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Arenobufagin

$250

  • Brand : BIOFRON

  • Catalogue Number : BF-A4003

  • Specification : 98%(HPLC)

  • CAS number : 464-74-4

  • Formula : C24H32O6

  • Molecular Weight : 416.51

  • PUBCHEM ID : 12305198

  • Volume : 20mg

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Catalogue Number

BF-A4003

Analysis Method

HPLC,NMR,MS

Specification

98%(HPLC)

Storage

2-8°C

Molecular Weight

416.51

Appearance

Powder

Botanical Source

Bufo gargarizans

Structure Type

Others

Category

Standards;Natural Pytochemical;API

SMILES

CC12CCC(CC1CCC3C2C(C(=O)C4(C3(CCC4C5=COC(=O)C=C5)O)C)O)O

Synonyms

Arenobufagin/(3β,5β,11α)-3,11,14-Trihydroxy-12-oxobufa-20,22-dienolide/5β-Bufa-20,22-dienolide, 3β,11α,14-trihydroxy-12-oxo-/ARENOBUFAGIN (REFERENCE GRADE)/Bufa-20,22-dienolide, 3,11,14-trihydroxy-12-oxo-, (3β,5β,11α)-

IUPAC Name

5-[(3S,5R,8R,9S,10S,11S,13R,14S,17R)-3,11,14-trihydroxy-10,13-dimethyl-12-oxo-2,3,4,5,6,7,8,9,11,15,16,17-dodecahydro-1H-cyclopenta[a]phenanthren-17-yl]pyran-2-one

Applications

Arenobufagin is a natural bufadienolide from toad venom; has potent antineoplastic activity against HCC HepG2 cells as well as corresponding multidrug-resistant HepG2/ADM cells.IC50 value: Target: in vitro: arenobufagin induced mitochondria-mediated apoptosis in HCC cells, with decreasing mitochondrial potential, as well as increasing Bax/Bcl-2 expression ratio, Bax translocation from cytosol to mitochondria. Arenobufagin also induced autophagy in HepG2/ADM cells. Autophagy-specific inhibitors (3-methyladenine, chloroquine and bafilomycin A1) or Beclin1 and Atg 5 small interfering RNAs (siRNAs) enhanced arenobufagin-induced apoptosis, indicating that arenobufagin-mediated autophagy may protect HepG2/ADM cells from undergoing apoptotic cell death [1]. arenobufagin inhibited vascular endothelial growth factor (VEGF)-induced viability, migration, invasion and tube formation in human umbilical vein endothelial cells (HUVECs) in vitro [2]. Arenobufagin blocked the Na+/K+ pump current in a dose-dependent manner with a half-maximal concentration of 0.29 microM and a Hill coefficient of 1.1 [3].in vivo: arenobufagin inhibited the growth of HepG2/ADM xenograft tumors, which were associated with poly (ADP-ribose) polymerase cleavage, light chain 3-II activation and mTOR inhibition [1]. Arenobufagin also suppressed sprouting formation from VEGF-treated aortic rings in an ex vivo model [2].

Density

1.4±0.1 g/cm3

Solubility

Methanol; Acetontrile; DMSO

Flash Point

219.3±25.0 °C

Boiling Point

637.2±55.0 °C at 760 mmHg

Melting Point

InChl

InChI=1S/C24H32O6/c1-22-9-7-15(25)11-14(22)4-5-17-19(22)20(27)21(28)23(2)16(8-10-24(17,23)29)13-3-6-18(26)30-12-13/h3,6,12,14-17,19-20,25,27,29H,4-5,7-11H2,1-2H3/t14-,15+,16-,17-,19-,20+,22+,23+,24+/m1/s1

InChl Key

JGDCRWYOMWSTFC-AZGSIFHYSA-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#:464-74-4) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

PMID

30272276

Abstract

Glioblastoma is the most common and lethal intracranial tumor type, characterized by high angiogenic and infiltrative capacities. To provide a novel insight into therapeutic strategies against glioblastoma, the cytotoxicity of arenobufagin and hellebrigenin was investigated in the human glioblastoma cell line, U-87. Similar dose-dependent cytotoxicity was observed in the cells, whereas no detectable toxicity was confirmed in mouse primary astrocytes. Treatment with each drug downregulated the expression levels of Cdc25C, Cyclin B1 and survivin, which occurred in parallel with G2/M phase arrest. Necrotic-like cell death was only observed in the cells treated with a relatively high concentration (>100 ng/ml). These results indicate that the two drugs exhibited distinct cytotoxicity against cancerous glial cells with high potency and selectivity, suggesting that growth inhibition associated with G2/M phase arrest and/or necrosis were attributed to their toxicities. Activation of the p38 mitogen activated protein kinase (MAPK) signaling pathway was also observed in treated cells. Notably, a specific inhibitor of p38 MAPK, SB203580, itself caused a significant decrease in cell viability, and further enhanced the cytotoxicity of the two drugs, suggesting an important pro-survival role for p38 MAPK. Given that p38 MAPK serves an essential role in promoting glioblastoma cell survival, developing a novel combination regimen of arenobufagin/hellebrigenin plus a p38 MAPK inhibitor may improve the efficacy of the two drugs, and may provide more therapeutic benefits to patients with glioblastoma. The qualitative assessment demonstrated the existence of arenobufagin in the cerebrospinal fluid of arenobufagin-treated rats, supporting its clinical application.

Title

Cytocidal effects of arenobufagin and hellebrigenin, two active bufadienolide compounds, against human glioblastoma cell line U-87.

Author

Han L1, Yuan B1, Shimada R1, Hayashi H1, Si N2, Zhao HY2, Bian B2, Takagi N1.

Publish date

2018 Dec;

PMID

30181060

Abstract

Arenobufagin is a naturally occurring bufadienolide showing promising antitumor activity accompanied however with apparent cardiac toxicity. Following the recent discovery that oxidative damage possibly be an important cause of the cardiac toxicity of cardenolides, a strategy fusing the antitumor agent arenobufagin with a benzoisoselenazol fragment, a reactive oxygen species (ROS) scavenger, has been developed. Six novel hybrids were synthesized and their ROS scavenging activities as well as their in vitro cytotoxicity against the human hepatocellular carcinoma cell line HepG2, an adriamycin-resistant subline HepG2/ADM, and the human myocardial cell line AC16 were evaluated. The results indicate that the hybrids exhibit various degrees of in vitro ROS scavenging activities, and weaker cytotoxicity than that of arenobufagin against the myocardial cell line AC16. These findings suggest the feasibility of a strategy in which the cardiotoxicity of the potential antitumor agent arenobufagin is reduced.

Copyright © 2018. Published by Elsevier Ltd.

KEYWORDS

Antitumor; Arenobufagin; Benzoisoselenazol; Hybridization; Reactive oxygen species

Title

Hybrids of arenobufagin and benzoisoselenazol reducing the cardiotoxicity of arenobufagin.

Author

Hou W1, Huang ZX1, Xu HG1, Lin J2, Zhang DM1, Peng QL1, Lin H1, Chang YQ1, Wang LH1, Yao Z1, Sun PH1, Chen WM3.

Publish date

2018 Nov 1

PMID

28987597

Title

Reflection on the selection of doses of arenobufagin in vivo anticancer study.

Author

Chen L1, Zhang D2.

Publish date

2018 Feb