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Telocinobufagin

$572

  • Brand : BIOFRON

  • Catalogue Number : BD-P0648

  • Specification : 98.0%(HPLC)

  • CAS number : 472-26-4

  • PUBCHEM ID : 259991

  • Volume : 25mg

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Catalogue Number

BD-P0648

Analysis Method

HPLC,NMR,MS

Specification

98.0%(HPLC)

Storage

2-8°C

Molecular Weight

Appearance

White crystalline powder

Botanical Source

Ch'an Su and other toad poisons

Structure Type

Steroids

Category

Standards;Natural Pytochemical;API

SMILES

CC12CCC(CC1(CCC3C2CCC4(C3(CCC4C5=COC(=O)C=C5)O)C)O)O

Synonyms

3,5,14-Trihydroxybufa-20,22-dienolide/Telobufotoxin/5β-Bufa-20,22-dienolide, 3β,5,14-trihydroxy-/Telecinobufagin/Telocinobufogenin/(3β,5β)-3,5,14-Trihydroxybufa-20,22-dienolide/Bufa-20,22-dienolide, 3,5,14-trihydroxy-, (3β,5β)-/Telocinobufagin

IUPAC Name

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

Applications

Telocinobufagin is one of anti-hepatoma constituent in Venenum Bufonis.

Density

1.3±0.1 g/cm3

Solubility

Methanol; Chloroform

Flash Point

201.0±23.6 °C

Boiling Point

589.6±50.0 °C at 760 mmHg

Melting Point

InChl

InChI=1S/C24H34O5/c1-21-9-5-16(25)13-23(21,27)11-7-19-18(21)6-10-22(2)17(8-12-24(19,22)28)15-3-4-20(26)29-14-15/h3-4,14,16-19,25,27-28H,5-13H2,1-2H3/t16-,17+,18-,19+,21+,22+,23-,24-/m0/s1

InChl Key

PBSOJKPTQWWJJD-ZBDZJSKLSA-N

WGK Germany

RID/ADR

HS Code Reference

2932110000

Personal Projective Equipment

Correct Usage

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

Meta Tag

provides coniferyl ferulate(CAS#:472-26-4) 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

30158457

Abstract

Cardiotonic steroids (CTS) are Na⁺/K⁺-ATPase (NKA) ligands that are elevated in volume-expanded states and associated with cardiac and renal dysfunction in both clinical and experimental settings. We test the hypothesis that the CTS telocinobufagin (TCB) promotes renal dysfunction in a process involving signaling through the NKA α-1 in the following studies. First, we infuse TCB (4 weeks at 0.1 µg/g/day) or a vehicle into mice expressing wild-type (WT) NKA α-1, as well as mice with a genetic reduction (~40%) of NKA α-1 (NKA α-1+/-). Continuous TCB infusion results in increased proteinuria and cystatin C in WT mice which are significantly attenuated in NKA α-1+/- mice (all p < 0.05), despite similar increases in blood pressure. In a series of in vitro experiments, 24-h treatment of HK2 renal proximal tubular cells with TCB results in significant dose-dependent increases in both Collagens 1 and 3 mRNA (2-fold increases at 10 nM, 5-fold increases at 100 nM, p < 0.05). Similar effects are seen in primary human renal mesangial cells. TCB treatment (100 nM) of SYF fibroblasts reconstituted with cSrc results in a 1.5-fold increase in Collagens 1 and 3 mRNA (p < 0.05), as well as increases in both Transforming Growth factor beta (TGFb, 1.5 fold, p < 0.05) and Connective Tissue Growth Factor (CTGF, 2 fold, p < 0.05), while these effects are absent in SYF cells without Src kinase. In a patient study of subjects with chronic kidney disease, TCB is elevated compared to healthy volunteers. These studies suggest that the pro-fibrotic effects of TCB in the kidney are mediated though the NKA-Src kinase signaling pathway and may have relevance to volume-overloaded conditions, such as chronic kidney disease where TCB is elevated.

KEYWORDS

Na+/K+-ATPase; cardiotonic steroids; fibrosis; kidney; signaling; telocinobufagin.

