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Euscaphic acid

$572

  • Brand : BIOFRON

  • Catalogue Number : BD-P0448

  • Specification : 98.0%(HPLC)

  • CAS number : 53155-25-2

  • Formula : C30H48O5

  • Molecular Weight : 488.7

  • PUBCHEM ID : 471426

  • Volume : 10mg

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Catalogue Number

BD-P0448

Analysis Method

Specification

98.0%(HPLC)

Storage

-20℃

Molecular Weight

488.7

Appearance

Powder

Botanical Source

This product is isolated and purified from the dried fruit of Ziziphus jujuba

Structure Type

Category

SMILES

CC1CCC2(CCC3(C(=CCC4C3(CCC5C4(CC(C(C5(C)C)O)O)C)C)C2C1(C)O)C)C(=O)O

Synonyms

Urs-12-en-28-oic acid, 2,3,19-trihydroxy-, (2α,3α)-/Jacarandic acid/(1R,2R,4aS,6aR,6aS,6bR,8aR,10S,11R,12aR,14bS)-1,10,11-trihydroxy-1,2,6a,6b,9,9,12a-heptamethyl-2,3,4,5,6,6a,7,8,8a,10,11,12,13,14b-tetradecahydropicene-4a-carboxylic acid/2α,3α,19α-Trihydroxyurs-12-en-28-oic acid/(2α,3α)-2,3,19-Trihydroxyurs-12-en-28-oic acid/tormentic acid/Euscaphic acid/2,3,19-trihydroxyurs-12-en-28-oic acid

IUPAC Name

Applications

Density

1.2±0.1 g/cm3

Solubility

Methanol; DMF

Flash Point

332.3±28.0 °C

Boiling Point

602.7±55.0 °C at 760 mmHg

Melting Point

InChl

InChl Key

OXVUXGFZHDKYLS-QUFHAEKXSA-N

WGK Germany

RID/ADR

HS Code Reference

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:53155-25-2) 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

31357075

Abstract

BACKGROUND:
Non-Small-Cell Lung Cancer (NSCLC) is the most-frequent cause of cancer death, and novel chemotherapeutic drugs for treating NSCLC are urgently needed. 2α, 3α, 23-trihydroxy-13α, 27-cyclours-11-en-28-oic acid (euscaphic acid G) is a new hexacyclic triterpene acid isolated by our group from Glechoma longituba (Nakai) Kupr. However, the underlying mechanisms responsible for the anticancer effects of hexacyclic triterpene acid have not been elucidated.

PURPOSE:
In the present work, we evaluated growth inhibitory effect of the new isolated hexacyclic triterpene acid and explored the underlying molecular mechanisms.

METHODS/STUDY DESIGNS:
Herbs were extracted and constituents were purified by chromatographic separation, including silica gel, ODS, MCI, Sephadex LH-20 and preparative HPLC. The compound structures were elucidated by the use of UV, NMR and MS spectral data. The anticancer activity of euscaphic acid G was evaluated by MTT assay. Cell cycle, apoptosis, reactive oxygen species and mitochondrial membrane potential were determined by flow cytometry. To display the possible mechanism of euscaphic acid G on NCI-H460 cells, RT-PCR, immunofluorescence and Western blot analysis were carried out.

RESULTS:
A new hexacyclic triterpene acid, euscaphic acid G, together with fifteen known triterpenoids, was isolated from the aerial parts of G. longituba. Our results showed that euscaphic acid G exerted strong anti-proliferative activity against NCI-H460 cells in a concentration- and time-dependent manner. Flow cytometry demonstrated euscaphic acid G arrested the cell cycle at G1 phase, induced cellular apoptosis, accompanied by ROS generation and mitochondrial membrane potential reduction. Mechanistic studies revealed that euscaphic acid G treatment inhibited IKKα/β phosphorylation and IκBα phosphorylation, which subsequently caused the blockage of NF-κB p65 phosphorylation and nuclear translocation.

CONCLUSION:
In conclusion, these results suggested that euscaphic acid G from G. longituba showed potential anticancer effects against lung cancer cells via inducing cell cycle arrest and apoptosis, at least partly, through NF-κB signaling pathways.

