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  • Brand : BIOFRON

  • Catalogue Number : BF-M3016

  • Specification : 98%

  • CAS number : 607-91-0

  • Formula : C11H12O3

  • Molecular Weight : 192.21

  • PUBCHEM ID : 4276

  • Volume : 100mg

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Catalogue Number


Analysis Method






Molecular Weight



Yellow liquid

Botanical Source

Ligusticum sinense

Structure Type



Standards;Natural Pytochemical;API




myristicine/4-methoxy-6-prop-2-en-1-yl-1,3-benzodioxole/6-Allyl-4-methoxy-1,3-benzodioxole/1,3-Benzodioxole, 4-methoxy-6-(2-propen-1-yl)-/Myristicin/4-Methoxy-6-(2-propen-1-yl)-1,3-benzodioxole/3-methoxy-4,5-methylenedioxyallylbenzene/1-allyl-4,5-methylenedioxy-3-methoxybenzene




1.1±0.1 g/cm3


Methanol; Ethyl Acetate; Chloroform

Flash Point

89.8±16.0 °C

Boiling Point

276.5±0.0 °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#:607-91-0) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Myristicin is widely distributed in spices and medicinal plants. The aim of this study was to explore the role of metabolic activation of myristicin in its potential toxicity through a metabolomic approach. The myristicin- N-acetylcysteine adduct was identified by comparing the metabolic maps of myristicin and 1′-hydroxymyristicin. The supplement of N-acetylcysteine could protect against the cytotoxicity of myristicin and 1′-hydroxymyristicin in primary mouse hepatocytes. When the depletion of intracellular N-acetylcysteine was pretreated with diethyl maleate in hepatocytes, the cytotoxicity induced by myristicin and 1′-hydroxymyristicin was deteriorated. It suggested that the N-acetylcysteine adduct resulting from myristicin bioactivation was closely associated with myristicin toxicity. Screening of human recombinant cytochrome P450s (CYPs) and treatment with CYP inhibitors revealed that CYP1A1 was mainly involved in the formation of 1′-hydroxymyristicin. Collectively, this study provided a global view of myristicin metabolism and identified the N-acetylcysteine adduct resulting from myristicin bioactivation, which could be used for understanding the mechanism of myristicin toxicity.


1′-hydroxymyristicin; metabolic activation; metabolomics; myristicin


Metabolic Activation of Myristicin and Its Role in Cellular Toxicity.


Zhu X1,2, Wang YK1,2, Yang XN1,3, Xiao XR1, Zhang T1,2, Yang XW4, Qin HB1, Li F1,5.

Publish date

2019 Apr 17




The present study describes physiologically based kinetic (PBK) models for the alkenylbenzene myristicin that were developed by extension of the PBK models for the structurally related alkenylbenzene safrole in rat and human. The newly developed myristicin models revealed that the formation of the proximate carcinogenic metabolite 1′-hydroxymyristicin in liver is at most 1.8 fold higher in rat than in human and limited for the ultimate carcinogenic metabolite 1′-sulfoxymyristicin to (2.8-4.0)-fold higher in human. In addition, a comparison was made between the relative importance of bioactivation for myristicin and safrole. Model predictions indicate that for these related compounds, the formation of the 1′-sulfoxy metabolites in rat and human liver is comparable with a difference of <2.2-fold over a wide dose range. The results from this PBK analysis support that risk assessment of myristicin may be based on the BMDL10 derived for safrole of 1.9-5.1 mg/kg bw per day. Using an estimated daily intake of myristicin of 0.0019 mg/kg bw per day resulting from the use of herbs and spices, this results in MOE values for myristicin that amount to 1000-2700, indicating a priority for risk management. The results obtained illustrate that PBK modeling provides insight into possible species differences in the metabolic activation of myristicin. Moreover, they provide an example of how PBK modeling can facilitate a read-across in risk assessment from a compound for which in vivo toxicity studies are available to a related compound for which tumor data are not reported, thus contributing to alternatives in animal testing.


Alkenylbenzenes; Myristicin; Physiologically based kinetic (PBK) modeling; Read-across-based risk assessment; Safrole


Physiologically based kinetic modeling of the bioactivation of myristicin.


Al-Malahmeh AJ1,2, Al-Ajlouni A3,4, Wesseling S3, Soffers AE3, Al-Subeihi A5, Kiwamoto R3, Vervoort J6, Rietjens IM3.

Publish date

2017 Feb




The effects of osmotic dehydration (OD) treatment on volatile compound (myristicin) content and the antioxidant capacity of nutmeg (Myristica fragrans) were studied. Fresh nutmeg pericarps were treated with varying sugar concentrations (60, 70, 80%) with different soaking periods at ambient temperature. The OD-treated nutmeg extracts were analyzed for myristicin content via Gas Chromatography Flame Ionization Detector. The phenolic content and antioxidant capacity were analyzed using Follin-Ciocalteu and a free radical scavenging activity assay. The myristicin content was highest (1.69 mg/100 mg) at 80% sugar concentration after 3 h of soaking. Total phenolic content and free radical scavenging activity were highest at 3 h of 80% sugar solution treatment with values of 76.90% and 1.75 mg GAE/g, respectively. OD treatment at varying sugar concentration levels and durations affects the production of myristicin and antioxidant composition. Treatment of nutmeg with OD at 80% sugar concentration for 3 h is preferable, resulting in an acceptable level of myristicin and high antioxidants.


Myristicin; Nutmeg; Solid phase extraction; Total phenolic content; Ultrasonic extraction


Effects of osmotic dehydration treatment on volatile compound (Myristicin) content and antioxidants property of nutmeg (Myristica fragrans) pericarp.


Rahman N1, Xin TB1, Kamilah H1, Ariffin F1.

Publish date

2018 Jan

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