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  • Brand : BIOFRON

  • Catalogue Number : BF-A3033

  • Specification : 98%

  • CAS number : 2883-98-9

  • Formula : C12H16O3

  • Molecular Weight : 208.25

  • PUBCHEM ID : 636822

  • Volume : 25mg

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Catalogue Number


Analysis Method






Molecular Weight



White crystalline powder

Botanical Source

Acorus gramineus

Structure Type



Standards;Natural Pytochemical;API




Benzene, 1,2,4-trimethoxy-5-[(1E)-1-propen-1-yl]-/trans-1,2,4-Trimethoxy-5-(1-propenyl)benzene/Asarin/1,2,4-trimethoxy-5-[(1E)-prop-1-en-1-yl]benzene/A-Asarion/trans-1,2,4-Trimethoxy-5-(1-propenyl)benzene,trans-1-Propenyl-2,4,5-trimethoxybenzene/Asaron/alpha-asarone/(E)-Asarone/benzene, 1,2,4-trimethoxy-5-[(1E)-1-propenyl]-/a-Asarone/α-Asarone/1,2,4-Trimethoxy-5-[(1E)-1-propen-1-yl]benzene/ASARONE,A/1,2,4-Trimethoxy-5-[(1E)-1-propen-1-yl]benzene/trans-Asarone/trans-2,4,5-trimethoxyphenylpropene/Asarone/trans-asaron/Etherophenol




1.0±0.1 g/cm3



Flash Point

107.7±23.8 °C

Boiling Point

296.0±0.0 °C at 760 mmHg

Melting Point

57-61 °C(lit.)


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#:2883-98-9) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Background: Neuropathic pain is an intractable and complex disease. Recent studies have shown a close relationship between endoplasmic reticulum (ER) stress and neuropathic pain. Here, we investigated the effect of α-asarone, an ER stress inhibitor, on chronic constriction injury (CCI)-induced neuropathic pain.
Methods: Two parts were included in this study. In part 1, rats were assigned to 7 groups: the sham group, the sham + α-asarone 20 mg/kg group, the CCI group, the CCI + vehicle group, the CCI + α-asarone 5 mg/kg group, the CCI + α-asarone 10 mg/kg group, and the CCI + α-asarone 20 mg/kg group. After surgery, the rats were treated with α-asarone or normal saline daily. Pain thresholds were measured, and samples of the L3-6 spinal cord were taken for western blotting and immunofluorescence on day 7. In part 2, rats were intrathecally implanted with PE-10 tubes and divided into 4 groups: the CCI + α-asarone 20 mg/kg group, the CCI + α-asarone 20 mg/kg + vehicle group, the CCI + α-asarone 20 mg/kg + SR9243 group, and the CCI group. Five rats in each group were separated for behavioral tests 1 hour after intrathecal injection. The rest of them were killed for western blotting on day 7.
Results: In this study, CCI surgery significantly induced mechanical allodynia and thermal hyperalgesia. CCI surgery significantly induced activation of ER stress (PERK-eIF2α, IRE1α, CHOP, and XBP-1s) in rats. However, treatment with 20 mg/kg of α-asarone significantly alleviated CCI-induced activation of ER stress. Behavioral results showed that daily treatment with 20 mg/kg of α-asarone significantly alleviated CCI-induced nociceptive behaviors, on day 7 (mechanical allodynia, P = .016, 95% confidence interval, 0.645-5.811; thermal hyperalgesia, P = .012, 95% confidence interval, 0.860-6.507). Furthermore, α-asarone induced upregulated expression of liver X receptor β (LXRβ) and downstream proteins in the spinal cord. The LXR antagonist SR9243 completely inhibited the anti-ER stress and antinociceptive effects of α-asarone in rats.
Conclusions: α-Asarone relieved CCI-induced neuropathic pain in an LXR-dependent manner. α-Asarone may be a potential agent for treatment of neuropathic pain.


