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Ganoderenic acid E


  • Brand : BIOFRON

  • Catalogue Number : BD-P0364

  • Specification : 98.0%(HPLC)

  • CAS number : 110241-23-1

  • Formula : C30H40O8

  • Molecular Weight : 528.642

  • PUBCHEM ID : 131801361

  • Volume : 10mg

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Catalogue Number


Analysis Method






Molecular Weight




Botanical Source

Structure Type






(E,2S)-6-[(7S,10S,12S,13R,14R)-7,12-dihydroxy-4,4,10,13,14-pentamethyl-3,11,15-trioxo-1,2,5,6,7,12,16,17-octahydrocyclopenta[a]phenanthren-17-yl]-2-methyl-4-oxohept-5-enoic acid


(E,2S)-6-[(7S,10S,12S,13R,14R)-7,12-dihydroxy-4,4,10,13,14-pentamethyl-3,11,15-trioxo-1,2,5,6,7,12,16,17-octahydrocyclopenta[a]phenanthren-17-yl]-2-methyl-4-oxohept-5-enoic acid



1.3±0.1 g/cm3


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

Flash Point

413.5±29.4 °C

Boiling Point

737.1±60.0 °C at 760 mmHg

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#:110241-23-1) 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.




AIM: To investigate the expression of tumor necrosis factor-alpha (TNF-α) and vascular endothelial growth factor (VEGF) in the development of esophageal varices in portal hypertensive rats.

METHODS: Thirty male Sprague-Dawley (SD) rats in the model group in which a two-stage ligation of portal vein plus ligation of the left adrenal vein was performed, were divided into three subgroups (M7, M14, and M21) in which the rats were kiued on the seventh day, the 14th d and the 21 d after the complete portal ligation. Thirty male SD rats, which underwent the sham operation in the control group, were also separated into three subgroups (C7, C14 and C21) corresponding to the models. The expression of TNF-α and VEGF in the esophagus of all the six subgroups of rats were measured with immunohistochemical SP technique.

RESULTS: The portal pressure in the three model subgroups was significantly higher than that in the corresponding control subgroups (23.82±1.83 vs 11.61±0.86 cmH2O, 20.90±3.27 vs 11.43±1.55 cmH2O and 20.68±2.27 vs 11.87±0.79 cmH2O respectively, P<0.01), as well as the number (9.3±1.6 vs 5.1±0.8, 11.1±0.8 vs 5.4±1.3 and 11.7±1.5 vs 5.2±1.1 respectively, P<0.01) and the total vascular area (78972.6±3527.8 vs 12993.5±4994.8 μm2, 107207.5±46461.4 vs 11862.6±5423.2 μm2 and 110241.4±49262.2 vs 11973.7±3968.5 μm2 respectively, P<0.01) of submucosal veins in esophagus. Compared to the corresponding controls, the expression of TNF-α and VEGF in M21 was significantly higher (2.23±0.30 vs 1.13±0.28 and 1.65±0.38 vs 0.56±0.30 for TNF-α and VEGF respectively, P <0.01), whereas there was no difference in M7 (1.14±0.38 vs 1.06±0.27 and 0.67±0.35 vs 0.50±0.24 for TNF-α and VEGF respectively, P>0.05) and M14 (1.20±0.25 vs 1.04±0.26 and 0.65±0.18 vs 0.53±0.25 for TNF-α and VEGF respectively, P>0.05). And the expression of TNF-α and VEGF in M21 was significantly higher than that in M7 (2.23±0.30 vs 1.14±0.38 and 1.65±0.38 vs 0.67±0.35 for TNF-α and VEGF respectively, P<0.01) and M14 (2.23±0.30 vs 1.20±0.25 and 1.65±0.38 vs 0.65±0.18 for TNF-α and VEGF respectively, P<0.01), but there was no difference between M7 and M14 (1.14±0.38 vs 1.20±0.25 and 0.67±0.35 vs 0.65±0.18 for TNF-α and VEGF respectively, P >0.05).

CONCLUSION: In the development of esophageal varices in portal hypertensive rats, increased TNF-α and VEGF may be not an early event, and probably play a role in weakening the esophageal wall and the rupture of esophageal varices.


