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  • Brand : BIOFRON

  • Catalogue Number : BF-H1006

  • Specification : 98%

  • CAS number : 6900-87-4

  • Formula : C33H45NO10

  • Molecular Weight : 615.711

  • PUBCHEM ID : 441737

  • Volume : 20mg

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Catalogue Number


Analysis Method






Molecular Weight



White powder

Botanical Source

Aconitum kusnezoffii,Aconitum carmichaelii

Structure Type







[(1S,2R,3R,4R,5R,6S,7S,8R,9R,13S,16S,17R,18R)-8-acetyloxy-5,7-dihydroxy-6,16,18-trimethoxy-13-(methoxymethyl)-11-methyl-11-azahexacyclo[,5.01,10.03,8.013,17]nonadecan-4-yl] benzoate


1.4±0.1 g/cm3


DMSO : 50 mg/mL (81.21 mM; Need ultrasonic)
H2O : < 0.1 mg/mL (insoluble)

Flash Point

359.8±31.5 °C

Boiling Point

671.3±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#:6900-87-4) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Background: Therapeutic applications of Fuzi (lateral root of Aconitum carmichaeli Debx) are seriously concerned with its toxic effects. Strategies and approaches to reducing toxicity are of great interest.

Purpose: We aimed to characterize the diurnal rhythm of Fuzi toxicity, and to determine the role of metabolism and pharmacokinetics in generating toxicity rhythmicity.

Methods: Toxicity was determined based on assessment of heart injury and animal survival after dosing mice with Fuzi decoction at different circadian time points. Circadian clock control of pharmacokinetics and toxicity was investigated using Bmal1-deficient (Bmal1-/-) mice.

Results: Fuzi exhibited a diurnal rhythmicity in cardiotoxicity (reflected by plasma CK-MB and LDH levels). The highest level of toxicity was observed at ZT10 (5 PM), while the lowest level of toxicity occurred at ZT22 (5 AM). Also, a higher mortality rate was observed at ZT10 and lower mortality rates at other times of the day. ZT10 dosing of Fuzi generated higher systemic exposures of three toxic alkaloid ingredients aconitine (AC), hypaconitine (HA) and mesaconitine (MA) compared to ZT22. This was accompanied by reduced the formation of the metabolites (N-deethyl-AC, didemethyl-HA and 2‑hydroxyl‑MA) at ZT10. Bmal1 ablation resulted in an increased level of Fuzi toxicity at ZT22, while having no influences when drug was dosed at ZT10. As a consequence, circadian time-dependent toxicity of Fuzi was lost in Bmal1-deficient mice. In addition, Bmal1 ablation increased the plasma concentrations of AC, HA and MA in mice after oral gavage of Fuzi, and reduced formation of their metabolites (N-deethyl-AC, didemethyl-HA and 2‑hydroxyl‑MA). Moreover, Fuzi metabolism in wild-type liver microsomes was more extensive at ZT22 than at ZT10. Bmal1 ablation abrogated circadian time-dependency of hepatic Fuzi metabolism.

Conclusions: Fuzi chronotoxicity in mice was attributed to time-varying hepatic metabolism and systemic exposure regulated by circadian clock. The findings may have implications in reducing Fuzi toxicity with a chronotherapeutic approach


Aconitine; Chronotherapeutics; Chronotoxicity; Circadian clock; Fuzi.


Zemin Yang 1, Yanke Lin 1, Lu Gao 1, Ziyue Zhou 1, Shuai Wang 1, Dong Dong 2, Baojian Wu 3

Publish date

2020 Feb;




Hypaconitine is an active and highly toxic constituent derived from Aconitum species. Here we aimed to determine the chronotoxicity of hypaconitine in mice, and to investigate a potential role of metabolism in hypaconitine chronotoxicity. Cardiac toxicity was assessed by measuring CK (creatine kinase) and LDH (lactate dehydrogenase) levels after hypaconitine administration to wild-type and Bmal1-/- (a clock disrupted model) mice at different times of day. The mRNA and protein levels of Cyp3a11 in mouse livers were determined by qPCR and western blotting, respectively. In vitro metabolism was assessed using liver microsomes. Pharmacokinetic study of hypaconitine was performed with wild-type mice. We observed injection time-dependent toxicity (i.e., a more severe toxicity during the light phase than the dark phase) for hypaconitine in mice. The chronotoxicity was attributed to a difference in systemic exposure of hypaconitine caused by time of day-dependent metabolism. Furthermore, circadian metabolism of hypaconitine was accounted for by the diurnal expression of Cyp3a11, a major enzyme for hypaconitine detoxification in the liver. Moreover, Bmal1 ablation in mice abolished the daily rhythm of Cyp3a11 expression and abrogated the time-dependency of hypaconitine toxicity. In conclusion, circadian Cyp3a11 metabolism contributed to chronotoxicity of hypaconitine in mice. This metabolism-based chronotoxicity would facilitate the formulation of best timing for drug administration.


Chronotoxicity; Circadian clock; Cyp3a11; Hypaconitine; Metabolism.


Circadian Cyp3a11 metabolism contributes to chronotoxicity of hypaconitine in mice


Yanke Lin 1, Ziyue Zhou 1, Zemin Yang 1, Lu Gao 1, Shuai Wang 1, Pei Yu 2, Baojian Wu 3

Publish date

2019 Aug 1;




Methodology/Principal Findings


Electrospray laser desorption ionization mass spectrometry; Emergency management; Herbal toxins; Point-of-care.


Rapid identification of herbal toxins using electrospray laser desorption ionization mass spectrometry for emergency care


Hung Su 1, Kuan-Ting Liu 2, Bai-Hsiun Chen 3, Yen-Ping Lin 1, Yu-Min Jiang 1, Yi-Hong Tsai 4, Fang-Rong Chang 5, Jentaie Shiea 6, Chi-Wei Lee 7

Publish date

2019 Apr

Description :

Effect of hypaconitine combined with liquiritin on the expression of calmodulin and connexin43 in rat cardiac muscle in vivo. PUMID/DOI:23058053 J Pharm Pharmacol. 2012 Nov;64(11):1654-8. The study indicated that Hypaconitine could inhibit CaM expression and Cx43 (Ser368) phosphorylation, and liquiritin could interfere with this kind of effect by synergistically inhibiting CaM expression and by antagonizing Cx43 (Ser368) dephosphorylation induced by Hypaconitine. Hypaconitine-induced QT prolongation mediated through inhibition of KCNH2 (hERG) potassium channels in conscious dogs. PUMID/DOI:25800797 J Ethnopharmacol. 2015 May 26;166:375-9. Hypaconitine is one of the main aconitum alkaloids in traditional Chinese medicines prepared with herbs from the genus Acotinum. These herbs are widely used for the treatment of cardiac insufficiency and arrhythmias. However, Acotinum alkaloids are known for their toxicity as well as their pharmacological activity, especially cardiotoxicity including QT prolongation, and the mechanism of this toxicity is not clear.These data suggest that Hypaconitine inhibits KCNH2 potassium channels and this effect might be the molecular mechanism underlying QT prolongation in conscious dogs.