepatitis C virus; hydroxyanthraquinone; hypericin; inhibitor; sennidin A

Title

Identification of Hydroxyanthraquinones as Novel Inhibitors of Hepatitis C Virus NS3 Helicase.

Author

Furuta A1,2, Tsubuki M3, Endoh M4, Miyamoto T1,2, Tanaka J5, Salam KA6, Akimitsu N7, Tani H8, Yamashita A9, Moriishi K10, Nakakoshi M11, Sekiguchi Y2, Tsuneda S12, Noda N13,14.

Publish date

2015 Aug 7

PMID

24931286

Abstract

Residual cancer cells and subsequent tumor relapse is an obstacle for curative cancer treatment. Tumor necrosis therapy (TNT) has recently been developed to cause residual tumor regression or destruction. Here, we exploited the avidity of the sennidin A (SA) tracer and radioiodinated SA (¹³¹I-SA) to necrotic tumors in order to further empower TNT. We showed high uptake and prolonged retention of SA in necrotic tumors and a quick clearance in other non-targeted tissues including the liver. On SPECT-CT images, tumor mass appeared persistently as a hotspot. Based on the prominent targetability of ¹³¹I-SA to the tumor necrosis, we designed a combinational theragnostic modality. The vascular disrupting agent (VDA) combretastatin A4 phosphate (CA4P) was used to cause massive tumor necrosis, which formed the target of ¹³¹I-SA that subsequently killed the residual tumor cells by cross-fire irradiation of beta particles. Consequently, ¹³¹I-SA combined with CA4P significantly inhibited tumor growth, extended tumor doubling time and prolonged mean animal survival. In conclusion, ¹³¹I-SA in combination with necrosis inducing drugs/therapies may generate synergetic tumoricidal effects on solid malignancies by means of primary debulking and secondary cleansing process.

Title

Necrosis targeted combinational theragnostic approach using radioiodinated Sennidin A in rodent tumor models.

Author

Ji Y1, Jiang C, Zhang X, Liu W, Gao M, Li Y, Wang J, Wang Q, Sun Z, Jiang X, Yao N, Wang X, Fang Z, Yin Z, Ni Y, Zhang J.

Publish date

2014 May 30


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