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Dehydroleucodin

$530

  • Brand : BIOFRON

  • Catalogue Number : AV-C10663

  • Specification : 98%

  • CAS number : 36150-07-9

  • Formula : C15H16O3

  • Molecular Weight : 244.29

  • PUBCHEM ID : 73440

  • Volume : 5mg

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Catalogue Number

AV-C10663

Analysis Method

HPLC,NMR,MS

Specification

98%

Storage

2-8°C

Molecular Weight

244.29

Appearance

Powder

Botanical Source

Structure Type

Sesquiterpenoids

Category

Standards;Natural Pytochemical;API

SMILES

CC1=C2C(C3C(CC1)C(=C)C(=O)O3)C(=CC2=O)C

Synonyms

DEHYDROACHILLIN/11,13-Dehydroleucodin Dehydroleucodin Leucodin Lidbeckialactone Mesatlantin E

IUPAC Name

(3aS,9aS,9bS)-6,9-dimethyl-3-methylidene-4,5,9a,9b-tetrahydro-3aH-azuleno[4,5-b]furan-2,7-dione

Applications

Density

1.2g/cm3

Solubility

C/EBPα; C/EBPβ; PPARγ; adipogenesis; mitotic clonal expansion; sesquiterpene lactone

Flash Point

203.1ºC

Boiling Point

450.6ºC at 760mmHg

Melting Point

InChl

InChI=1S/C15H16O3/c1-7-4-5-10-9(3)15(17)18-14(10)13-8(2)6-11(16)12(7)13/h6,10,13-14H,3-5H2,1-2H3/t10-,13-,14-/m0/s1

InChl Key

SKNVIAFTENCNGB-BPNCWPANSA-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#:36150-07-9) 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

29663555

Abstract

Aberrant levels of preadipocyte differentiation, triggered by adipocyte hyperplasia and hypertrophy, results in the obesogenic phenotype. Obesity is a risk factor for several metabolic disorders. In this paper, dehydroleucodine inhibited the accumulation of lipid droplets and decreased the elevations of triglycerides, and this inhibitory effect occurred during the early stage of adipogenesis. Thus, not only did dehydroleucodine downregulate the expression of C/EBPα and PPARγ, it also strongly blocked the expression of C/EBPβ, an early stage biomarker of early adipogenesis, in a concentration-dependent manner. The proliferation of preadipocytes was dramatically suppressed when dehydroleucodine was added to the medium as early as 24 hr. These results indicate that dehydroleucodine may specifically affect mitotic clonal expansion to inhibit preadipocyte differentiation. Dehydroleucodine arrested the cell cycle at the G0 /G1 phase, increased p27 and decreased both cyclins A and D and their partners (e.g., CDK2 and CDK4). Additionally, dehydroleucodine decreased phosphorylation of Erk1/2 and Akt. Furthermore, dehydroleucodine downregulated expression of histone demethylase JMJD2B as well as repressed the expression of histone methyltransferase MLL4, which in turn diminished the expression of C/EBPβ and PPARγ, respectively. Collectively, our results indicate that dehydroleucodine inhibits preadipocyte differentiation by blocking mitotic clonal expansion via cell cycle arrest, which may be mediated by regulation of selective histone methylation/demethylation in transcription activation during the early step of adipogenesis.

Copyright ? 2018 John Wiley & Sons, Ltd.

KEYWORDS

C/EBPα; C/EBPβ; PPARγ; adipogenesis; mitotic clonal expansion; sesquiterpene lactone

Title

Dehydroleucodine inhibits mitotic clonal expansion during adipogenesis through cell cycle arrest.

Author

Abood S1, Veisaga ML2, Lopez LA3, Barbieri MA1,2,4,5.

Publish date

2018 Aug

PMID

26718258

Abstract

Malignant melanoma represents the fastest growing public health risk of all cancer types worldwide. Several strategies and anti-cancer drugs have been used in an effort to improve treatments, but the development of resistance to anti-neoplastic drugs remains the major cause of chemotherapy failure in melanomas. Previously, we showed that the sesquiterpene lactone, dehydroleucodine (DhL), promotes the accumulation of DNA damage markers, such as H2AX and 53BP1, in human tumor cells. Also DhL was shown to trigger either cell senescence or apoptosis in a concentration-dependent manner in HeLa and MCF7 cells. Here, we evaluated the effects of DhL on B16F0 mouse melanoma cells in vitro and in a pre-clinical melanoma model. DhL inhibited the proliferation of B16F0 cells by inducing senescence or apoptosis in a concentration-dependent manner. Also, DhL reduced the expression of the cell cycle proteins cyclin D1 and B1 and the inhibitor of apoptosis protein, survivin. In melanomas generated by subcutaneous injection of B16F0 cells into C57/BL6 mice, the treatment with 20 mg DhL /Kg/day in preventive, simultaneous and therapeutic protocols reduced tumor volumes by 70%, 60% and 50%, respectively. DhL treatments reduced the number of proliferating, while increasing the number of senescent and apoptotic tumor cells. To estimate the long-term effects of DhL, a mathematical model was applied to fit experimental data. Extrapolation beyond experimental time points revealed that DhL administration following preventive and therapeutic protocols is predicted to be more effective than simultaneous treatments with DhL in restricting tumor growth.

Copyright ? 2015 Elsevier Ireland Ltd. All rights reserved.

KEYWORDS

Apoptosis; Dehydroleucodine; Mathematical model; Melanoma; Premature senescence; Sesquiterpene lactones

Title

Dehydroleucodine inhibits tumor growth in a preclinical melanoma model by inducing cell cycle arrest, senescence and apoptosis.

Author

Costantino VV1, Lobos-Gonzalez L2, IbaNez J1, Fernandez D1, Cuello-Carrion FD3, Valenzuela MA2, Barbieri MA4, Semino SN1, Jahn GA3, Quest AF5, Lopez LA6.

Publish date

2016 Mar 1

PMID

27057812

Abstract

The sesquiterpene lactones dehydroleucodine (1) and leucodine (2) were isolated from Gynoxys verrucosa, a species used in traditional medicine in southern Ecuador. The activity of these compounds was determined against eight acute myeloid leukemia (AML) cell lines and compared with their activity against normal peripheral blood mononuclear cells. Compound 1 showed cytotoxic activity against the tested cell lines, with LD50 values between 5.0 and 18.9 μM. Compound 2 was inactive against all of the tested cell lines, demonstrating that the exocyclic methylene in the lactone ring is required for cytotoxic activity. Importantly, compound 1 induced less toxicity to normal blood cells than to AML cell lines and was active against human AML cell samples from five patients, with an average LD50 of 9.4 μM. Mechanistic assays suggest that compound 1 has a similar mechanism of action to parthenolide (3). Although these compounds have significant structural differences, their lipophilic surface signatures show striking similarities.

Title

Dehydroleucodine, a Sesquiterpene Lactone from Gynoxys verrucosa, Demonstrates Cytotoxic Activity against Human Leukemia Cells.

Author

OrdoNez PE1,2,3, Sharma KK4, Bystrom LM4, Alas MA4, Enriquez RG5, Malagon O2, Jones DE3, Guzman ML4, Compadre CM1.

Publish date

2016 Apr 22