We Offer Worldwide Shipping
Login Wishlist



  • Brand : BIOFRON

  • Catalogue Number : BF-R2003

  • Specification : 98%

  • CAS number : 472-11-7

  • Formula : C27H42O4

  • Molecular Weight : 430.62

  • PUBCHEM ID : 441893

  • Volume : 20mg

In stock

Checkout Bulk Order?

Catalogue Number


Analysis Method






Molecular Weight



White crystal

Botanical Source

root of Ophiopogon japonicus

Structure Type



Standards;Natural Pytochemical;API




(1β,3β,25R)-Spirost-5-ene-1,3-diol/25D-Spirost-5-ene-1|A,3|A-diol/(25R)-Spirost-5-ene-1b,3b-diol/(25R)-Spirost-5-ene-1β,3β-diol/(1β,3β,25R)-Spirost-5-en-1,3-diol/Spirost-5-en-1,3-diol, (1β,3β,25R)-




1.2±0.1 g/cm3


Methanol; Acetone

Flash Point

294.4±30.1 °C

Boiling Point

563.1±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#:472-11-7) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Ruscogenin, an important steroid sapogenin derived from Ophiopogon japonicus, has been shown to inhibit cerebral ischemic injury. However, its potential molecular action on blood-brain barrier (BBB) dysfunction after stroke remains unclear. This study aimed to investigate the effects of ruscogenin on BBB dysfunction and the underlying mechanisms in middle cerebral artery occlusion/reperfusion (MCAO/R)-injured mice and oxygen-glucose deprivation/reoxygenation (OGD/R)-injured mouse brain microvascular endothelial cells (bEnd.3). The results demonstrated that administration of ruscogenin (10 mg/kg) decreased the brain infarction and edema, improved neurological deficits, increased cerebral brain flow (CBF), ameliorated histopathological damage, reduced evans blue (EB) leakage and upregulated the expression of tight junctions (TJs) in MCAO/R-injured mice. Meanwhile, ruscogenin (0.1-10 µM) treatment increased cell viability and trans-endothelial electrical resistance (TEER) value, decreased sodium fluorescein leakage, and modulated the TJs expression in OGD/R-induced bEnd.3 cells. Moreover, ruscogenin also inhibited the expression of interleukin-1β (IL-1β) and caspase-1, and markedly suppressed the expression of Nucleotide-binding domain (NOD)-like receptor family, pyrin domain containing 3 (NLRP3) and thiredoxin-interactive protein (TXNIP) in vivo and in vitro. Furthermore, ruscogenin decreased reactive oxygen species (ROS) generation and inhibited the mitogen-activated protein kinase (MAPK) pathway in OGD/R-induced bEnd.3 cells. Our findings provide some new insights into its potential application for the prevention and treatment of ischemic stroke.


MAPK; blood-brain barrier; inflammasome; ischemic stroke; ruscogenin.


Ruscogenin Attenuates Cerebral Ischemia-Induced Blood-Brain Barrier Dysfunction by Suppressing TXNIP/NLRP3 Inflammasome Activation and the MAPK Pathway


Guosheng Cao 1 , Nan Jiang 2 , Yang Hu 3 , Yuanyuan Zhang 4 , Guangyun Wang 5 , Mingzhu Yin 6 , Xiaonan Ma 7 , Kecheng Zhou 8 , Jin Qi 9 , Boyang Yu 10 , Junping Kou 11