α-Asarone Alleviated Chronic Constriction Injury-Induced Neuropathic Pain Through Inhibition of Spinal Endoplasmic Reticulum Stress in an Liver X Receptor-Dependent Manner


Yulong Gui 1 2 , Aiyuan Li 1 , Jie Zhang 1 , Guan Li 1 , Xia Ruan 1 , Qulian Guo 2 , Wangyuan Zou 2

Publish date

2018 Sep




α-asarone is natural bioactive compound that has been reported to have many benefits and medicinal properties. The present study aimed to assess the protective effect of α-asarone against doxorubicin (DOX) induced nephrotic syndrome in rats. An experimental nephrotic syndrome was induced by single intravenous injection of DOX (7 mg/kg) in rats. Animals were orally administered α-asarone (10 and 20 mg kg-1 d-1) for 4 weeks. Blood, urine and kidney tissues were collected for analyses at the end of the study. Treatment with α-asarone significantly improved kidney function by significantly inhibiting proteinuria, hypoalbuminemia, dyslipidemia, and restored antioxidant enzyme activities in kidney tissue. Furthermore, α-asarone ameliorated mRNA and protein expression of NF-κB, TNF-α, IL-6, and podocin in the kidney. Histopathological evidence also confirmed the protective effects of α-asarone against DOX-induced nephrotic syndrome. In conclusion, α-asarone has an anti-nephritic effect that might be attributed to its antioxidant, hypolipidaemic and anti-inflammatory activities.


α-Asarone Reduce Proteinuria by Restoring Antioxidant Enzymes Activities and Regulating Necrosis Factor κB Signaling Pathway in Doxorubicin-Induced Nephrotic Syndrome


Brijesh Sutariya 1 , Madhusudan Saraf 2

Publish date

2018 Feb




α-asarone, a bioactive compound found in Acorus plant species, has been shown to exhibit neuroprotective, anti-oxidative, anti-inflammatory, and cognitive-enhancing effects. However, the effects of α-asarone on spinal cord injury (SCI) have not yet been elucidated. The present study investigated the effects of α-asarone on the mRNA of pro-inflammatory cytokines, macrophage polarization toward an anti-inflammatory M2 phenotype, and angiogenesis in rats with compressive SCI. α-Asarone was orally administered (10 mg/kg) once per day for 14 days following moderate static compression SCI. Compared to controls, α-asarone treatment significantly improved locomotor score, prevented neuroinflammation, and facilitated angiogenesis in the spinal cord at 14 days after SCI. Furthermore, α-asarone significantly reduced the TNF-α, IL-1β, IL-6, monocyte chemoattractant protein 1 (MCP-1), macrophage inflammatory protein 2 (MIP-2), and inducible nitric oxide synthase (iNOS) levels but increased the IL-4, IL-10, and arginase 1 levels at 24 h after SCI. At 7 and 14 days after SCI, immunohistochemistry showed reduced reactive gliosis and neuroinflammation and an increased expression of M2 macrophage markers and angiogenesis. The results suggest that the inhibition of pro-inflammatory cytokines, macrophage polarization toward an anti-inflammatory M2 phenotype, and angiogenesis by α-asarone may be some of the mechanisms underlying the α-asarone-mediated neuroprotective effects on an injured spinal cord.


M2 polarization; anti-inflammation; neuroprotection; spinal cord injury; α-asarone.


Oral Administration of α-Asarone Promotes Functional Recovery in Rats With Spinal Cord Injury


Min-Jae Jo 1 , Hemant Kumar 1 , Hari P Joshi 1 , Hyemin Choi 1 , Wan-Kyu Ko 1 , J M Kim 1 , Sean S S Hwang 1 , Song Y Park 1 , Seil Sohn 1 , Alvin B Bello 2 , Kyoung-Tae Kim 3 , Soo-Hong Lee 2 , Xiang Zeng 4 , Inbo Han 1

Publish date

2018 May 7

Description :

Alpha-Asarone is one of the main psychoactive compounds, and possesses an antidepressant-like activity in mice.IC50 value:Target:In vitro: The results indicated that α-asarone significantly attenuated the LPS-stimulated increase in neuroinflammatory responses and suppressed pro-inflammatory cytokine production in BV-2 cells. Mechanistic study revealed that α-asarone?inhibited the LPS-stimulated activation via regulation of nuclear factor kappa-B by blocking degradation of inhibitor kappa B-alpha signaling in BV-2 microglial cells. [2]In vivo: The present results reveal that the acute treatment of α-asarone elicited biphasic responses on immobility such that the duration of the immobility time is significantly reduced at lower doses (15 and 20 mg/kg, i.p.) but increased at higher doses (50 and 100 mg/kg, i.p.) in the TST. Besides, α-asarone at higher doses (50 and 100 mg/kg, i.p.) significantly decreased the spontaneous locomotor activity.[1]