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β-Elemonic acid

$198

  • Brand : BIOFRON

  • Catalogue Number : BF-E2011

  • Specification : 98%

  • CAS number : 28282-25-9

  • Formula : C30H46O3

  • Molecular Weight : 454.68

  • PUBCHEM ID : 15559100

  • Volume : 20mg

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Catalogue Number

BF-E2011

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

454.68

Appearance

Powder

Botanical Source

Boswellia serrata

Structure Type

Terpenoids

Category

Standards;Natural Pytochemical;API

SMILES

CC(=CCCC(C1CCC2(C1(CCC3=C2CCC4C3(CCC(=O)C4(C)C)C)C)C)C(=O)O)C

Synonyms

(5β,13α,14β,20S)-3-Oxolanosta-8,24-dien-21-oic acid/Lanosta-8,24-dien-21-oic acid, 3-oxo-, (5β,13α,14β,20S)-/(2S)-6-methyl-2-[(10S,14S,17S)-4,4,10,13,14-pentamethyl-3-oxo-1,2,5,6,7,11,12,15,16,17-decahydrocyclopenta[a]phenanthren-17-yl]hept-5-enoic acid/beta-Elemonic acid

IUPAC Name

(2S)-6-methyl-2-[(5R,10S,13S,14S,17S)-4,4,10,13,14-pentamethyl-3-oxo-1,2,5,6,7,11,12,15,16,17-decahydrocyclopenta[a]phenanthren-17-yl]hept-5-enoic acid

Density

1.07

Solubility

Methanol; Ethyl Acetate

Flash Point

309.6±26.6 °C

Boiling Point

565.2±50.0 °C at 760 mmHg

Melting Point

216-219 ºC

InChl

InChI=1S/C30H46O3/c1-19(2)9-8-10-20(26(32)33)21-13-17-30(7)23-11-12-24-27(3,4)25(31)15-16-28(24,5)22(23)14-18-29(21,30)6/h9,20-21,24H,8,10-18H2,1-7H3,(H,32,33)/t20-,21-,24-,28+,29-,30+/m0/s1

InChl Key

XLPAINGDLCDYQV-XUWOXAENSA-N

WGK Germany

RID/ADR

HS Code Reference

2938900000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:28282-25-9) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

26530631

Abstract

β-elemonic acid, a known triterpene, exhibits anti-inflammatory effects, yet research on the pharmacological effects of β-elemonic acid is rare. We investigated the anticancer effects and the related molecular mechanisms of β-elemonic acid on human non-small cell lung cancer (NSCLC) A549 cells. The effects of β-elemonic acid on the growth of A549 cells were studied using a 3-(4,5)-2,5-diphenyltetrazolium bromide (MTT) assay. Apoptosis was detected using Annexin V staining. The effect of β-elemonic acid on the cell cycle of A549 cells was assessed using the propidium iodide method. The change in reactive oxygen species (ROS) was detected using a dichlorodihydrofluorescein diacetate (DCFH-DA) assay with microscopic examination. The expression levels of Bcl-2 family proteins, mitogen-activated protein kinase (MAPK) family proteins and cyclooxygenase 2 (COX-2) were detected using western blot analysis. Our data revealed that β-elemonic acid strongly induced human A549 lung cancer cell death in a dose- and time-dependent manner as determined by the MTT assay. β-elemonic acid-induced cell death was considered to be apoptotic when the phosphatidylserine exposure was observed using Annexin V staining. The death of human A549 lung cancer cells was caused by apoptosis induced by activation of ROS activity, increase in the sub-G1 proportion, downregulation of Bcl-2 expression, upregulation of Bax expression and inhibition of the MAPK signaling pathways. These results clearly demonstrated that β-elemonic acid inhibits proliferation by inducing hypoploid cells and cell apoptosis. Moreover, the anticancer effects of β-elemonic acid were related to the MAPK signaling pathway, ROS activation and glutathione depletion in human A549 lung cancer cells.

