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  • Brand : BIOFRON

  • Catalogue Number : BF-A4018

  • Specification : 98%(HPLC)

  • CAS number : 24502-78-1

  • Formula : C18H18O6

  • Molecular Weight : 330.33

  • PUBCHEM ID : 479501

  • Volume : 20mg

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Catalogue Number


Analysis Method






Molecular Weight



Red crystalline powder

Botanical Source

Arnebia euchroma

Structure Type



Standards;Natural Pytochemical;API




1'O-acetylshikonin/(1R)-1-(5,8-Dihydroxy-1,4-dioxo-1,4-dihydro-2-naphthalenyl)-4-methyl-3-penten-1-yl acetate/1,4-Naphthalenedione, 2-[(1R)-1-(acetyloxy)-4-methyl-3-penten-1-yl]-5,8-dihydroxy-/O-Acetylshikonin/Shikonin acetate/acethylshikonin/1,4-Naphthalenedione, 2-[1- (acetyloxy)-4-methyl-3-pentenyl]-5,8-dihydroxy-, (R)-/(1R)-1-(5,8-Dihydroxy-1,4-dioxo-1,4-dihydronaphthalen-2-yl)-4-methylpent-3-en-1-yl acetate/Acetylshikonin: 1,4-Naphthalenedione,2-[1-(acetyloxy)-4-methyl-3-pentenyl]-5,8-dihydroxy-, (R)-,/Shikonin,acetyl/acetyl shikonin/(R)-1-(5,8-dihydroxy-1,4-dioxo-1,4-dihydronaphthalen-2-yl)-4-methylpent-3-enyl acetate


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


1.3±0.1 g/cm3


Methanol; Ethyl Acetate

Flash Point

201.3±23.6 °C

Boiling Point

553.2±50.0 °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#:24502-78-1) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Cerebrovascular smooth muscle cell proliferation and migration contribute to hyperplasia in case of cerebrovascular remodeling and stroke. In the present study, we investigated the effects of acetylshikonin, the main ingredient of a Chinese traditional medicine Zicao, on human brain vascular smooth muscle cell (HBVSMCs) proliferation and migration induced by angiotensin II (AngII), and the underlying mechanisms. We found that acetylshikonin treatment significantly inhibited AngII-induced HBVSMCs proliferation and cell cycle transition from G1 to S phase. Wound-healing assay and Transwell assay showed that AngII-induced cell migration and invasion were markedly attenuated by acetylshikonin. In addition, AngII challenge significantly induced Wnt/β-catenin signaling activation, as evidenced by increased β-catenin phosphorylation and nuclear translocation and GSK-3β phosphorylation. However, acetylshikonin treatment inhibited the activation of Wnt/β-catenin signaling. Consequently, western blotting analysis revealed that acetylshikonin effectively reduced the expression of downstream target genes in AngII-treated cells, including c-myc, survivin and cyclin D1, which contributed to the inhibitory effect of acetylshikonin on HBVSMCs proliferation. Further, stimulation with recombinant Wnt3a dramatically reversed acetylshikonin-mediated inhibition of proliferation and cell cycle transition in HBVSMCs. Our study demonstrates that acetylshikonin prevents AngII-induced cerebrovascular smooth muscle cells proliferation and migration through inhibition of Wnt/β-catenin pathway, indicating that acetylshikonin may present a potential option for the treatment of cerebrovascular remodeling.


Acetylshikonin; Angiotensin II; Cerebrovascular smooth muscle cells; Proliferation; Wnt/β-catenin pathway.


