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  • Brand : BIOFRON

  • Catalogue Number : BF-E1010

  • Specification : 98%

  • CAS number : 552-58-9

  • Formula : C15H12O6

  • Molecular Weight : 288.25

  • PUBCHEM ID : 440735

  • Volume : 20mg

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Catalogue Number


Analysis Method






Molecular Weight



Light yellow powder

Botanical Source

Arachis hypogaea

Structure Type



Standards;Natural Pytochemical;API




(S)-3',4',5,7-Tetrahydroxyflavanone/T66 BO EVT&J CR CQ DQ& GQ IQ &&S Form/(2S)-2-(3,4-Dihydroxyphenyl)-5,7-dihydroxy-2,3-dihydro-4H-chromen-4-one/(S)-2-(3,4-Dihydroxyphenyl)-2,3-dihydro-5,7-dihydroxy-4H-1-benzopyran-4-one/4H-1-Benzopyran-4-one, 2-(3,4-dihydroxyphenyl)-2,3-dihydro-5,7-dihydroxy-, (2S)-/Eriodictiol/(S)-2-(3,4-Dihydroxyphenyl)-2,3-dihydro-5,7-dihydroxy-4-benzopyrone/Eriodictyol




1.6±0.1 g/cm3



Flash Point

241.9±25.0 °C

Boiling Point

625.2±55.0 °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#:552-58-9) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Eriodictyol, a flavonoid isolated from Lyonia ovalifolia, was found to be the most potent insulin secretagogue in our preliminary studies. Here, we explored mechanism(s) of insulin secretory activity of eriodictyol in vitro and in vivo. Mice islets and MIN6 cells were incubated in basal and stimulatory glucose containing eriodictyol with or without agonist/antagonist. Secreted insulin and cAMP contents were measured using ELISA kits. K+- and Ca2+-channels currents were recorded with patch-clamp technique. Oral glucose tolerance test and plasma insulin was evaluated in non-diabetic and diabetic rats. Eriodictyol stimulated insulin secretion from mice islets and MIN6 cells only at stimulatory glucose concentrations with maximum effect at 200μM. Eriodictyol showed no pronounced effect on inward rectifying K+ and Ca2+ currents. Furthermore, in KCl depolarized islets, in the presence of diazoxide, insulin secretory ability of eriodictyol was enhanced. IBMX, a phosphodiesterase inhibitor, significantly (P<0.001) enhanced eriodictyol-induced insulin secretion at 16.7mM glucose in comparison to eriodictyol or IBMX alone. The cAMP content after eriodictyol exposure was also increased. Eriodictyol-induced insulin secretion was partially inhibited by adenylate cyclase inhibitor (SQ22536) and completely inhibited by PKA inhibitor (H-89), suggesting that the eriodictyol effect is more on PKA. Molecular docking studies showed the best binding affinities of eriodictyol with PKA. Eriodictyol improved glucose tolerance and enhanced plasma insulin in non-diabetic and diabetic rats. Eriodictyol also lowered blood glucose in diabetic rats upon chronic treatment. Taken together, it can be concluded that eriodictyol, a novel insulin secretagogue, exerts an exclusive glucose-dependent insulinotropic effect through cAMP/PKA pathway.

Copyright © 2017 Elsevier B.V. All rights reserved.


Eriodictyol; Insulin secretion; Mice islets; Protein kinase A; cAMP


Eriodictyol stimulates insulin secretion through cAMP/PKA signaling pathway in mice islets.


Hameed A1, Hafizur RM2, Hussain N3, Raza SA1, Rehman M3, Ashraf S1, Ul-Haq Z1, Khan F1, Abbas G3, Choudhary MI4.

