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Ilexgenin A


  • Brand : BIOFRON

  • Catalogue Number : BD-P0718

  • Specification : 98.0%(HPLC)

  • CAS number : 108524-94-3

  • Formula : C30H46O6

  • Molecular Weight : 502.7

  • PUBCHEM ID : 21672638

  • Volume : 25mg

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Catalogue Number


Analysis Method





Molecular Weight



Botanical Source

Structure Type





Myriaboric acid/Urs-12-ene-24,28-dioic acid, 3,19-dihydroxy-, (3β)-/(3β)-3,19-Dihydroxyurs-12-ene-24,28-dioic acid


(3S,4R,4aR,6aR,6bS,8aS,11R,12R,12aS,14aR,14bR)-3,12-dihydroxy-4,6a,6b,11,12,14b-hexamethyl-1,2,3,4a,5,6,7,8,9,10,11,12a,14,14a-tetradecahydropicene-4,8a-dicarboxylic acid



1.2±0.1 g/cm3


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

Flash Point

362.9±28.0 °C

Boiling Point

653.3±55.0 °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#:108524-94-3) 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.




Because large, prospective, population-based data sets describing maternal outcomes are typically not available in low- and middle-income countries, it is difficult to monitor maternal mortality rates over time and to identify factors associated with maternal mortality. Early identification of risk factors is essential to develop comprehensive intervention strategies preventing pregnancy-related complications. Our objective was to describe maternal mortality rates in a large, multi-country dataset and to determine maternal, pregnancy-related, delivery and postpartum characteristics that are associated with maternal mortality.

We collected data describing all pregnancies from 2010 to 2013 among women enrolled in the multi-national Global Network for Women’s and Children’s Health Research Maternal and Neonatal Health Registry (MNHR). We reported the proportion of mothers who died per pregnancy and the maternal mortality ratio (MMR). Generalized linear models were used to evaluate the relationship of potential medical and social factors and maternal mortality and to develop point and interval estimates of relative risk associated with these factors. Generalized estimating equations were used to account for the correlation of outcomes within cluster to develop appropriate confidence intervals.

We recorded 277,736 pregnancies and 402 maternal deaths for an MMR of 153/100,000 live births. We observed an improvement in the total MMR from 166 in 2010 to 126 in 2013. The MMR in Latin American sites (91) was lower than the MMR in Asian (178) and African sites (125). When adjusted for study site and the other variables, no formal education (RR 3.2 [1.5, 6.9]), primary education only (RR 3.4 [1.6, 7.5]), secondary education only (RR 2.5 [1.1, 5.7]), lack of antenatal care (RR 1.8 [1.2, 2.5]), caesarean section delivery (RR 1.9 [1.3, 2.8]), hemorrhage (RR 3.3 [2.2, 5.1]), and hypertensive disorders (RR 7.4 [5.2, 10.4]) were associated with higher risks of death.

The MNHR identified preventable causes of maternal mortality in diverse settings in low- and middle-income countries. The MNHR can be used to monitor public health strategies and determine their association with reducing maternal mortality.

Trial Registration NCT01073475


Risk factors for maternal death and trends in maternal mortality in low- and middle-income countries: a prospective longitudinal cohort analysis


Melissa Bauserman,corresponding author1 Adrien Lokangaka,2 Vanessa Thorsten,3 Antoinette Tshefu,2 Shivaprasad S Goudar,4 Fabian Esamai,5 Ana Garces,6 Sarah Saleem,7 Omrana Pasha,7 Archana Patel,8 Albert Manasyan,9 Mabel Berrueta,10 Bhala Kodkany,4 Elwyn Chomba,9 Edward A Liechty,11 K Michael Hambidge,12 Nancy F Krebs,12 Richard J Derman,13 Patricia L Hibberd,14 Fernando Althabe,10 Waldemar A Carlo,15 Marion Koso-Thomas,16 Robert L Goldenberg,17 Dennis D Wallace,3 Elizabeth M McClure,3 and Carl L Bose1

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To improve care and control for patients with adult-onset asthma, a better understanding of determinants of their risk and outcomes is important. We investigated how associations between asthma, asthma control and obesity may be modified by patient demographic characteristics.

This retrospective study of adults enrolled in several health plans across the U.S. (n = 2,860,305) examined the interacting effects of obesity, age, race, and sex on adult-onset asthma and asthma control. Multivariable adjusted Cox and logistic regression models estimated hazard ratios (HR), and 95 % confidence intervals (CI) for the associations between body mass index (BMI) and study outcomes, and interactions of BMI with demographic characteristics.

Compared with individuals who had a BMI <25 kg/m2, the hazard of adult-onset asthma progressively increased with increasing BMI, from a 12 % increase among persons with a BMI of 25.0-29.9 kg/m2 (HR 1.12, 95 % CI 1.10, 1.14) to an almost 250 % increase among persons with a BMI ≥50 kg/m2 (HR 2.49, 95 % CI 2.38, 2.60). The magnitude of the association between obesity and asthma risk was greater for women (compared with men) and lower for Blacks (compared with non-Hispanic Whites). Among individuals with asthma, obesity was associated with poorly controlled and high-risk asthma. Conclusions The present study demonstrates that the magnitude of the associations between obesity and adult-onset asthma incidence and control are modified by race, age, and sex. Understanding the role of obesity in the development of adult-onset asthma will help to improve asthma treatment algorithms and to develop targeted interventions.


Asthma, Adult-onset, Obesity, Race, Sex, Ethnicity


Interacting effects of obesity, race, ethnicity and sex on the incidence and control of adult-onset asthma


Corinna Koebnick,corresponding author1 Heidi Fischer,1 Matthew F. Daley,2 Assiamira Ferrara,3 Michael A. Horberg,4 Beth Waitzfelder,5 Deborah Rohm Young,1 and Michael K. Gould1

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Idiopathic pulmonary arterial hypertension (IPAH) continues to be one of the most serious intractable diseases that might start with activation of several triggers representing the genetic susceptibility of a patient. To elucidate what essentially contributes to the onset and progression of IPAH, we investigated factors playing an important role in IPAH by searching discrepant or controversial expression patterns between our murine model and those previously published for human IPAH. We employed the mouse model, which induced muscularization of pulmonary artery leading to hypertension by repeated intratracheal injection of Stachybotrys chartarum, a member of nonpathogenic and ubiquitous fungus in our envelopment.

Microarray assays with ontology and pathway analyses were performed with the lungs of mice. A comparison was made of the expression patterns of biological pathways between our model and those published for IPAH.

Some pathways in our model showed the same expression patterns in IPAH, which included bone morphogenetic protein (BMP) signaling with down-regulation of BMP receptor type 2, activin-like kinase type 1, and endoglin. On the other hand, both Wnt/planar cell polarity (PCP) signaling and its downstream Rho/ROCK signaling were found alone to be activated in IPAH and not in our model.

Activation of Wnt/PCP signaling, in upstream positions of the pathway, found alone in lungs from end stage IPAH may play essential roles in the pathogenesis of the disease.


Pulmonary Vascular Remodeling, Stachybotrys chartarum, BMP signaling, BMPR2, PCP pathway


Gene expression analysis of a murine model with pulmonary vascular remodeling compared to end-stage IPAH lungs


Kayoko Shimodaira, Yoichiro Okubo, Eri Ochiai, Haruo Nakayama, Harutaka Katano, Megumi Wakayama, Minoru Shinozaki, Takao Ishiwatari, Daisuke Sasai, Naobumi Tochigi, Tetsuo Nemoto, Tsutomu Saji, Katsuhiko Kamei, Kazutoshi Shibuya

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