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Bufotalidin

$807

  • Brand : BIOFRON

  • Catalogue Number : BD-P0837

  • Specification : 98.0%(HPLC&TLC)

  • CAS number : 465-90-7

  • Formula : C24H32O6

  • Molecular Weight : 416.514

  • PUBCHEM ID : 259577

  • Volume : 25mg

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Catalogue Number

BD-P0837

Analysis Method

HPLC,NMR,MS

Specification

98.0%(HPLC&TLC)

Storage

2-8°C

Molecular Weight

416.514

Appearance

Powder

Botanical Source

Bufonis Venenum

Structure Type

Miscellaneous

Category

SMILES

CC12CCC3C(C1(CCC2C4=COC(=O)C=C4)O)CCC5(C3(CCC(C5)O)C=O)O

Synonyms

(3S,5S,8R,9S,10S,13R,14S,17R)-3,5,14-trihydroxy-13-methyl-17-(6-oxopyran-3-yl)-2,3,4,6,7,8,9,11,12,15,16,17-dodecahydro-1H-cyclopenta[a]phenanthrene-10-carbaldehyde

IUPAC Name

(3S,5S,8R,9S,10S,13R,14S,17R)-3,5,14-trihydroxy-13-methyl-17-(6-oxopyran-3-yl)-2,3,4,6,7,8,9,11,12,15,16,17-dodecahydro-1H-cyclopenta[a]phenanthrene-10-carbaldehyde

Applications

Density

1.419g/cm3

Solubility

Soluble in Chloroform,Dichloromethane,Ethyl Acetate,DMSO,Acetone,etc.

Flash Point

215ºC

Boiling Point

626.3ºC at 760 mmHg

Melting Point

InChl

InChI=1S/C24H32O6/c1-21-8-5-18-19(6-10-23(28)12-16(26)4-9-22(18,23)14-25)24(21,29)11-7-17(21)15-2-3-20(27)30-13-15/h2-3,13-14,16-19,26,28-29H,4-12H2,1H3/t16-,17+,18-,19+,21+,22-,23-,24-/m0/s1

InChl Key

TVKPTWJPKVSGJB-XHCIOXAKSA-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#:465-90-7) 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

30587014

Abstract

Three new bufadienolides 14β, 16β-dihydroxy-3β-[β-D-glucopyranosyl-(1→6)-(β-D-glucopyranosyl)oxy]-5α-bufa-20, 22-dienolide (1), 14β-hydroxy-3β-[β-D-glucopyranosyl-(1→4)-(β-D-glucopyranosyl)oxy]-5α-bufa-20, 22-dienolide (2) and hellebrigenin-3-O-β-D-glucosyl-(1→4)-β-D-glucoside (3), together with eight known bufadienolides (4-11) were isolated from the roots and rhizomes of Helleborus thibetanus. Their structures were elucidated by extensive spectroscopic methods and acid hydrolysis. Compounds 1-7 were evaluated for their cytotoxic activity against HCT116, A549 and HepG2 tumor cell lines. Compound 1 exhibited moderate cytotoxicity against HepG2 cells with IC50 value of 15.1 ± 1.72 μM. Compounds 5 and 6 exhibited moderate cytotoxicity against HCT116 cells with IC50 values of 15.12 ± 0.58 μM and 13.17 ± 2.34 μM, respectively.

KEYWORDS

Helleborus thibetanus Franch; bufadienolide glycosides; cytotoxic activity; structure identification.

Title

New cytotoxic bufadienolides from the roots and rhizomes of Helleborus thibetanus Franch

Author

Yuze Li 1, Huawei Zhang 2, Xiaofei Liang 2, Bei Song 1, Xudong Zheng 1, Rui Wang 1, Li Liu 1, Xiaomei Song 2, Jianli Liu 1

Publish date

2020 Apr

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

Lingyu Han 1, Bo Yuan 1, Ryota Shimada 1, Hideki Hayashi 1, Nan Si 2, Hai-Yu Zhao 2, Baolin Bian 2, Norio Takagi 1

Publish date

2018 Dec;

PMID

24954031

Abstract

Hellebrigenin, one of bufadienolides belonging to cardioactive steroids, was found in skin secretions of toads and plants of Helleborus and Kalanchoe genera. In searching for natural constituents with anti-hepatoma activities, we found that hellebrigenin, isolated from traditional Chinese medicine Venenum Bufonis, potently reduced the viability and colony formation of human hepatocellular carcinoma cells HepG2, and went on to explore the underlying molecular mechanisms. Our results demonstrated that hellebrigenin triggered DNA damage through DNA double-stranded breaks and subsequently induced cell cycle G2/M arrest associated with up-regulation of p-ATM (Ser(1981)), p-Chk2 (Tyr(68)), p-CDK1 (Tyr(15)) and Cyclin B1, and down-regulation of p-CDC25C (Ser(216)). It was also found that hellebrigenin induced mitochondrial apoptosis, characterized by Bax translocation to mitochondria, disruption of mitochondrial membrane potential, release of cytochrome c into cytosol and sequential activation of caspases and PARP. In addition, Akt expression and phosphorylation were inhibited by hellebrigenin, whereas Akt silencing with siRNA significantly blocked cell cycle arrest but enhanced apoptosis induced by hellebrigenin. Activation of Akt by human insulin-like growth factor I (hIGF-I) could obviously attenuate hellebrigenin-induced cell death. In summary, our study is the first to report the efficacy of hellebrigenin against HepG2 and elucidated its molecular mechanisms including DNA damage, mitochondria collapse, cell cycle arrest and apoptosis, which will contribute to the development of hellebrigenin into a chemotherapeutic agent in the treatment of liver cancer.

KEYWORDS

Akt; Apoptosis; Cell cycle; DNA damage; Hellebrigenin; Hepatocellular carcinoma.

Title

Hellebrigenin induces cell cycle arrest and apoptosis in human hepatocellular carcinoma HepG2 cells through inhibition of Akt

Author

Li-Juan Deng 1, Li-Ping Hu 1, Qun-Long Peng 1, Xiao-Lin Yang 1, Liang-Liang Bai 1, Anita Yiu 2, Yong Li 1, Hai-Yan Tian 1, Wen-Cai Ye 3, Dong-Mei Zhang 4

Publish date

2014 Aug 5