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  • Brand : BIOFRON

  • Catalogue Number : BF-O2003

  • Specification : 98%

  • CAS number : 28608-75-5

  • Formula : C21H20O11

  • Molecular Weight : 448.38

  • PUBCHEM ID : 5281675

  • Volume : 20mg

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Catalogue Number


Analysis Method






Molecular Weight



Yellow powder

Botanical Source

Trigonella foenum-graecum,Vitex negundo,Gelsemium elegans,Gleditsia sinensis,Adonis coerulea

Structure Type



Standards;Natural Pytochemical;API




isoorientin/(1S)-1,5-Anhydro-1-[2-(3,4-dihydroxyphenyl)-5,7-dihydroxy-4-oxo-4H-chromen-8-yl]-D-glucitol/2-(3,4-Dihydroxyphenyl)-5,7-dihydroxy-8-[(2S,3R,4R,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)tetrahydro-2H-pyran-2-yl]-4H-chromen-4-one/Orientin 8-C-β-D-glucopyranoside/3',4',5,7-tetrahydroxyflavone-8-C-glucoside/2-(3,4-Dihydroxyphenyl)-5,7-dihydroxy-8-[(2S,3R,4R,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)tetrahydro-2H-pyran-2-yl]-4H-chromen-4-on/Luteolin-8-C-glucoside/3',4',5,7-tetrahydroxyflavone 8-glucoside/4H-1-Benzopyran-4-one, 2-(3,4-dihydroxyphenyl)-8-β-D-glucopyranosyl-5,7-dihydroxy-/D-Glucitol, 1,5-anhydro-1-C-[2-(3,4-dihydroxyphenyl)-5,7-dihydroxy-4-oxo-4H-1-benzopyran-8-yl]-, (1S)-/Orientin/lutexin/2-(3,4-Dihydroxyphenyl)-5,7-dihydroxy-8-[(2S,3R,4R,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)tetrahydro-2H-pyran-2-yl]-4H-chromen-4-one/2-(3,4-Dihydroxyphenyl)-8-b-D-glucopyranosyl-5,7-dihydroxy-4H-1-benzopyran-4-one




1.8±0.1 g/cm3



Flash Point

289.1±27.8 °C

Boiling Point

816.1±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#:28608-75-5) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Alzheimer’s disease (AD) is the most common cause of dementia and is characterized by the presence of β-amyloid (Aβ) plaques and defective autophagy in the brain, which is believed to cause neuronal dysfunction. By using APP/PS1 transgenic AD mice, we investigated the influence of orientin (Ori) on cognitive function and its underlying mechanisms in AD models. Our data indicated that Ori improved spatial learning and memory in APP/PS1 mice, possibly through decreasing brain Aβ deposition and attenuating autophagy impairment. Ori decreased the LC3-II/I ratio, p62 and cathepsin D (Ctsd) protein levels and the number of autolysosomes, whereas the protein levels of Ulk1 and Beclin-1 were no different between the control and treatment groups, indicating increased autolysosome clearance and thus a decreased Aβ burden in the brain. Our results showed that Ori could enhance autolysosome clearance, decrease brain Aβ deposition and improve learning and memory in AD mice.


Alzheimer’s disease; Amyloid beta deposits; Autophagy; Orientin


Orientin Improves Cognition by Enhancing Autophagosome Clearance in an Alzheimer's Mouse Model.


Zhong Y1, Zheng QY2, Sun CY1, Zhang Z1, Han K3, Jia N4.

Publish date

2019 Oct




Flavone C-glycosides are difficult to be deglycosylated using traditional chemical methods due to their solid carbon-carbon bond between sugar moieties and aglycones; however, some bacteria may easily cleave this bond because they generate various specific enzymes.

A bacterial strain, named W12-1, capable of deglycosylating orientin, vitexin, and isovitexin to their aglycones, was isolated from human intestinal bacteria in this study and identified as Enterococcus faecalis based on morphological examination, physiological and biochemical identification, and 16S rDNA sequencing. The strain was shown to preferentially deglycosylate the flavone C-glycosides on condition that the culture medium was short of carbon nutrition sources such as glucose and starch, and its deglycosylation efficiency was negatively correlated with the content of the latter two substances.

This study provided a new bacterial resource for the cleavage of C-glycosidic bond of flavone C-glycosides and reported the carbon nutrition sources reduction induced deglycosylation for the first time.


Deglycosylation; Enterococcus faecalis; Flavone C-glycosides; Reduced carbon nutrition source induction


A newly isolated human intestinal bacterium strain capable of deglycosylating flavone C-glycosides and its functional properties.


Zheng S1, Geng D1, Liu S1, Wang Q1, Liu S1, Wang R2.