Acetylshikonin Attenuates Angiotensin II-induced Proliferation and Motility of Human Brain Smooth Muscle Cells by Inhibiting Wnt/β-catenin Signaling


Zequn Li 1 , Zhiyuan Yan 1 , Chunbo Xu 1 , Yiqun Dong 1 , Ye Xiong 1 , Yongyue Dai 2

Publish date

2018 Jul




Acetylshikonin is a biologically active compound with anti-cancer and anti-inflammatory activity, which is isolated from the roots of Lithospermum erythrorhizoma. An inhibitory effect of acetylshikonin against CYP2J2 activity was discovered recently. Based on this result, this study was expanded to evaluate the inhibitory effects of acetylshikonin against nine different cytochrome P450 (P450) isoforms in human liver microsomes (HLMs) using substrate cocktails incubation assay. Acetylshikonin showed a strong inhibitory effect against all P450s tested with IC50 values of 1.4-4.0 μ m. Pre-incubation of acetylshikonin with HLMs and NADPH did not alter the inhibition potency, indicating that acetylshikonin is not a mechanism-based inhibitor. SKF-525A, a widely used non-specific P450 inhibitor, had no inhibitory activity against CYP1A2, 2A6, 2E1 and 2J2, while it showed an inhibitory effect against CYP2B6, CYP2C19 and 2D6 with IC50 values of 2.5, 3.6 and 0.5 μ m, respectively. Our findings indicate that acetylshikonin may be a novel general P450 inhibitor, which could replace SKF-525A.


Acetylshikonin; Angiotensin II; Cerebrovascular smooth muscle cells; Proliferation; Wnt/β-catenin pathway.


Acetylshikonin Is a Novel Non-Selective Cytochrome P450 Inhibitor


Jong Cheol Shon 1 , Nguyen Minh Phuc 2 , Won Cheol Kim 1 , Jae Kyung Heo 1 , Zhexue Wu 1 , Hyunyoung Lee 1 , Kwang-Hyeon Liu 1

Publish date

2017 Dec




Diabetic nephropathy (DN) is the major cause of end-stage renal disease in diabetic patients. Zicao, a well-known Chinese traditional medicine, has attracted much attention due to its beneficial effects in various medical fields. In this study, we attempted to investigate the effects and mechanisms of action of acetylshikonin, the main ingredient of Zicao, on renal dysfunction in DN. Our results showed that administration with acetylshikonin not only decreased blood urea nitrogen, urine creatinine and the mean kidney-to-body weight ratio in streptozotocin-induced diabetic mice, but also restored the loss of body weight, whereas the blood glucose was not changed. Masson’s trichrome staining showed that acetylshikonin treatment resulted in a marked decrease in kidney fibrosis from diabetic mice. The increased expression of fibrosis proteins, such as plasminogen activator inhibitor type 1 (PAI-1), connective tissue growth factor, and collagen III and IV, were reduced after acetylshikonin administration. In addition, the expressions of interleukin-1β, interleukin-6, monocyte chemoattractant protein-1, intercellular adhesion molecule 1 and infiltration of macrophages in kidney tissues were decreased in acetylshikonin-treated diabetic mice. Acetylshikonin led to a reduction of transforming growth factor-β1 (TGF-β1) expression and Smad-2/3 phosphorylation, as accompanied by increased Smad7 expression. Furthermore, in vitro treatment with acetylshikonin markedly attenuated TGF-β1-induced the PAI-1, collagen III and IV, and Smad-2/3 phosphorylation in HK2 immortalized human proximal tubule epithelial cells. Acetylshikonin also prevented epithelial-to-mesenchymal transition induced by TGF-β1. Collectively, our study provides evidences that acetylshikonin attenuates renal fibrosis though inhibiting TGF-β1/Smad signaling pathway, suggesting that acetylshikonin may be a novel therapeutic agent for the treatment of DN.


Acetylshikonin; Diabetic nephropathy; Inflammation; Renal fibrosis; TGF-β1/Smad.


Acetylshikonin From Zicao Ameliorates Renal Dysfunction and Fibrosis in Diabetic Mice by Inhibiting TGF-β1/Smad Pathway


Zezhao Li 1 , Zhen Hong 2 , Zhiqing Peng 3 , Yongcai Zhao 4 , Rusheng Shao 2

Publish date

2018 Jul

Description :

Acetylshikonin, derived from the root of Lithospermum erythrorhizon, has anti-cancer and antiinflammation activity. Acetylshikonin is a non-selective cytochrome P450 inhibitor against all P450s (IC50 values range from 1.4-4.0 μM). Acetylshikonin is an AChE inhibitor and exhibits potent antiapoptosis activity[1][2][3].