Portal hypertension, Esophageal varices, Tumor necrosis factor-alpha, Vascular endothelial growth factor


Expression of TNF-α and VEGF in the esophagus of portal hypertensive rats


Zhao-Hui Yin, Xun-Yang Liu, Rang-Lang Huang, and Shu-Ping Ren

Publish date

2005 Feb 28




Pulmonary arterial hypertension (PAH) is a rare condition that can ultimately lead to right heart failure and death. In this study we estimated the health care costs and resource utilization associated with PAH in a large US managed care health plan.

Subjects with claims-based evidence of PAH from 1/1/2004 to 6/30/2010 (identification period) were selected. To be included in the final PAH study sample, subjects were required to have ≥2 claims with a primary PH diagnosis; ≥2 claims with a PAH related-diagnosis (connective tissue diseases, congenital heart diseases, portal hypertension); and ≥1 claim with evidence of a PAH-indicated medication. The earliest date of a claim with evidence of PAH-indicated medication during the identification period was set as the index date. Health care costs and resource utilization were compared between an annualized baseline period and a 12 month follow-up period.

504 PAH subjects were selected for the final study cohort. Estimated average total health care costs were approximately 16% lower in the follow-up period compared to the baseline period (follow-up costs = $98,243 [SD = 110,615] vs. baseline costs = $116,681 [SD = 368,094], p < 0.001), but substantively high in each period relative to costs reported for other chronic diseases. Pharmacy costs were significantly higher in the follow-up period vs. the baseline period, ($38,514 [SD = 34,817] vs. $6,440 [SD = 12,186], p < 0.001) but medical costs were significantly lower in the follow-up vs. baseline ($59,729 [SD = 106,683] vs. $110,241 [SD = 368,725], p < 0.001). These costs were mirrored in health-care resource utilization estimates. The average counts of ambulatory visits and inpatient stays were lower in the follow-up vs. the baseline (both p < 0.001). Results varied in exploratory analyses when less restrictive subject identification algorithms were used. Conclusions Subjects with evidence of PAH had substantively high health care costs. Medical costs appeared to decrease following PAH medication use, but with a concomitant increase in pharmacy costs. Electronic supplementary material The online version of this article (doi:10.1186/s12913-014-0676-0) contains supplementary material, which is available to authorized users.


PAH, Costs, Resource use, Retrospective, Managed care, Pulmonary arterial hypertension


The economic burden of pulmonary arterial hypertension (PAH) in the US on payers and patients


Mirko Sikirica, Serban R Iorga, Tim Bancroft, and Jesse Potashcorresponding author

Publish date





Cognitive development in childhood is negatively affected by socioeconomic disadvantage. This study examined whether differences in fetal environment might mediate the association between family socioeconomic position and child development.

Data were linked from the Scottish Longitudinal Study, maternity inpatient records and the Child Health Surveillance Programme – Pre School for 32,238 children. The outcome variables were based on health visitor assessment of gross motor, hearing and language, vision and fine motor, and social development. Socioeconomic position was measured using parental social class and highest qualification attained. Random-effects logistic regression models were estimated to account for multiple reviews and familial clustering. Mediation analysis was conducted using the Karlson-Holm-Breen method.

Hearing and language, vision and fine motor, and social development were associated with lower parental social class and lower parental educational qualifications after adjustment for fetal environment. Fetal environment partially mediated the estimated effect of having parents without educational qualifications for hearing and language (β = 0·15; 95% confidence interval (CI) = 0·07, 0·23), vision and fine motor (β = 0·19; CI = 0·10, 0·28) and social development (β = 0·14; CI = 0·03 to 0·25).

Socioeconomic position predicted hearing and language, vision and fine motor, and social development but not gross motor development. For children of parents without educational qualifications, fetal environment appears to contribute to a part of the socioeconomic gradient in child development abnormalities but post-natal environment appears to still explain the majority of the gradient and for other children most of it.

Electronic supplementary material
The online version of this article (10.1186/s12939-017-0698-4) contains supplementary material, which is available to authorized users.


Birth weight, Lifecourse/childhood circumstances, Child health, Health inequalities, Socioeconomic


Socioeconomic disadvantage, fetal environment and child development: linked Scottish administrative records based study


Christopher James Playford,corresponding author1 Chris Dibben,2,3 and Lee Williamson3

Publish date