Publish date

2019 May 28




Previous evidence show foods and beverages rich in polyphenolic compounds to have favourable effects on the cardiovascular system.

The current study assessed the modulation of oxidative stress and associated inflammation induced by diesel exhaust particles (DEP – SRM 2975) by pre-treatment of human umbilical vein endothelial cells (HUVECs) with aqueous extracts of rooibos [fermented (FR) as well as green form (GR)] and honeybush [fermented form (FH)].

HUVEC are either exposed to DEP (10 µg/ml) for 4 h or pre-treated with 40 and 60 µg/ml of FR or GH or FR, or 50 µg/ml orientin (OR) for 6 h prior to DEP exposure.

In vitro antioxidant capacity of the extracts was assessed and the polyphenol contents were also assessed by HPLC. ROS, cell viability, lactate dehydrogenase leakage, lipid peroxidation, GSH:GSSG ratios, conjugated diene and protein carbonyl levels were determined as indices of oxidative stress and cytotoxicity. RT-qPCR and western blot were used to assess inflammatory cytokines and antioxidant genes expression.

DEP caused a dose and time-dependent increase in ROS production, significant (p < 0.001) increase in protein carbonyl (PC) formation, thiobarbituric acid reactive substances and conjugated dienes levels (p < 0.01) and a significant reduction in glutathione (GSH) redox status. Pre-incubation with either the herbal extracts or orientin attenuated these effects. The significant increase in IL-1α, IL-6, IL-8, VCAM-1 and ATF4 gene expression caused by DEP (10 µg/ml) were also attenuated by the presence of the FR, GR and FH extracts, and OR . Pre-treatment with the rooibos extracts or flavone orientin enhanced cell viability, reduced LDH leakage, enhanced mRNA expression of NQO1 and Nrf2, but repressed CYP1B1 mRNA induced by DEP. Western blot showed both the herbal tea extracts and orientin to enhance NQO1 and γGSC protein induction by DEP.

Taken together, the herbal extracts offer protection against DEP-induced oxidative stress and inflammatory response.

Copyright © 2019 Elsevier GmbH. All rights reserved.


Diesel exhaust particles; Endothelial cells; Honeybush; Inflammation; Oxidative stress; Rooibos


Rooibos (Aspalathus linearis) and honeybush (Cyclopia species) modulate the oxidative stress associated injury of diesel exhaust particles in human umbilical vein endothelial cells.


Lawal AO1, Davids LM2, Marnewick JL3.

Publish date

2019 Jun

Description :