Publish date

2016 Aug 29




Background: Hepatocellular carcinoma (HCC) is the third-leading cause of cancer-related mortality with poor prognosis and treatment. More effective strategies should be studied in HCC.
Methods: After treated with ruscogenin, the cell proliferation was assessed by CCK-8 method. Cell migration and invasion were estimated using wound healing and transwell assays. Pathological changes of lung tissue were observed by HE staining and IHC methods. MMP-2, MMP-9, uPA, VEGF and HIF-1α levels were measured using ELISA, RT-qPCR and WB tests. PI3K/Akt/mTOR pathway related molecules were detected using WB analysis.
Results: The results indicated the hypotoxicity of ruscogenin. Meanwhile, ruscogenin showed obvious interruption on the cancer cell migration and invasion, and inhibition on the metastatic foci in pulmonary tissue. Significantly, ruscogenin decreased the levels of MMP-2, MMP-9, uPA, VEGF and HIF-1α, down-regulated the phosphorylation of Akt, mTOR.
Conclusion: The present study indicated a novel use of ruscogenin in suppressing HCC metastasis by reducing the expression of MMP-2, MMP-9, uPA, VEGF and HIF-1α via regulating the PI3K/Akt/mTOR signaling pathway.


MAPK; blood-brain barrier; inflammasome; ischemic stroke; ruscogenin.


Ruscogenin Suppressed the Hepatocellular Carcinoma Metastasis via PI3K/Akt/mTOR Signaling Pathway


Hui Hua 1 , Yu Zhu 2 , Yu-He Song 3

Publish date

2018 May




Ruscogenin, a natural steroidal sapogenin, presents in both food and medicinal plants. It has been found to exert significant anti-inflammatory activities. Considering that activation of neutrophil is a key feature of inflammatory diseases, this study was performed to investigate the inhibitory effect of ruscogenin and its underlying mechanisms responsible for neutrophil activation. Ruscogenin displayed potent antioxidative effects against Formyl-Met-Leu-Phe (FMLP)-induced extra- and intracellular superoxide generation in mouse bone marrow neutrophils, with IC50 values of 1.07±0.32 μM and 1.77±0.46 μM, respectively. Phorbol myristate acetate (PMA)-elicited extra- and intracellular superoxide generation were also suppressed by ruscogenin, with IC50 values of 1.56±0.46 μM and 1.29±0.49 μM, respectively. However, ruscogenin showed weak inhibition in NaF-induced response. Inhibition of superoxide generation was mediated neither by a superoxide-scavenging ability nor by a cytotoxic effect. Furthermore, ruscogenin inhibited the membrane translocation of p47phox and p67phox. It reduced FMLP-induced phosphorylation of cytosolic phospholipase A2 (cPLA2) and p21-activated kinase (PAK). The cellular cyclic adenosine monophosphate (cAMP) levels and protein kinase A (PKA) expression were increased by ruscogenin. Moreover, ruscogenin inhibited phosphorylation of protein kinase B (Akt), p38 mitogen-activated protein kinase (p38MAPK), extracellular signal-regulated kinase 1 and 2 (ERK1/2), and c-Jun N-terminal kinase (JNK). In addition, the inhibitory effects of ruscogenin on superoxide production and the phosphorylation of Akt, p38MAPK, and ERK1/2 were reversed by PKA inhibitor (H89), suggesting a PKA-dependent mechanism. In summary, our data suggest that ruscogenin inhibits activation of neutrophil through cPLA2, PAK, Akt, MAPKs, cAMP, and PKA signaling pathways. Increased PKA activity is associated with suppression of the phosphorylation of Akt, p38MAPK, and ERK1/2 pathways.


NADPH oxidase; Neutrophils; Ruscogenin; Signaling pathways; Superoxide anion.


Ruscogenin Suppresses Mouse Neutrophil Activation: Involvement of Protein Kinase A Pathway


Y N Lin 1 , R Jia 1 , Y H Liu 1 , Y Gao 1 , L L Wang 1 , J P Kou 2 , B Y Yu 3

Publish date

2015 Nov

Description :

Ruscogenin, an important steroid sapogenin derived from Ophiopogon japonicus, attenuates cerebral ischemia-induced blood-brain barrier dysfunction by suppressing TXNIP/NLRP3 inflammasome activation and the MAPK pathway and exerts significant anti-inflammatory and anti-thrombotic activities[1][2].