We Offer Worldwide Shipping
Login Wishlist



  • Brand : BIOFRON

  • Catalogue Number : BF-L3017

  • Specification : 98%

  • CAS number : 260413-62-5

  • Formula : C33H40O18

  • Molecular Weight : 724.67

  • PUBCHEM ID : 10417462

  • Volume : 25mg

In stock

Checkout Bulk Order?

Catalogue Number


Analysis Method






Molecular Weight



White needle crystal

Botanical Source

Ligustrum lucidum,Olea europaea

Structure Type



Standards;Natural Pytochemical;API




5-Hydroxy-2-(4-hydroxyphenyl)-4-oxo-4H-chromen-7-yl 6-deoxy-α-L-mannopyranosyl-(1->2)-[6-deoxy-α-L-mannopyranosyl-(1->6)]-β-D-glucopyranoside/ligustroflavone/4H-1-Benzopyran-4-one, 7-[[O-6-deoxy-α-L-mannopyranosyl-(1->2)-O-[6-deoxy-α-L-mannopyranosyl-(1->6)]-β-D-glucopyranosyl]oxy]-5-hydroxy-2-(4-hydroxyphenyl)-




1.7±0.1 g/cm3


Methanol; Ethanol; Water

Flash Point

325.2±27.8 °C

Boiling Point

1028.5±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#:260413-62-5) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Receptor-interacting protein kinase 1/3 (RIPK1/3) and mixed lineage kinase domain-like (MLKL)-mediated necroptosis contributes to brain injury after ischemic stroke. Ligustroflavone is an ingredient of common privet with activities of anti-inflammation and complement inhibition. This study aims to explore the effect of ligustroflavone on ischemic brain injury in stroke rat and the underlying mechanisms. A rat model of ischemic stroke was established by middle cerebral artery occlusion (MCAO), which showed ischemic injury (increase in neurological deficit score and infarct volume) and upregulation of necroptosis-associated proteins (RIPK1, RIPK3 and MLKL/p-MLKL). Administration of ligustroflavone (30 mg/kg, i.g.) 15 min before ischemia evidently improved neurological function, reduced infarct volume, and decreased the levels of necroptosis-associated proteins except the RIPK1. Consistently, hypoxia-cultured PC12 cells (O2/N2/CO2, 1:94:5, 8 h) caused cellular injury (LDH release and necroposis) concomitant with up-regulation of necroptosis-associated proteins, and these phenomena were blocked in the presence of ligustroflavone (25 μM) except the elevated RIPK1 levels. Using the Molecular Operating Environment (MOE) program, we identified RIPK1, RIPK3, and MLKL as potential targets of ligustroflavone. Further studies showed that the interaction between RIPK3 and RIPK1 or MLKL was significantly enhanced, which was blocked in the presence of ligustroflavone. Based on these observations, we conclude that ligustroflavone protects rat brain from ischemic injury, and its beneficial effect is related to the prevention of necroptosis through a mechanism involving targeting RIPK1, RIPK3, and/or MLKL.


Ligustroflavone; Mixed lineage kinase domain-like (MLKL); Necroptosis; Receptor-interacting protein kinase 1 (RIPK1); Receptor-interacting protein kinase 3 (RIPK3).


Ligustroflavone Reduces Necroptosis in Rat Brain After Ischemic Stroke Through Targeting RIPK1/RIPK3/MLKL Pathway


Yi-Yue Zhang 1 , Wei-Ning Liu 1 , Yue-Qi Li 2 , Xiao-Jie Zhang 1 3 , Jie Yang 4 , Xiu-Ju Luo 5 , Jun Peng 6 7

Publish date

2019 Sep




Ligustroflavone is one major compound contained in active fraction from Fructus Ligustri Lucidi (the fruit of Ligustrum lucidum), which could regulate parathyroid hormone (PTH) levels and improve calcium balance by acting on calcium-sensing receptors (CaSR). This study aimed to explore the potency of ligustroflavone as a CaSR antagonist and its protective effects against diabetic osteoporosis in mice. LF interacted well with the allosteric site of CaSR shown by molecular docking analysis, increased PTH release of primary parathyroid gland cells and suppressed extracellular calcium influx in HEK-293 cells. The serum level of PTH attained peak value at 2

h and maintained high during the period of 1

h and 3

h than that before treatment in mice after a single dose of LF. Treatment of diabetic mice with LF inhibited the decrease in calcium level of serum and bone and the enhancement in urinary calcium excretion as well as elevated circulating PTH levels. Trabecular bone mineral density and micro-architecture were markedly improved in diabetic mice upon to LF treatment for 8 weeks. LF reduced CaSR mRNA and protein expression in the kidneys of diabetic mice. Taken together, ligustroflavone could transiently increase PTH level and regulate calcium metabolism as well as prevent osteoporosis in diabetic mice, suggesting that ligustroflavone might be an effective antagonist on CaSR.


Ligustroflavone; Mixed lineage kinase domain-like (MLKL); Necroptosis; Receptor-interacting protein kinase 1 (RIPK1); Receptor-interacting protein kinase 3 (RIPK3).


Protective Effects of Ligustroflavone, an Active Compound From Ligustrum Lucidum, on Diabetes-Induced Osteoporosis in Mice: A Potential Candidate as Calcium-Sensing Receptor Antagonist


Rui Feng 1 , Fan Ding 1 , Xiu-Hua Mi 2 , Shu-Fen Liu 1 3 , Ai-Ling Jiang 4 , Bi-Hui Liu 5 , Yin Lian 5 , Qi Shi 1 3 , Yong-Jun Wang 1 3 , Yan Zhang 1 3 `

Publish date





A selective and sensitive liquid chromatography-electrospray ionization tandem mass spectrometry (LC-ESI-MS/MS) method was developed for the simultaneous determination of ligustroflavone and rhoifolin in rat plasma. Chromatographic separation was performed on a Venusil HILIC column using an isocratic mobile phase consisting of acetonitrile/water/formic acid (75:25:0.1, v/v/v). The detection was achieved using a triple-quadrupole tandem MS in negative ionization through selected reaction monitoring (SRM) mode. The calibration curves of both analytes in plasma showed good linearity over the concentration ranges of 3-300 ng/mL for ligustroflavone, and 2-200 ng/mL for rhoifolin. This assay was used to investigate the pharmacokinetics of ligustroflavone and rhoifolin in rats.
© The Author 2016. Published by Oxford University Press. All rights reserved. For Permissions, please email: journals.permissions@oup.com.


Development and Validation of an LC-ESI-MS/MS Method for Simultaneous Determination of Ligustroflavone and Rhoifolin in Rat Plasma and Its Application to a Pharmacokinetic Study


Hong Liu 1 , Cheng Xu 2 , Wei Wang 3 , Yue Zhao 4

Publish date

2017 Mar 1

Description :

Ligustroflavone, extracted from Ligustrum lucidum, is a potential candidate as calcium-sensing receptor (CaSR) antagonist. Ligustroflavone exhibits protective effects against diabetic osteoporosis in mice[1].