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  • Brand : BIOFRON

  • Catalogue Number : BD-D0731

  • Specification : HPLC≥98%

  • CAS number : 52438-12-7

  • Formula : C20H22O6

  • Molecular Weight : 358.39

  • PUBCHEM ID : 479500

  • Volume : 10mg

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Catalogue Number


Analysis Method






Molecular Weight



White crystalline powder

Botanical Source

Lithospermum erythrorhizon

Structure Type



Standards;Natural Pytochemical;API




(R)-1-(1,4-Dihydro-5,8-dihydroxy-1,4-dioxonaphthalen-2-yl)-4-methyl-3-pentenyl=isobutyrate/2-Methylpropanoic acid (R)-1-[(1,4-dioxo-5,8-dihydroxy-1,4-dihydronaphthalene)-2-yl]-4-methyl-3-pentenyl ester/1-(2,6-Diphenyltetrahydro[1,3]dioxino[5,4-d][1,3]dioxin-4-yl)ethane-1,2-diol (non-preferred name)/1-(2,6-Diphenyltetrahydro[1,3]dioxino[5,4-d][1,3]dioxin-4-yl)-1,2-ethanediol/5,8-DIHYDROXY-2-(1-ISOBUTYRYLOXY-4-METHYL-3-PENTENYL)-1,4-NAPHTHALENEDIONE/2-[1-(Isobutyryloxy)-4-methyl-3-pentenyl]-5,8-dihydroxy-1,4-naphthoquinone/Isobutylshikonin/(1,3:2,4) Dibenzylidene sorbitol (DBS)


[(1R)-1-(5,8-dihydroxy-1,4-dioxonaphthalen-2-yl)-4-methylpent-3-enyl] 2-methylpropanoate



1.3±0.1 g/cm3


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

Flash Point

295.6±28.7 °C

Boiling Point

565.2±45.0 °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#:52438-12-7) 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.




Hypertension is a major risk factor for many cardiovascular diseases and leads to subsequent concomitant pathologies such as left ventricular hypertrophy (LVH). Translational approaches using large animals get more important as they allow the use of standard clinical procedures in an experimental setting. Therefore, the aim of this study was to establish a minimally invasive ovine hypertension model using chronic angiotensin II (ANG II) treatment and to characterize its effects on cardiac remodeling after 8 weeks. Sheep were implanted with osmotic minipumps filled with either vehicle control (n = 7) or ANG II (n = 9) for 8 weeks. Mean arterial blood pressure in the ANG II‐treated group increased from 87.4 ± 5.3 to 111.8 ± 6.9 mmHg (P = 0.00013). Cardiovascular magnetic resonance imaging showed an increase in left ventricular mass from 112 ± 12.6 g to 131 ± 18.7 g after 7 weeks (P = 0.0017). This was confirmed by postmortem measurement of left ventricular wall thickness which was higher in ANG II‐treated animals compared to the control group (18 ± 4 mm vs. 13 ± 2 mm, respectively, P = 0.002). However, ANG II‐treated sheep did not reveal any signs of fibrosis or inflammatory infiltrates as defined by picrosirius red and H&E staining on myocardial full thickness paraffin sections of both atria and ventricles. Measurements of plasma high‐sensitivity C‐reactive protein and urinary 8‐iso‐prostaglandin F2α were inconspicuous in all animals. Furthermore, multielectrode surface mapping of the heart did not show any differences in epicardial conduction velocity and heterogeneity. These data demonstrate that chronic ANG II treatment using osmotic minipumps presents a reliable, minimally invasive approach to establish hypertension and nonfibrotic LVH in sheep


Angiotensin II, CMR, hypertension, left ventricular hypertrophy


Development of nonfibrotic left ventricular hypertrophy in an ANG II‐induced chronic ovine hypertension model


Niklas Klatt, 1 , 2 , † Katharina Scherschel, 1 , 2 , † Claudia Schad, 1 , 2 Denise Lau, 2 , 3 Aline Reitmeier, 1 , 2 Pawel Kuklik, 1 Kai Muellerleile, 3 Jin Yamamura, 4 Tanja Zeller, 2 , 3 Daniel Steven, 5 Stephan Baldus, 5 Benjamin Schaffer, 1 Christiane Jungen, 1 , 2 Christian Eickholt, 1 Katharina Wassilew, 6 , 7 , 8 Edzard Schwedhelm, 2 , 9 Stephan Willems, 1 , 2 and Christian Meyercorresponding author 1 , 2