Title

Telocinobufagin, a Novel Cardiotonic Steroid, Promotes Renal Fibrosis via Na⁺/K⁺-ATPase Profibrotic Signaling

Author

David J Kennedy 1 , Fatimah K Khalaf 2 , Brendan Sheehy 3 , Malory E Weber 4 , Brendan Agatisa-Boyle 5 , Julijana Conic 6 , Kayla Hauser 7 , Charles M Medert 8 , Kristen Westfall 9 , Philip Bucur 10 , Olga V Fedorova 11 , Alexei Y Bagrov 12 , W H Wilson Tang 13 14 15

Publish date

2018 Aug 29

PMID

25687199

Abstract

Ideal potential vaccine adjuvants to stimulate a Th1 immune response are urgently needed to control intracellular infections in clinical applications. Telocinobufagin (TBG), an active component of Venenum bufonis, exhibits immunomodulatory activity. Therefore, we investigated whether TBG enhances the Th1 immune response to ovalbumin (OVA) and formalin-inactivated Salmonella typhimurium (FIST) in mice. TBG augmented serum OVA- and FIST-specific IgG and IgG2a and the production of IFNγ by antigen-restimulated splenocytes. TBG also dramatically enhanced splenocyte proliferative responses to concanavalin A, lipopolysaccharide, and OVA and substantially increased T-bet mRNA levels and the CD3(+)/CD3(+)CD4(+)/CD3(+)CD8(+) phenotype in splenocytes from OVA-immunized mice. In in vivo protection studies, TBG significantly decreased the bacterial burdens in the spleen and prolonged the survival time of FIST-immunized mice challenged with live S. typhimurium. In vivo neutralization of IFNγ with anti-IFNγ mAbs led to a significant reduction in FIST-specific IgG2a and IFNγ levels and in anti-Salmonella effect in TBG/FIST-immunized mice. In conclusion, these results suggest that TBG enhances a Th1 immune response to control intracellular infections.

KEYWORDS

Na+/K+-ATPase; cardiotonic steroids; fibrosis; kidney; signaling; telocinobufagin.

Title

Telocinobufagin Enhances the Th1 Immune Response and Protects Against Salmonella Typhimurium Infection

Author

Shuai-Cheng Wu 1 , Ben-Dong Fu 1 , Hai-Qing Shen 1 , Peng-Fei Yi 1 , Li-Yan Zhang 1 , Shuang Lv 1 , Xun Guo 1 , Fang Xia 1 , Yong-Li Wu 1 , Xu-Bin Wei 2

Publish date

2015 Apr

PMID

29725474

Abstract

Telocinobufagin (TBG), an active ingredient of Venenumbufonis, exhibits an immunomodulatory activity. However, its antimetastatic activity in breast cancer remains unknown. The present study investigated whether TBG prevents breast cancer metastasis and evaluated its regulatory mechanism. TBG inhibited the migration and invasion of 4T1 breast cancer cells. Furthermore, TBG triggered the collapse of F-actin filaments in breast cancer. The epithelial-mesenchymal transition (EMT) markers, vimentin and fibronectin, were downregulated following TBG treatment. However, E-cadherin was upregulated following TBG treatment. Snail, a crucial transcriptional factor of EMT, was downregulated following TBG treatment. Signaling pathway markers, including phosphorylated protein kinase B (P-Akt), p-mechanistic target of rapamycin (mTOR) and p-extracellular signal-regulated kinase (ERK), were decreased following TBG treatment. The same results were obtained from in vivo experiments. In conclusion, in vitro and in vivo experiments reveal that TBG inhibited migration, invasion and EMT via the phosphoinositide 3-kinase (PI3K)/Akt/ERK/Snail signaling pathway in breast cancer.

KEYWORDS

epithelial-mesenchymal transition; invasion; migration; snail; telocinobufagin.

Title

Telocinobufagin Inhibits the Epithelial-Mesenchymal Transition of Breast Cancer Cells Through the Phosphoinositide 3-kinase/protein Kinase B/extracellular Signal-Regulated kinase/Snail Signaling Pathway

Author

Yuxue Gao 1 , Lihong Shi 2 , Zhen Cao 1 , Xuetao Zhu 1 , Feng Li 1 , Ruyan Wang 1 , Jinyuan Xu 1 , Jinyi Zhong 1 , Baogang Zhang 3 , Shijun Lu 3

Publish date

2018 May