Orientin improves depression-like behavior and BDNF in chronic stressed mice. PUMID/DOI:25788013 Mol Nutr Food Res. 2015 Jun;59(6):1130-42. Orientin, a phenolic compound abundant in some fruits, millet, and herbs, has been shown to have antioxidant properties. This study investigated the potential antidepressant effects of Orientin against chronic stress and its underlying mechanisms.||METHODS AND RESULTS:||The chronic unpredictable mild stress (CUMS) model was used to investigate the effects of Orientin on behavior and biochemical alterations in mice. After 2 weeks of the CUMS protocol, the mice were treated with Orientin (20 mg/kg and 40 mg/kg, oral gavage) for 3 weeks. Administration of Orientin significantly alleviated the CUMS-induced depression-like behavior, including sucrose preference reduction, locomotor activity decline, and hypomotility. Orientin treatment attenuated the oxidative stress markers and increased the concentrations of serotonin and norepinephrine in the hippocampus and prefrontal cortex of CUMS mice. Orientin treatment also increased the brain-derived neurotrophic factor and synapse-associated proteins (synaptophysin and postsynaptic density protein 95) of CUMS mice.||CONCLUSION:||Orientin exerts antidepressant-like effects on CUMS mice, specifically by improving central oxidative stress, neurotransmission, and neuroplasticity. Therefore, supplementation with Orientin-enriched food or fruit could be beneficial as a preventive strategy for chronic stress-induced depression. Neuroprotective effects of orientin on hydrogen peroxide?induced apoptosis in SH?SY5Y cells. PUMID/DOI:24366367 Mol Med Rep. 2014 Mar;9(3):947-54. Neurodegenerative diseases remain a global issue which affects the ageing population. Efforts towards determining their aetiologies to understand their pathogenic mechanisms are underway in order to identify a pathway through which therapeutic measures can be applied. One such pathogenic mechanism, oxidative stress (OS), is widely considered to be involved in neurodegenerative disease. Antioxidants, most notably flavonoids, have promising potential for therapeutic use as shown in in vitro and in vivo studies. In view of the importance of flavonoids for combating OS, this study investigated the neuroprotective effects of orientin, which has been reported to be capable of crossing the blood?brain barrier. The maximum non?toxic dose (MNTD) of orientin against SH?SY5Y neuroblastoma cells was determined using a 3?(4,5?dimethylthiazol?2?yl)?2,5?diphenyltetrazolium bromide (MTT) assay. The effects of the MNTD and the half MNTD (?MNTD) of orientin on cell cycle progression and intracellular reactive oxygen species (ROS) levels, as well as the activity of caspases 3/7, 8 and 9 after exposure to 150 μM of hydrogen peroxide (H2O2) were also determined using flow cytometry, a 2',7'?dichlorodihydrofluorescein?diacetate (DCFH?DA) assay and caspase assay kits, respectively. The results revealed that orientin at ≤20 μM was not cytotoxic to SH?SY5Y cells. After treatment with orientin at the MNTD, the percentage of apoptotic cells was significantly reduced compared with that in cells treated with 150 μM H2O2 alone. The results also showed that, although orientin at the MNTD and ?MNTD did not reduce intracellular ROS levels, it significantly inhibited the activity of caspases 3/7. Caspase 9 was significantly inactivated with orientin at the MNTD. Findings from this study suggest that the neuroprotection conferred by orientin was the result of the intracellular mediation of caspase activity. Radiation protection by the ocimum flavonoids orientin and vicenin: mechanisms of action. PUMID/DOI:11023610 Radiat Res. 2000 Oct;154(4):455-60. The antioxidant activity of Orientin/vicenin (10-500 microM) was studied by measuring inhibition of hydroxyl radicals generated by the Fenton reaction (Fe(3+)-EDTA-ascorbic acid-H(2)O(2)) in vitro. The compounds were also tested for possible pro-oxidant and iron chelation activities at the above concentrations in the in vitro system. Orientin and vicenin provided almost equal protection against radiation-induced lipid peroxidation in mouse liver. Both compounds showed a significantly greater free radical-inhibiting activity in vitro than DMSO. Neither Orientin nor vicenin showed any pro-oxidant activity at the concentrations tested. Both compounds inhibited free radical formation in the absence of EDTA. Free radical scavenging appears to be a likely mechanism of radiation protection by these flavonoids. Orientin alleviates cognitive deficits and oxidative stress in Aβ1-42-induced mouse model of Alzheimer's disease. PUMID/DOI:25497709 Life Sci. 2015 Jan 15;121:104-9. Previous studies have demonstrated that Orientin (Ori) possesses antioxidation capabilities in vitro. Therefore, current study is to demonstrate that Orientin can activate Nrf2/HO-1 signaling and alleviate apoptosis induced by Aβ1-42, and ameliorate cognitive deficits in AD mice.||KEY FINDINGS:||Results indicated that Orientin could ameliorate cognitive deficits in AD mice. Levels of oxidative stress, indicated by production of reactive oxygen species (ROS), 3-nitrotyrosine (3-NT), 4-hydroxy-nonenal (4-HNE) and 8-hydroxy-2'-deoxyguanosine (8-OHdG), were significantly decreased after Orientin treatment. In addition, the current study showed that Orientin could attenuate mitochondrial dysfunction induced by Aβ1-42, and subsequently inhibited the mitochondrial apoptotic pathway. Orientin induced the nuclear translocation of Nrf2, which enhanced the expression of HO-1 and activation of the redox signaling pathway.||SIGNIFICANCE:||Orientin might alleviate cognitive deficits and oxidative stress in AD mice, which might be a potential therapeutic drug for AD. Orientin-induced cardioprotection against reperfusion is associated with attenuation of mitochondrial permeability transition. PUMID/DOI:21283956 Planta Med. 2011 Jul;77(10):984-91. After myocardial ischemia, opening of the mPTP is a critical determinant of cell death. The relationship of Orientin and mPTP in mediating reperfusion-induced cardiomyocytes injury is still elusive. Here, our results indicate that the protective effect of Orientin in H9c2 cells subjected to I/R injury is associated with depression of the mPTP opening, resultant mitochondrial dysfunction, and apoptosis. Further investigation of cellular mechanisms revealed that these effects were associated with inhibition of reactive oxygen species (ROS) generation, repolarization of mitochondrial membrane potential (Δψ(m)), suppression of mitochondrial cytochrome C release, enhancement of the Bcl-2 level, and inhibition of Bax and Smac/DIABLO levels. Furthermore, these beneficial effects of Orientin were blocked by the phosphatidylinositol 3-kinase (PI3K) inhibitor wortmannin, and Orientin could enhance Akt phosphorylation. In summary, we demonstrate that Orientin protects H9c2 cardiomytocytes against I/R-induced apoptosis by modulating the mPTP opening, and this role of Orientin may involve the PI3K/Akt signaling pathway.