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Epimagnolin B Sale

(Synonyms: 表木兰脂素 B) 目录号 : GC38618

Epimagnolin B 是从木兰中分离得到的一种具有抗炎活性的双环氧木质素。Epimagnolin B 抑制 LPS 激活的小胶质细胞中 NO 的产生。Epimagnolin B 具有抗过敏作用。

Epimagnolin B Chemical Structure

Cas No.:1134188-26-3

规格 价格 库存 购买数量
1mg
¥1,008.00
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5mg
¥3,024.00
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10mg
¥5,139.00
现货

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Sample solution is provided at 25 µL, 10mM.

产品文档

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产品描述

Epimagnolin B is a bisepoxylignan isolated from Magnolia fargesii, with anti-inflammatory activity and antiallergic effects. Epimagnolin B inhibits NO production in LPS-activated microglia. Epimagnolin B exhibited antiallergic effects[1][2].

Epimagnolin B exhibits antiallergic effects without affecting the viability of BMMCs[1].

[1]. Kim JY, et al. In vitro anti-inflammatory activity of lignans isolated from Magnolia fargesii. Bioorg Med Chem Lett. 2009 Feb 1;19(3):937-40. [2]. Xing Zhang, et al. Bioassay-guided isolation of bisepoxylignans from the flower buds of Magnolia biondii Pamp and their antiallergic effects.  RSC Advances. July 2017;7(54):34236-34243.

Chemical Properties

Cas No. 1134188-26-3 SDF
别名 表木兰脂素 B
Canonical SMILES COC1=C(OC)C(OC)=CC([C@@H]2[C@]3([H])[C@]([C@H](C4=CC(OC)=CC(OC)=C4)OC3)([H])CO2)=C1
分子式 C23H28O7 分子量 416.46
溶解度 Soluble in DMSO 储存条件 Store at -20°C
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溶解性数据

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1 mg 5 mg 10 mg
1 mM 2.4012 mL 12.006 mL 24.0119 mL
5 mM 0.4802 mL 2.4012 mL 4.8024 mL
10 mM 0.2401 mL 1.2006 mL 2.4012 mL
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Research Update

In vitro anti-inflammatory activity of lignans isolated from Magnolia fargesii

Bioorg Med Chem Lett 2009 Feb 1;19(3):937-40.PMID:19110419DOI:10.1016/j.bmcl.2008.11.103.

The overproduction of nitric oxide (NO) and prostaglandin E(2) (PGE(2)) causes neurodegenerative diseases, such as Alzheimer's disease and Parkinson's disease. Four lignans, (+)-eudesmin (1), (+)-magnolin (2), (+)-yangambin (3) and a new structure named as Epimagnolin B (4) were isolated from Magnolia fargesii (Magnoliaceae) as the inhibitors of NO production in LPS-activated microglia. The most potent compound 4 inhibited the production of NO and PGE(2) and the expression of respective enzyme iNOS and COX-2 through the suppression of I-kappaB-alpha degradation and nuclear translocation of p65 subunit of NF-kappaB.