Copyright © 2019 Elsevier GmbH. All rights reserved.

KEYWORDS

Anticancer; Glechoma longituba; Hexacyclic triterpene acid; Lung cancer; Nuclear factor-κB

Title

NF-κB inhibitory and cytotoxic activities of hexacyclic triterpene acid constituents from Glechoma longituba.

Author

Ouyang XL1, Qin F2, Huang RZ3, Liang D2, Wang CG3, Wang HS4, Liao ZX5.

Publish date

2019 Oct

PMID

29328385

Abstract

Interleukin-1β (IL-1β) accelerates degradation of the cartilage matrix and induces apoptosis of chondrocytes. Tormentic acid (TA) is a triterpene isolated from the stem bark of the Vochysia divergens plant, which has been demonstrated to exert in vitro inhibitory activity against hepatocyte apoptosis. However, the effects of TA on IL‑1β‑induced apoptosis of human chondrocytes remain unclear. Therefore, the present study investigated the in vitro effects of TA on human osteoarthritic chondrocyte apoptosis cultivated in the presence of IL‑1β. Human chondrocytes were pretreated with or without various concentrations of TA and then co‑incubated in the absence or presence of IL‑1β for 24 h. Cell viability was determined using the MTT assay, and cell apoptosis was detected using a Nucleosome ELISA kit. Caspase‑3 activity was detected using a caspase‑3 colorimetric assay kit. The levels of B‑cell lymphoma 2 (Bcl‑2)‑associated X protein (Bax), Bcl‑2, phosphorylated (p)‑phosphoinositide 3‑kinase (PI3K), PI3K, p‑protein kinase B (Akt) and Akt were measured by western blotting. The results revealed that pretreatment with TA inhibited IL‑1β‑induced cytotoxicity and apoptosis in chondrocytes. In addition, TA pretreatment increased B‑cell lymphoma (Bcl)‑2 expression, and decreased caspase‑3 activity and Bax expressionin human chondrocytes. In addition, pretreatment with TA markedly increased the expression of p‑PI3K and p‑Akt in IL‑1β‑induced chondrocytes. Collectively, these results indicate that TA inhibits IL‑1β‑induced chondrocyte apoptosis by activating the PI3K/Akt signaling pathway. Therefore, TA may be considered a potential therapeutic target for the treatment of osteoarthritis

Title

Tormentic acid inhibits IL-1β-induced chondrocyte apoptosis by activating the PI3K/Akt signaling pathway.

Author

Yang Y1, Wang Y2, Zhao M3, Jia H1, Li B1, Xing D1.

Publish date

2018 Mar;

PMID

28705120

Abstract

To explore the anticancer compounds from tormentic acid derivatives, a quantitative structure-activity relationship (QSAR) model was developed by the multiple linear regression methods. The developed QSAR model yielded a high activity-descriptors relationship accuracy of 94% referred by regression coefficient (r2 = .94) and a high activity prediction accuracy of 91%. The QSAR study indicates that chemical descriptors, chiV5, T_T_Cl_7, T_2_T_4, SsCH3count, and Epsilon3 are significantly correlated with anticancer activity. This validated model was further been used for virtual screening and thus identification of new potential breast cancer inhibitors. Lipinski’s rule of five, ADMET risk and synthetic accessibility are used to filter false positive hits. Filtered compounds were then docked to identify the possible target binding pocket, to obtain a set of aligned ligand poses and to prioritize the predicted active compounds. The scrutinized compounds, as well as their metabolites, were predicted and analyzed for different pharmacokinetics parameters such as absorption, distribution, metabolism, excretion, and toxicity. Finally, the top-ranked compound NB-12 was evaluated by system pharmacology approach. Later studied the metabolic networks, disease biomarker networks, pathway maps, drug-target networks and generate significant gene networks. The strategy applied in this research work may act as a framework for rational design of potential anticancer drugs.

KEYWORDS

ADMET; QSAR; drug designing; system pharmacology; virtual screening

Title

QSAR, docking, ADMET, and system pharmacology studies on tormentic acid derivatives for anticancer activity.

Author

Alam S1,2, Khan F1,2,3.

Publish date

2018 Jul