Title

β-Elemonic Acid Inhibits the Cell Proliferation of Human Lung Adenocarcinoma A549 Cells: The Role of MAPK, ROS Activation and Glutathione Depletion

Author

Tsu-Tuan Wu 1 , Chien-Lin Lu 2 , Hen-I Lin 3 , Bing-Fang Chen 3 , Guey-Mei Jow 3

Publish date

2016 Jan

PMID

32113150

Abstract

Background: Osteosarcoma (OS) is a significant threat to the lives of children and young adults. Although neoadjuvant chemotherapy is the first choice of treatment for OS, it is limited by serious side-effects and cancer metastasis. β-Elemonic acid (β-EA), an active component extracted from Boswellia carterii Birdw., has been reported to exhibit potential anti-inflammatory and anticancer activities. However, the anti-tumor effects and underlying mechanisms on OS as well as pharmacokinetic characteristics of β-EA remain unknown.
Purpose: This study was aimed to investigating the anti-tumor effects of β-EA on human OS, the underlying mechanisms, and the pharmacokinetic and tissue distribution characteristics.
Study design and methods: Cell viability and colony formation assays were performed to determine the effect of β-EA cell on cell proliferation. Apoptosis rates, mitochondrial membrane potential and cell cycle features were analyzed by flow cytometry. qRT-PCR, Western blot, immunofluorescence and immunohistochemical assays were conducted to evaluate the expression levels of genes or proteins related to the pathways affected by β-EA in vitro and in vivo. Cell migration and invasion were evaluated in wound healing and Transwell chamber assays. The effects and pharmacokinetic characteristics of β-EA in vivo were evaluated by analyzing tumor suppression, pharmacokinetics and tissue distribution.
Results: Explorations indicated that endoplasmic reticulum (ER) stress conditions provoked by β-EA activated the PERK/eIF2α/ATF4 branch of the unfolded protein reaction (UPR), stimulating C/EBP homologous protein (CHOP)-regulated apoptosis and inducing Ca2+ leakage leading to caspase-dependent apoptosis. Furthermore, β-EA induced G0/G1 cell cycle arrest and inhibited metastasis of HOS and 143B cells by attenuating Wnt/β-catenin signaling effects, which included decreased levels of p-Akt(Ser473), p-Gsk3β (Ser9), Wnt/β-catenin target genes (c-Myc and CyclinD1) along with a decline in nuclear β-catenin accumulation. The fast absorption, short elimination half-life, and linear pharmacokinetic characteristics of β-EA were also revealed. The distribution of β-EA was detected in the tumor and bone tissues.
Conclusions: Overall, both in vitro and in vivo investigations showed the potential of β-EA for the treatment of human OS. The pharmacokinetic profile and considerable distribution in the tumor and bone tissues warrant further preclinical or even clinical studies.

Title

β-Elemonic Acid Inhibits the Growth of Human Osteosarcoma Through Endoplasmic Reticulum (ER) Stress-Mediated PERK/eIF2α/ATF4/CHOP Activation and Wnt/β-catenin Signal Suppression

Author

Ang Zhao 1 , Zhanjie Zhang 1 , Yanfen Zhou 1 , Xin Li 1 , Xiaotian Li 2 , Bo Ma 3 , Qi Zhang 4

Publish date

2020 Feb 7

PMID

30917586

Abstract

The purpose of this research was to extract and separate the compounds from frankincense, and then evaluate their anti-inflammatory effects. The isolated compound was a representative tetracyclic triterpenes of glycine structure according to ¹H-NMR and 13C-NMR spectra, which is β-elemonic acid (β-EA). We determined the content of six different localities of frankincense; the average content of β-EA was 41.96 mg/g. The toxic effects of β-EA administration (400, 200, 100 mg/kg) for four weeks in Kunming (KM) mice were observed. Compared with the control group, the body weight of mice, the visceral coefficients and serum indicators in the β-EA groups showed no systematic variations. The anti-inflammatory effects of β-EA were evaluated in LPS-induced RAW264.7 cells, xylene-induced induced ear inflammation in mice, carrageenin-induced paw edema in mice, and cotton pellet induced granuloma formation in rats. β-EA inhibited overproduction of tumor necrosis factor-α(TNF-α), interleukin-6 (IL-6), monocyte chemotactic protein 1 (MCP-1), soluble TNF receptor 1 (sTNF R1), Eotaxin-2, Interleukin 10 (IL-10) and granulocyte colony-stimulating factor (GCSF) in the RAW264.7 cells. Intragastric administration with β-EA (300, 200, and 100 mg/kg in mice, and 210, 140, and 70 mg/kg in rats) all produced distinct anti-inflammatory effects in vivo in a dose-dependent manner. Following treatment with β-EA (300 mg/kg, i.g.), the NO level in mice ears and PGE2 in mice paws both decreased (p < 0.01). In conclusion, our study indicates that β-EA could be a potential anti-inflammatory agent for the treatment of inflammatory diseases.

