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β,β-Dimethylacrylshikonin

$210

  • Brand : BIOFRON

  • Catalogue Number : AV-H05035

  • Specification : 98%

  • CAS number : 24502-79-2

  • Formula : C21H22O6

  • Molecular Weight : 370.4

  • PUBCHEM ID : 479499

  • Volume : 20mg

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Catalogue Number

AV-H05035

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

370.4

Appearance

Brown ceramic powder

Botanical Source

Lithospermum erythrorhizon/Lithospermum erythrospermum, Lithospermum euchromum, Alkanna tinctoria, Alkanna hirsutissima and Jatropha glandulifera

Structure Type

Category

Standards;Natural Pytochemical;API

SMILES

CC(=CCC(C1=CC(=O)C2=C(C=CC(=C2C1=O)O)O)OC(=O)C=C(C)C)C

Synonyms

(BETA,BETA-DIMETHYLACRYL)SHIKONIN/2-Butenoic acid, 3-methyl-, (1R)-1-(1,4-dihydro-5,8-dihydroxy-1,4-dioxo-2-naphthalenyl)-4-methyl-3-pentenyl ester/dmask/1,4-Naphthalenedione, 5,8-dihydroxy-2-[(1R,3E)-1-hydroxy-4,8-dimethyl-6-oxo-3,7-nonadien-1-yl]-2-Butenoic acid, 3-methyl-, 1-(1,4-dihydro-5,8-dihydroxy-1,4-dioxo-2-naphthalenyl)-4-methyl-3-pentenyl ester, (R)-/(1R)-1-(5,8-Dihydroxy-1,4-dioxo-1,4-dihydro-2-naphthalenyl)-4-methyl-3-penten-1-yl 3-methyl-2-butenoate/2-Butenoic acid, 3-methyl-, (1R)-1-(1,4-dihydro-5,8-dihydroxy-1,4-dioxo-2-naphthalenyl)-4-methyl-3-penten-1-yl ester/Senecioylshikonin/Dimethylacrylshikonin/Isoarnebin I/b,b-Dimethylacrylshikonin/5,8-Dihydroxy-2-[(1R,3E)-1-hydroxy-4,8-dimethyl-6-oxo-3,7-nonadien-1-yl]-1,4-naphthoquinone/(β,β-DiMethylacryl)shikonin

IUPAC Name

[(1R)-1-(5,8-dihydroxy-1,4-dioxonaphthalen-2-yl)-4-methylpent-3-enyl] 3-methylbut-2-enoate

Applications

β,β-Dimethylacrylshikonin is a naphthoquinone derivative isolated from Arnebia nobilis, promotes angiogenesis by inducing eNOS, VEGF and HIF-1α expression through the PI3K-dependent pathway. Arnebin 1 has anti-tumor activity[1].

Density

1.3±0.1 g/cm3

Solubility

Flash Point

362.8±28.0 °C

Boiling Point

653.2±55.0 °C at 760 mmHg

Melting Point

103ºC

InChl

InChl Key

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#:24502-79-2) 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

30678506

Abstract

OBJECTIVE:
To examine the effects of arnebin-1 on nonalcoholic fatty liver disease (NAFLD) induced by a high-fat diet (HFD).

METHODS:
Male Sprague-Dawley rats were fed an HFD for 10 weeks and then treated with arnebin-1 at a dose of 5, 10 or 20 mg/kg/day by gavage for a further 12 weeks of a 22-week HFD. Peripheral blood and liver tissues were collected for biochemical and histopathological examination. The mechanisms of arnebin-1 on liver fibrosis and insulin resistance (IR) were determined by Western blotting and real-time quantitative polymerase chain reaction.

RESULTS:
Arnebin-1 treatment attenuated the increase of total cholesterol, triglycerides, low-density lipoprotein cholesterol, aspartate aminotransferase and alanine aminotransferase in serum and lipid accumulation in the livers of HFD-fed rats. Furthermore, arnebin-1 abrogated HFD-induced liver fibrosis and the increase of fibrotic biomarkers. The HFD-induced decrease of hepatic proliferator-activated receptor γ and pro-matrix-metalloproteinase (MMP)-9 levels and the increase of tissue inhibitor of metalloproteinase-1 (TIMP-1) levels were reversed after arnebin-1. Arnebin-1 attenuated IR through activating the insulin receptor substrate-1/Akt/mTOR signalling pathway.

CONCLUSION:
This study demonstrated that arnebin-1 ameliorates NAFLD, in part, by attenuating hepatic fibrosis and IR, suggesting that arnebin-1 may be a therapeutic agent for NAFLD treatment.

