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Forsythoside B


Catalogue Number : BF-F2007
Specification : 98%
CAS number : 81525-13-5
Formula : C34H44O19
Molecular Weight : 756.7
PUBCHEM ID : 23928102
Volume : 20mg

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Catalogue Number


Analysis Method






Molecular Weight



Off-white crystalline powder

Botanical Source

Lamiophlomis rotata,Callicarpa kwangtungensis,Phlomis umbrosa,Schnabelia tetrodonta,Syringa pubescens

Structure Type



Standards;Natural Pytochemical;API




2-(3,4-Dihydroxyphenyl)ethyl 3-O-(6-deoxy-α-L-mannopyranosyl)-6-O-[(2R,3R,4R)-3,4-dihydroxy-4-(hydroxymethyl)tetrahydro-2-furanyl]-4-O-[(2E)-3-(3,4-dihydroxyphenyl)-2-propenoyl]-β-D-glucopyrano side/β-D-Glucopyranoside, 2-(3,4-dihydroxyphenyl)ethyl 3-O-(6-deoxy-α-L-mannopyranosyl)-4-O-[(2E)-3-(3,4-dihydroxyphenyl)-1-oxo-2-propen-1-yl]-6-O-[(2R,3R,4R)-tetrahydro-3,4-dihydroxy-4-(hydroxymeth yl)-2-furanyl]-/Forsythoside B


[(2R,3R,4R,5R,6R)-2-[[(2R,3R,4R)-3,4-dihydroxy-4-(hydroxymethyl)oxolan-2-yl]oxymethyl]-6-[2-(3,4-dihydroxyphenyl)ethoxy]-5-hydroxy-4-[(2S,3R,4R,5R,6S)-3,4,5-trihydroxy-6-methyloxan-2-yl]oxyoxan-3-yl] (E)-3-(3,4-dihydroxyphenyl)prop-2-enoate


1.7±0.1 g/cm3


Methanol; Water; Acetontrile; DMSO

Flash Point

323.9±27.8 °C

Boiling Point

1040.3±65.0 °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#:81525-13-5) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Acute lung injury (ALI), which is mainly triggered by infection, pneumonia, vasculitis, and sepsis, has no specific and effective therapy except for primary supportive treatment or bedside care. Excessive inflammation caused by innate immune cells is the major characteristic of ALI. Forsythoside B, a phenylethanoside compound, possesses good antioxidant and anti-bacterial properties in vivo and in vitro. In this study, the therapeutic potential of forsythoside B and its mechanism of action were investigated in a lipopolysaccharide (LPS)-induced ALI mouse model. The results showed that LPS-induced edema exudation and lung pathological changes in mice were significantly suppressed by forsythoside B pre-treatment. Furthermore, it also attenuated lung inflammation caused by LPS stimulation, evidenced by decreased inflammatory cell infiltration and down-regulated expression of cytokines, chemokines, and inducible enzymes. The anti-inflammation property of forsythoside B was confirmed in vitro using LPS-stimulated RAW 264.7 macrophages. Moreover, it alleviated LPS-induced inflammation by inhibiting the activation of TLR4/NF-κB signaling pathway in vivo and in vitro. In conclusion, the results demonstrated that forsythoside B protects against LPS-induced ALI by attenuating inflammatory cell infiltration and suppressing TLR4/NF-κB-mediated lung inflammation. Therefore, it might be a potential therapeutic agent for ALI caused by sepsis.

Copyright © 2018 Elsevier B.V. All rights reserved.


Acute lung injury; Forsythoside B; Inflammation; Lipopolysaccharide; TLR4/NF-κB pathway


Protective effect of forsythoside B against lipopolysaccharide-induced acute lung injury by attenuating the TLR4/NF-κB pathway.


Liu JX1, Li X2, Yan FG2, Pan QJ1, Yang C1, Wu MY3, Li G4, Liu HF5.

Publish date

2019 Jan




In recent years, hypersensitivity reactions to the Shuanghuanglian injection have attracted broad attention. However, the componential chief culprits inducing the reactions and the underlying mechanisms involved have not been completely defined. In this study, we used a combination of approaches based on the mouse model, human umbilical vein endothelial cell monolayer, real-time cellular monitoring, immunoblot analysis, pharmacological inhibition, and molecular docking. We demonstrated that forsythoside A and forsythoside B contributed to Shuanghuanglian injection-induced pseudoallergic reactions through activation of the RhoA/ROCK signaling pathway. Forsythoside A and forsythoside B could trigger dose-dependent vascular leakage in mice. Moreover, forsythoside A and forsythoside B slightly elicited mast cell degranulation. Correspondingly, treatment with forsythoside A and forsythoside B disrupted the endothelial barrier and augmented the expression of GTP-RhoA, p-MYPT1, and p-MLC2 in a concentration-dependent manner. Additionally, the ROCK inhibitor effectively alleviated forsythoside A/forsythoside B-induced hyperpermeability in both the endothelial cells and mice. Similar responses were not observed in the forsythoside E-treated animals and cells. These differences may be related to the potential of the tested compounds to react with RhoA-GTPγS and form stable interactions. This study innovatively revealed that some forsythosides may cause vascular leakage, and therefore, limiting their contents in injections should be considered.


RhoA/ROCK signaling pathway; Shuanghuanglian injection; forsythoside A; forsythoside B; forsythoside E; pseudo-allergic reactions


Forsythoside A and Forsythoside B Contribute to Shuanghuanglian Injection-Induced Pseudoallergic Reactions through the RhoA/ROCK Signaling Pathway.


Han J1, Zhang Y1, Pan C1, Xian Z1, Pan C1, Zhao Y1, Li C1, Yi Y1, Wang L1, Tian J1, Liu S1, Wang D1, Meng J1, Liang A1.

Publish date

2019 Dec 12




The present study investigated the effects of Forsythoside B on an experimental model of sepsis induced by caecal ligation and puncture (CLP) in rats and elucidated the potential mechanism in cultured RAW 264.7 cells. Results showed that Forsythoside B concentration-dependently down-regulated the levels of TNF-α, IL-6 and high-mobility group-box 1 protein (HMGB1) in lipopolysaccharide (LPS)-stimulated RAW264.7 cells, inhibited the IκB kinase (IKK) pathway and modulated nuclear factor (NF)- κB. Intravenous injection (i.v.) of Forsythoside B alone or plus Imipenem reduced serum levels of TNF-α, IL-6, HMGB1, triggering receptor expressed on myeloid cells (TREM-1) and endotoxin, while the serum level of IL-10 was up-regulated and myeloperoxidase (MPO) in lung, liver and small intestine was reduced. Meanwhile, i.v. of Forsythoside B alone or plus Imipenem reduced CLP-induced lethality in rats. These data indicated that the antisepsis effect of Forsythoside B is mediated by decreasing local and systemic levels of a wide spectrum of inflammatory mediators. Its antisepsis mechanism may be that Forsythoside B binds to LPS and reduces the biological activity of serum LPS, and inhibits NF-κB activition. Our studies enhance the case for the use of Forsythoside B in sepsis. Forsythoside B itself has promise as a therapy for the treatment of sepsis in humans.

Copyright © 2011 John Wiley & Sons, Ltd.


Forsythoside B protects against experimental sepsis by modulating inflammatory factors.


Jiang WL1, Yong-Xu, Zhang SP, Zhu HB, Jian-Hou.

Publish date

2012 Jul