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Chebulic acid


  • Brand : BIOFRON

  • Catalogue Number : BD-P0434

  • Specification : 98.0%(HPLC)

  • CAS number : 23725-05-5

  • PUBCHEM ID : 71308174

  • Volume : 10mg

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Catalogue Number


Analysis Method






Molecular Weight



Botanical Source

Chebulae Fructus

Structure Type



Standards;Natural Pytochemical;API




(S)-2-((3S,4S)-3-carboxy-5,6,7-trihydroxy-1-oxoisochroman-4-yl)succinic acid/Chebulic acid


(2S)-2-[(3S,4S)-3-carboxy-5,6,7-trihydroxy-1-oxo-3,4-dihydroisochromen-4-yl]butanedioic acid


Chebulic acid, a phenolcarboxylic acid compound isolated from Terminalia chebula, has potent anti-oxidant activity, which breaks the cross-links of proteins induced by advanced glycation end-products (AGEs) and inhibits the formation of AGEs. Chebulic acid is effective in controlling elevated metabolic parameters, oxidative stress and renal damage, supporting its beneficial effect in diabetic nephropathy[1][2].




Methanol; Water

Flash Point

Boiling Point

Melting Point



InChl Key


WGK Germany


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#:23725-05-5) 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.




Astrocytic glutamate transporter excitatory amino acid transporter (EAAT) 1, also known as glutamate aspartate transporter (GLAST) in rodents, is one of two glial glutamate transporters that are responsible for removing excess glutamate from synaptic clefts to prevent excitotoxic neuronal death. Despite its important role in neurophysiological functions, the molecular mechanisms of EAAT1 regulation at the transcriptional level remain to be established. Here, we report that NF-κB is a main positive transcription factor for EAAT1, supported by the following: 1) EAAT1 contains two consensus sites for NF-κB, 2) mutation of NF-κB binding sites decreased EAAT1 promoter activity, and 3) activation of NF-κB increased, whereas inhibition of NF-κB decreased EAAT1 promoter activity and mRNA/protein levels. EGF increased EAAT1 mRNA/protein levels and glutamate uptake via NF-κB. The transcription factor yin yang 1 (YY1) plays a role as a critical negative regulator of EAAT1, supported by the following: 1) the EAAT1 promoter contains multiple consensus sites for YY1, 2) overexpression of YY1 decreased EAAT1 promoter activity and mRNA/protein levels, and 3) knockdown of YY1 increased EAAT1 promoter activity and mRNA/protein levels. Manganese decreased EAAT1 expression via YY1. Epigenetic modifiers histone deacetylases (HDACs) served as co-repressors of YY1 to further decrease EAAT1 promoter activity, whereas inhibition of HDACs reversed manganese-induced decrease of EAAT1 expression. Taken together, our findings suggest that NF-κB is a critical positive regulator of EAAT1, mediating the stimulatory effects of EGF, whereas YY1 is a negative regulator of EAAT1 with HDACs as co-repressors, mediating the inhibitory effects of manganese on EAAT1 regulation.


astrocyte, epidermal growth factor (EGF), glutamate, manganese, NF-κB transcription factor


Transcriptional Regulation of the Astrocytic Excitatory Amino Acid Transporter 1 (EAAT1) via NF-κB and Yin Yang 1 (YY1)*


Pratap Karki,‡ Clifford Kim,§ Keisha Smith,‡ Deok-Soo Son,‡ Michael Aschner,¶ and Eunsook Lee‡,1

Publish date

2015 Sep 25




Despite numerous descriptions of rapid effects of corticosterone on neuronal function, the intracellular mechanisms responsible for these changes remain elusive. The present comprehensive analysis reveals that signaling from a membrane-located G protein-coupled receptor activates PKC, Akt/PKB, and PKA, which subsequently trigger the phosphorylation of the tyrosine kinases Pyk2, Src, and Abl. These changes induce rapid cytoskeletal rearrangements (increased PSD-95 co-clustering) within the post-synaptic density; these events are accompanied by increased surface NMDA receptor expression, reflecting corticosterone-induced inhibition of NMDA receptor endocytosis. Notably, none of these signaling mechanisms require de novo protein synthesis. The observed up-regulation of ERK1/2 (downstream of NMDA receptor signaling) together with the fact that c-Abl integrates cytoplasmic and nuclear functions introduces a potential mechanism through which rapid signaling initiated at the plasma membrane may eventually determine the long term integrated response to corticosterone by impacting on the transcriptional machinery that is regulated by classical, nuclear mineralocorticoid, and glucocorticoid receptors.


G Protein-coupled Receptors (GPCR), Glucocorticoids, Glutamate Receptors Ionotropic (AMPA, NMDA), Neurons, Nonreceptor-tyrosine Kinase, Hippocampus


Non-receptor-tyrosine Kinases Integrate Fast Glucocorticoid Signaling in Hippocampal Neurons


Silei Yang,‡,1 Francesco Roselli,‡§,1,2 Alexandre V. Patchev,‡,3 Shuang Yu,‡ and Osborne F. X. Almeida‡,4

Publish date

2013 Aug 16




Healthy People 2020 (HP2020) calls for a 10% to 15% reduction in death rates from 2007 to 2020 for selected cancers. Trends in death rates can be used to predict progress toward meeting HP2020 targets.

We used mortality data from 1975 through 2009 and population estimates and projections to predict deaths for all cancers and the top 23 cancers among men and women by race. We apportioned changes in deaths from population risk and population growth and aging.

From 1975 to 2009, the number of cancer deaths increased among white and black Americans primarily because of an aging white population and a growing black population. Overall, age-standardized cancer death rates (risk) declined in all groups. From 2007 to 2020, rates are predicted to continue to decrease while counts of deaths are predicted to increase among men (15%) and stabilize among women (increase <10%). Declining death rates are predicted to meet HP2020 targets for cancers of the female breast, lung and bronchus, cervix and uterus, colon and rectum, oral cavity and pharynx, and prostate, but not for melanoma. Conclusion Cancer deaths among women overall are predicted to increase by less than 10%, because of, in part, declines in breast, cervical, and colorectal cancer deaths among white women. Increased efforts to promote cancer prevention and improve survival are needed to counter the impact of a growing and aging population on the cancer burden and to meet melanoma target death rates.


Meeting the Healthy People 2020 Objectives to Reduce Cancer Mortality


Hannah K. Weir, PhD,corresponding author Trevor D. Thompson, BS, Ashwini Soman, MBBS, MPH, Bjorn Møller, PhD, Steven Leadbetter, MS, and Mary C. White, ScD

Publish date