KEYWORDS

Nonalcoholic fatty liver disease; arnebin-1; fibrosis; insulin resistance; lipid accumulation; liver injury

Title

Protective role of arnebin-1 in rats with nonalcoholic fatty liver disease.

Author

Yang W1, Yang M1, Yao H1, Ma Y1, Ren X1, Teng L1, Wang T1.

Publish date

2019 Mar

PMID

30380804

Abstract

Skin cancer is currently diagnosed as one in every three cancers. Melanoma, the most aggressive form of skin cancer, is responsible for 79% of skin cancer deaths and the incidence is rising faster than in any other solid tumor type. Previously, we have demonstrated that dimethylacrylshikonin (DMAS), isolated from the roots of Onosma paniculata (Boraginaceae), exhibited the lowest IC50 values against different tumor types out of several isolated shikonin derivatives. DMAS was especially cytotoxic towards melanoma cells and led to apoptosis and cell cycle arrest. In this study, we performed a comprehensive gene expression study to investigate the mechanism of action in more detail. Gene expression signature was compared to vehicle-treated WM164 control cells after 24 h of DMAS treatment; where 1192 distinct mRNAs could be identified as expressed in all replicates and 89 were at least 2-fold differentially expressed. DMAS favored catabolic processes and led in particular to p62 increase which is involved in cell growth, survival, and autophagy. More in-depth experiments revealed that DMAS led to autophagy, ROS generation, and loss of mitochondrial membrane potential in different melanoma cells. It has been reported that the induction of an autophagic cell death represents a highly effective approach in melanoma therapy.

KEYWORDS

ROS generation; autophagy; melanoma; mitochondrial membrane potential; p62; β-β-dimethylacrylshikonin

Title

Comparative Gene Expression Analysis in WM164 Melanoma Cells Revealed That β-β-Dimethylacrylshikonin Leads to ROS Generation, Loss of Mitochondrial Membrane Potential, and Autophagy Induction.

Author

Kretschmer N1, Deutsch A2, Durchschein C3, Rinner B4, Stallinger A5, Higareda-Almaraz JC6,7,8, Scheideler M9,10,11, Lohberger B12, Bauer R13.

Publish date

2018 Oct 30

PMID

30217260

Abstract

BACKGROUND:
Chordoma, slow growing bone tumours originating from remnants of the notochord, leave affected patients with a median survival of six years. The high recurrence rate of chordoma, together with limited treatment options and bad overall prognosis, make the development of new treatment options urgently necessary.

PURPOSE:
In this study, the potential of two natural products, silibinin and β-β-dimethylacrylshikonin (DMAS), was tested on clival (MUG-CC1 and UM-Chor1) as well as sacral (MUG-Chor1 and U-CH2) chordoma cell lines. The treatment was administered both as single- and combined therapy.

METHODS:
For investigation of cell viability, the Cell Titer 96 Aqueous Non-Radioactive Cell Proliferation Assay Kit was used. Apoptosis induction was studied by flow cytometry, (Annexin V/SYTOX Green, caspase-3) and RT-qPCR. Pathway analyses were performed by western blot.

RESULTS:
Both drugs were found to reduce cell viability alone as well as in combination in a dose dependent manner, with DMAS being more efficient than silibinin. The mode of cell death was mainly apoptosis in DMAS treated samples, while the combination therapy led to apoptosis as well as late-apoptosis/necrosis. Silibinin therapy alone, although reducing cell viability, did not lead to significant apoptotic effects in the performed assays. Focussing on the molecular mechanism of DMAS induced apoptosis, it was found that major genes of the mitochondrial apoptosis pathway, like NOXA and PUMA were overexpressed. Additionally, western blot experiments showed a decrease of ERK/pERK, STAT3/pSTAT3 (Tyr705) and AKT/pAKT expression/activation levels under DMAS treatment.

CONCLUSION:
DMAS is a promising new candidate for chordoma therapy, while silibinin or a combination of both is less favourable.

Copyright ? 2018. Published by Elsevier GmbH.

KEYWORDS

Apoptosis; Chordoma; Silibinin; β-β-dimethylacrylshikonin

Title

Influence of silibinin and β-β-dimethylacrylshikonin on chordoma cells.

Author

Jahanafrooz Z1, Stallinger A2, Anders I2, Kleinegger F3, Lohberger B4, Durchschein C5, Bauer R5, Deutsch A6, Rinner B7, Kretschmer N5.

Publish date

2018 Oct 1