KEYWORDS

Frankincense; anti-inflammatory; triterpene; β-elemonic acid.

Title

Evaluation of Anti-Inflammatory Activities of a Triterpene β-Elemonic Acid in Frankincense In Vivo and In Vitro

Author

Yue Zhang 1 2 , Ying-Li Yu 3 4 , Hua Tian 5 , Ru-Yu Bai 6 , Ya-Nan Bi 7 , Xiao-Mei Yuan 8 , Li-Kang Sun 9 10 , Yan-Ru Deng 11 , Kun Zhou 12 13 14

Publish date

2019 Mar


Description :

Bioactive constituents from Boswellia papyrifera. PUMID/DOI:15730241 J Nat Prod. 2005 Feb;68(2):189-93. Phytochemical investigation of the stem bark extract of Boswellia papyrifera afforded two new stilbene glycosides, trans-4',5-dihydroxy-3-methoxystilbene-5-O-{alpha-L-rhamnopyranosyl-(1-->2)-[alpha-L-rhamnopyranosyl-(1-->6)]-beta-D-glucopyranoside (1), trans-4',5-dihydroxy-3-methoxystilbene-5-O-[alpha-L-rhamnopyranosyl-(1-->6)]-beta-D-glucopyranoside (2), and a new triterpene, 3alpha-acetoxy-27-hydroxylup-20(29)-en-24-oic acid (3), along with five known compounds, 11-keto-beta-boswellic acid (4), Beta-Elemonic acid (7), 3alpha-acetoxy-11-keto-beta-boswellic acid (8), beta-boswellic acid (9), and beta-sitosterol (10). The stilbene glycosides exhibited significant inhibition of phosphodiesterase I and xanthine oxidase. The triterpenes (3-9) exhibited prolyl endopeptidase inhibitory activities. β-Elemonic acid inhibits the cell proliferation of human lung adenocarcinoma A549 cells: The role of MAPK, ROS activation and glutathione depletion. PUMID/DOI:26530631 Oncol Rep. 2016 Jan;35(1):227-34. Beta-Elemonic acid, a known triterpene, exhibits anti-inflammatory effects, yet research on the pharmacological effects of Beta-Elemonic acid is rare. We investigated the anticancer effects and the related molecular mechanisms of Beta-Elemonic acid on human non-small cell lung cancer (NSCLC) A549 cells. The effects of Beta-Elemonic acid on the growth of A549 cells were studied using a 3-(4,5)-2,5-diphenyltetrazolium bromide (MTT) assay. Apoptosis was detected using Annexin V staining. The effect of Beta-Elemonic acid on the cell cycle of A549 cells was assessed using the propidium iodide method. The change in reactive oxygen species (ROS) was detected using a dichlorodihydrofluorescein diacetate (DCFH-DA) assay with microscopic examination. The expression levels of Bcl-2 family proteins, mitogen-activated protein kinase (MAPK) family proteins and cyclooxygenase 2 (COX-2) were detected using western blot analysis. Our data revealed that β-elemonic acid strongly induced human A549 lung cancer cell death in a dose- and time-dependent manner as determined by the MTT assay. Beta-Elemonic acid-induced cell death was considered to be apoptotic when the phosphatidylserine exposure was observed using Annexin V staining. The death of human A549 lung cancer cells was caused by apoptosis induced by activation of ROS activity, increase in the sub-G1 proportion, downregulation of Bcl-2 expression, upregulation of Bax expression and inhibition of the MAPK signaling pathways. These results clearly demonstrated that Beta-Elemonic acid inhibits proliferation by inducing hypoploid cells and cell apoptosis. Moreover, the anticancer effects of Beta-Elemonic acid were related to the MAPK signaling pathway, ROS activation and glutathione depletion in human A549 lung cancer cells.