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Catalogue Number : BF-C2013
Specification : 98%
CAS number : 84605-18-5
Formula : C30H50O5
Molecular Weight : 490.71
Volume : 20mg

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Catalogue Number


Analysis Method






Molecular Weight



Botanical Source

Sapogenin from Astragalus galegiformis

Structure Type








1.2±0.1 g/cm3


DMSO : ≥ 100 mg/mL (203.78 mM)
H2O : < 0.1 mg/mL (insoluble)
*"≥" means soluble, but saturation unknown.

Flash Point

327.1±31.5 °C

Boiling Point

617.2±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#:84605-18-5) 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.




Background: Refractory wound healing is a severe complication of diabetes with a significant socioeconomic burden. Whereas current therapies are insufficient to accelerate repair, stem cell-based therapy is increasingly recognized as an alternative that improves healing outcomes. The aim of the present study is to explore the role of cycloastragenol (CAG), a naturally occurring compound in Astragali Radix, in ameliorating refractory cutaneous wound healing in vitro, which may provide a new insight into therapeutic strategy for diabetic wounds.

Methods: Human epidermal stem cells (EpSCs) obtained from nine patients were exposed to CAG, with or without DKK1 (a Wnt signaling inhibitor). A lentiviral short hairpin RNA (shRNA) system was used to establish the telomerase reverse transcriptase (TERT) and β-catenin knockdown cell line. Cell counting kit-8, scratch wound healing, and transwell migration assay were used to determine the effects of CAG in cell growth and migration. The activation of TERT, β-catenin, and c-Myc was determined using real-time qPCR and western blot analysis. Chromatin immunoprecipitation (ChIP) was performed to evaluate the associations among CAG, TERT, and Wnt/β-catenin signals.

Results: CAG not only promoted the proliferation and migration ability of EpSCs but also increased the expression levels of TERT, β-catenin, c-Myc. These effects of CAG were most pronounced at a dose of 0.3 μM. Notably, the CAG-promoted proliferative and migratory abilities of EpSCs were abrogated in TERT and β-catenin-silenced cells. In addition, the ChIP results strongly suggested that CAG-modulated TERT was closely associated with the activation of Wnt/β-catenin signaling.

Conclusion: Our data indicate that CAG is a TERT activator of EpSCs and is associated with their proliferation and migration, a role it may play through the activation of Wnt/β-catenin signaling.


The Potential Role of Cycloastragenol in Promoting Diabetic Wound Repair In Vitro


Yi Cao 1, Li Xu 2, Xiaohong Yang 2, Yuan Dong 3, Hongbin Luo 2, Fengling Xing 4, Qiongxiang Ge 2

Publish date

2019 Dec 18;




Psoriasis is a common chronic inflammatory skin disease, and the infiltrated macrophages in psoriatic skin lesions play a key role in the progression of this uncontrolled cutaneous inflammation. However, the current therapeutic strategies for patients with psoriasis are not satisfactory. Here, we report that cycloastragenol (CAG), a natural active small compound isolated from Astragalus membranaceus, significantly ameliorated imiquimod (IMQ)-induced psoriasiform dermatitis in mice by targeting proinflammatory macrophages. CAG significantly reduced the clinical scores, decreased the epidermal thickness, and ameliorated the deteriorating histopathology observed in IMQ-induced mice. CAG treatment specifically reduced the dermal infiltration of macrophages, rather than of dendritic cells, neutrophils, or T lymphocytes, into psoriatic skin. CAG dose-dependently decreased the level of proinflammatory cytokines, including IL-1β, TNF-α and IL-6, in murine psoriatic skin and serum, as well as in IMQ-stimulated, bone-marrow-derived macrophages. When compared to the control group, CAG significantly decreased IMQ-triggered NLRP3 inflammasome activation and gasdermin D-mediated cell pyroptosis in these proinflammatory macrophages. CAG also suppressed the assembly of the NLRP3 inflammasome complex. Taken together, the results show that CAG selectively modulates macrophage function by inhibiting NLRP3 inflammasome-mediated pyroptosis to ameliorate IMQ-induced psoriasis-like skin inflammation in mice. Our findings also identify an effective drug candidate for the treatment of psoriasis.


Cycloastragenol; Imiquimod; NLRP3 inflammasome; Psoriasis; Pyroptosis.


Inhibition of NLRP3 inflammasome-mediated pyroptosis in macrophage by cycloastragenol contributes to amelioration of imiquimod-induced psoriasis-like skin inflammation in mice


Guoliang Deng 1, Wenjun Chen 2, Peng Wang 1, Tianying Zhan 3, Wei Zheng 1, Zhengbing Gu 4, Xiaomei Wang 5, Xiaoyun Ji 6, Yang Sun 7

Publish date

2019 Sep




Background: Cycloastragenol (CAG), a triterpene aglycone is commonly prescribed for treating hypertension, cardiovascular disease, diabetic nephropathy, viral hepatitis, and various inflammatory-linked diseases.

Hypothesis: We investigated CAG for its action on signal transducer and activator of transcription 3 (STAT3) activation cascades, and its potential to sensitize gastric cancer cells to paclitaxel-induced apoptosis.

Methods: The effect of CAG on STAT3 phosphorylation and other hallmarks of cancer was deciphered using diverse assays in both SNU-1 and SNU-16 cells.

Results: We observed that CAG exhibited cytotoxic activity against SNU-1 and SNU-16 cells to a greater extent as compared to normal GES-1 cells. CAG predominantly caused negative regulation of STAT3 phosphorylation at tyrosine 705 through the abrogation of Src and Janus-activated kinases (JAK1/2) activation. We noted that CAG impaired translocation of STAT3 protein as well as its DNA binding activity. It further decreased cellular proliferation and mediated its anticancer effects predominantly by causing substantial apoptosis rather than autophagy. In addition, CAG potentiated paclitaxel-induced anti-oncogenic effects in gastric tumor cells.

Conclusions: Our results indicate that CAG can function to impede STAT3 activation in human gastric tumor cells and therefore it may be a suitable candidate agent for therapy of gastric cancer.


Apoptosis; Cancer; Cycloastragenol; Paclitaxel; STAT3.


Cycloastragenol can negate constitutive STAT3 activation and promote paclitaxel-induced apoptosis in human gastric cancer cells


Sun Tae Hwang 1, Chulwon Kim 1, Jong Hyun Lee 1, Arunachalam Chinnathambi 2, Sulaiman Ali Alharbi 2, Omar H M Shair 2, Gautam Sethi 3, Kwang Seok Ahn 4

Publish date

2019 Jun