Publish date

2016 Sep;




Human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) represent an unlimited source of human CMs that could be a standard tool in drug research. However, there is concern whether hiPSC-CMs express all cardiac ion channels at physiological level and whether they might express non-cardiac ion channels. In a control hiPSC line, we found large, “noisy” outward K+ currents, when we measured outward potassium currents in isolated hiPSC-CMs. Currents were sensitive to iberiotoxin, the selective blocker of big conductance Ca2+-activated K+ current (IBK,Ca). Seven of 16 individual differentiation batches showed a strong initial repolarization in the action potentials (AP) recorded from engineered heart tissue (EHT) followed by very early afterdepolarizations, sometimes even with consecutive oscillations. Iberiotoxin stopped oscillations and normalized AP shape, but had no effect in other EHTs without oscillations or in human left ventricular tissue (LV). Expression levels of the alpha-subunit (KCa1.1) of the BKCa correlated with the presence of oscillations in hiPSC-CMs and was not detectable in LV. Taken together, individual batches of hiPSC-CMs can express sarcolemmal ion channels that are otherwise not found in the human heart, resulting in oscillating afterdepolarizations in the AP. HiPSC-CMs should be screened for expression of non-cardiac ion channels before being applied to drug research.


human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs), iPS cells, stem cells, big conductance calcium activated potassium channel (BK), Maxi-K, slo1, KCa1.1, iberiotoxin, long QT syndrome


Case Report on: Very Early Afterdepolarizations in HiPSC-Cardiomyocytes—An Artifact by Big Conductance Calcium Activated Potassium Current (Ibk,Ca)


Andras Horvath,1,2,3,†‡ Torsten Christ,1,2,*† Jussi T. Koivumaki,4 Maksymilian Prondzynski,1,2,§ Antonia T. L. Zech,1,2 Michael Spohn,5 Umber Saleem,1,2 Ingra Mannhardt,1,2 Barbel Ulmer,1,2 Evaldas Girdauskas,2,6 Christian Meyer,3,7 Arne Hansen,1,2 Thomas Eschenhagen,1,2 and Marc D. Lemoine1,2,7,*

Publish date

2020 Jan;




In most vertebrates, the liver produces bile that is necessary to emulsify absorbed fats and enable the digestion of lipids in the small intestine as well as to excrete bilirubin and other metabolic products. In the liver, the experimental obstruction of the extrahepatic biliary system initiates a complex cascade of pathological events that leads to cholestasis and inflammation resulting in a strong fibrotic reaction originating from the periportal fields. Therefore, surgical ligation of the common bile duct has become the most commonly used model to induce obstructive cholestatic injury in rodents and to study the molecular and cellular events that underlie these pathophysiological mechanisms induced by inappropriate bile flow. In recent years, different surgical techniques have been described that either allow reconnection or reanastomosis after bile duct ligation (BDL), e.g., partial BDL, or other microsurgical methods for specific research questions. However, the most frequently used model is the complete obstruction of the common bile duct that induces a strong fibrotic response after 21 to 28 days. The mortality rate can be high due to infectious complications or technical inaccuracies. Here we provide a detailed surgical procedure for the BDL model in mice that induce a highly reproducible fibrotic response in accordance to the 3R rule for animal welfare postulated by Russel and Burch in 1959.


Medicine, Issue 96, bile duct ligation, cholestasis, bile obstruction, hepatic fibrosis, inflammation, extracellular matrix, jaundice, mouse


Bile Duct Ligation in Mice: Induction of Inflammatory Liver Injury and Fibrosis by Obstructive Cholestasis


Carmen G. Tag, 1 Sibille Sauer-Lehnen, 1 Sabine Weiskirchen, 1 Erawan Borkham-Kamphorst, 1 Rene H. Tolba, 2 Frank Tacke, 3 and Ralf Weiskirchen 1

Publish date