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Brusatol

$225

  • Brand : BIOFRON

  • Catalogue Number : BF-B4006

  • Specification : 98%(HPLC)

  • CAS number : 14907-98-3

  • Formula : C26H32O11

  • Molecular Weight : 520.531

  • PUBCHEM ID : 73432

  • Volume : 25mg

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Catalogue Number

BF-B4006

Analysis Method

HPLC,NMR,MS

Specification

98%(HPLC)

Storage

-20℃

Molecular Weight

520.531

Appearance

White crystalline powder

Botanical Source

Brucea javanica

Structure Type

Terpenoids

Category

Standards;Natural Pytochemical;API

SMILES

CC1=C(C(=O)CC2(C1CC3C45C2C(C(C(C4C(C(=O)O3)OC(=O)C=C(C)C)(OC5)C(=O)OC)O)O)C)O

Synonyms

Picras-3-en-21-oic acid, 13,20-epoxy-3,11,12-trihydroxy-15-[(3-methyl-1-oxo-2-buten-1-yl)oxy]-2,16-dioxo-, methyl ester, (11β,12α,15β)-/Methyl (11β,12α,15β)-3,11,12-trihydroxy-15-[(3-methylbut-2-enoyl)oxy]-2,16-dioxo-13,20-epoxypicras-3-en-21-oate/Methyl (11β,12α,15β)-3,11,12-trihydroxy-15-[(3-methyl-2-butenoyl)oxy]-2,16-dioxo-13,20-epoxypicras-3-en-21-oate

IUPAC Name

methyl (1R,2S,3R,6R,8R,13S,14R,15R,16S,17S)-10,15,16-trihydroxy-9,13-dimethyl-3-(3-methylbut-2-enoyloxy)-4,11-dioxo-5,18-dioxapentacyclo[12.5.0.01,6.02,17.08,13]nonadec-9-ene-17-carboxylate

Density

1.5±0.1 g/cm3

Solubility

Methanol

Flash Point

242.2±26.4 °C

Boiling Point

724.3±60.0 °C at 760 mmHg

Melting Point

InChl

InChI=1S/C26H32O11/c1-10(2)6-15(28)37-18-20-25-9-35-26(20,23(33)34-5)21(31)17(30)19(25)24(4)8-13(27)16(29)11(3)12(24)7-14(25)36-22(18)32/h6,12,14,17-21,29-31H,7-9H2,1-5H3/t12-,14+,17+,18+,19+,20+,21-,24-,25+,26-/m0/s1

InChl Key

ZZZYHIMVKOHVIH-VILODJCFSA-N

WGK Germany

RID/ADR

HS Code Reference

2932990000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:14907-98-3) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

31183074

Abstract

Background: Natural products from herbal medicines have long been investigated for their potentials as cancer therapeutics. Besides the development of several herbal medicine-derived anti-cancer agents, such as paclitaxel, vincristine and podophyllotoxin, many recent laboratory findings demonstrated that brusatol, a quassinoid from the seeds of Brucea sumatrana, exhibits potent tumor suppressing effect with improved disease outcome. Our recent finding further demonstrated that brusatol synergizes with the intrinsic metabolic burden in cancer cells.
Main body: Here, we summarized the recent investigations of brusatol as an experimental therapeutic for human malignancies, such as leukemia, lung cancer, pancreatic cancer and brain tumor. We also discussed the molecular target brusatol, with a focus on the Nuclear factor erythroid 2-related factor 2 (NRF2)-guided gene transcription, as well as glutathione de novo synthesis. Further, we discussed the challenges and future applications of brusatol for cancer therapy.
Conclusion: In conclusion, we believe increasing evidences have shown the value of brusatol as a novel strategy for cancer treatment, which may indicate future drug development and clinical translation.

KEYWORDS

Brusatol; Cancer; NRF2; Oxidative stress; Synthetic lethality.