Publish date

2018 Feb 5




Osteoarthritis (OA) is a degenerative disease of joints, which is closely associated with cartilage degradation. Eriodictyol, a natural flavonoid compound, has been reported to have anti-inflammatory and anti-osteoclastogenic effects. However, the effect of eriodictyol on inflammatory response in OA has not been investigated. Our results showed that eriodictyol attenuated the inhibition of cell viability in IL-1β-stimulated chondrocytes. In addition, eriodictyol inhibited the expressions of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2), and the production of prostaglandin E2 (PGE2) and nitric oxide (NO), which were induced by IL-1β. The induction of inflammatory cytokines and matrix metalloproteinases (MMPs) caused by IL-1β stimulation was also attenuated by eriodictyol. Furthermore, eriodictyol pretreatment inhibited IκBα degradation and the level of p-p65, and enhanced the up-regulation of nuclear factor (erythroid-derived 2)-like 2 (Nrf2) and heme oxygenase 1 (HO-1) in IL-1β-stimulated chondrocytes. Si-Nrf2 treatment significantly inhibited the expressions of Nrf2 and HO-1 in chondrocytes. Additionally, si-Nrf2 transfection also abolished the anti-inflammatory effects of eriodictyol in chondrocytes. These findings indicated that eriodictyol exhibited anti-inflammatory effect in IL-1β-stimulated chondrocytes. The effect was mediated by inhibiting NF-κB via activating the Nrf2/HO-1 signaling pathway.

Copyright © 2018 Elsevier Masson SAS. All rights reserved.


Chondrocytes; Eriodictyol; Inflammatory response; NF-κB; Nrf2/HO-1 signaling; Osteoarthritis (OA)


Eriodictyol inhibits IL-1β-induced inflammatory response in human osteoarthritis chondrocytes.


Wang Y1, Chen Y1, Chen Y2, Zhou B1, Shan X1, Yang G3.

Publish date

2018 Nov




Eriodictyol, a natural flavonoid mainly distributed in citrus fruits and peanut, has been well-documented with possession of excellent anti-inflammatory, antioxidant, and anticancer bioactivities. This work focus on the protective effects of eriodictyol on LPS-induced neuroinflammation, amyloidogenesis, cognitive impairment, and the potential mechanisms involved. Behavioral tests and histological examinations showed that eriodictyol significantly prevented the memory and neuronal damage triggered by LPS. Consistently, eriodictyol (100 mg/kg) reduced the formation of Aβ1-42 by 28.37 ± 16.71 pg/mL compared to the LPS group. In addition, high dose eriodictyol (100 mg/kg) also equilibrated the cholinergic system via suppressing AChE activity (0.1996 ± 0.0831 U/mgprot) and elevating ChAT activity (41.81 ± 24.72 U/g) as well as ACh level (5.093 ± 3.531 μg/mgprot) compared to the LPS group. Western blot results indicated that compared to the LPS group, eriodictyol suppressed LPS-induced glial overactivation (84.29% ± 27.21%) and regulated inflammatory mediators and cytokines by inhibiting the NF-κB and MAPK pathways. These results indicated that eriodictyol alleviated amyloidogenesis and memory impairment triggered by LPS via inhibiting TLR4, MAPKs, and PI3K/Akt, and activating Sirt1 pathways and thus blocking downstream translocation of NF-κB, which offers a potential nutritional preventive strategy for neuroinflammation diseases such as Alzheimer’s disease (AD).


MAPKs; NF-κB; eriodictyol; lipopolysaccharide; neuroinflammation


Eriodictyol Attenuates LPS-Induced Neuroinflammation, Amyloidogenesis, and Cognitive Impairments via the Inhibition of NF-κB in Male C57BL/6J Mice and BV2 Microglial Cells.


He P1, Yan S1, Zheng J1, Gao Y1, Zhang S1, Liu Z1, Liu X1, Xiao C1.

Publish date

2018 Oct 3

Description :

Eriodictyol is a flavonoid isolated from the Chinese herb, with antioxidant and anti-inflammatory activity. Eriodictyol induces Nrf2 signaling pathway.