Title

Brusatol, an NRF2 Inhibitor for Future Cancer Therapeutic

Author

Sabrina J Cai 1 , Yang Liu 1 , Sue Han 1 , Chunzhang Yang 1

Publish date

2019 Jun 6.

PMID

29849873

Abstract

Although gemcitabine is the standard chemotherapy treatment for advanced pancreatic cancer, its benefits are quite limited due to prevalent chemoresistance, and the mechanism underlying gemcitabine chemoresistance remains unclear. Currently, Nrf2 has been deemed as a significant contributor to gemcitabine chemoresistance in pancreatic cancer. Brusatol is a unique inhibitor of the Nrf2 pathway, and in previous studies, we determined that brusatol exhibits the effects of growth inhibition and proapoptosis in pancreatic cancer cells. Due to these data, we speculate that brusatol can reverse gemcitabine-induced Nrf2 activation and propose that it can enhance gemcitabine efficacy in treating pancreatic cancer. In this study, we first proved that brusatol can effectively inhibit the Nrf2 signalling pathway and increase ROS accumulation in pancreatic cancer cells. Next, we demonstrated that brusatol can abrogate gemcitabine-induced Nrf2 activation in pancreatic cancer cells. In addition, we discovered that brusatol potentiates gemcitabine-induced growth inhibition and apoptosis in human pancreatic cancer cells. In nude mice with PANC-1 xenografts, treatment with a combination of brusatol and gemcitabine considerably reduced in vivo tumour growth compared with control treatment or treatment with either brusatol or gemcitabine alone. Immunohistochemical staining also showed that Nrf2 expression levels were reduced in brusatol-treated xenograft tumour tissues. In summary, our results suggest that brusatol is capable of enhancing the antitumour effects of gemcitabine in both pancreatic cancer cells and PANC-1 xenografts via suppressing the Nrf2 pathway.

Title

Brusatol Enhances the Chemotherapy Efficacy of Gemcitabine in Pancreatic Cancer via the Nrf2 Signalling Pathway

Author

Yukai Xiang 1 , Wen Ye 1 , Chaohao Huang 1 , Dinglai Yu 1 , Hao Chen 1 , Tuo Deng 1 , Fan Zhang 1 , Bin Lou 1 , Jie Zhang 1 , Keqing Shi 2 , Bicheng Chen 1 2 , Mengtao Zhou 1 2

Publish date

2018 Apr 18

PMID

28455228

Abstract

Brusatol, isolated from brucea, has been proved to exhibit anticancer influence on various kind of human malignancies. However, the role that brusatol plays in pancreatic cancer is seldom known by the public. Through researches brusatol was proved to inhibit growth and induce apoptosis in both PATU-8988 and PANC-1 cells by decreasing the expression level of Bcl-2 and increasing the expression levels of Bax, Cleaved Caspase-3. Then we found the activation of the JNK, p38 MAPK and inactivation of the NF-κb, Stat3 are related with the potential pro-apoptotic signaling pathways. However, SP600125 could not only abrogated the JNK activation caused by brusatol, but also reverse the p38 activation and the decrease of Bcl-2 as SB203580 did. Besides, SP600125 and SB203580 also reversed the inactivation of NF-κb and Stat3. Furthermore, BAY 11-7082 and S3I-201 indeed had the similar effect as brusatol had on the expression of Phospho-Stat3 and Bcl-2. To sum up, we came to a conclusion that in pancreatic cancer, brusatol do inhibit growth and induce apoptosis. And we inferred that brusatol illustrates anticancer attribution via JNK/p38 MAPK/NF-κb/Stat3/Bcl-2 signaling pathway.

KEYWORDS

Apoptosis; Brusatol; JNK/p38 MAPK/NF-κb/Stat3/Bcl-2; Pancreatic cancer.

Title

Brusatol Inhibits Growth and Induces Apoptosis in Pancreatic Cancer Cells via JNK/p38 MAPK/NF-κb/Stat3/Bcl-2 Signaling Pathway

Author

Yukai Xiang 1 , Wen Ye 1 , Chaohao Huang 1 , Bin Lou 1 , Jie Zhang 1 , Dinglai Yu 1 , Xince Huang 1 , Bicheng Chen 2 , Mengtao Zhou 3

Publish date

2017 Jun 10


Description :

Brusatol, isolated from the Brucea javanica plant, inhibits Nrf2.