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  • Brand : BIOFRON

  • Catalogue Number : BF-S1017

  • Specification : 98%

  • CAS number : 72063-39-9

  • Formula : C28H32O15

  • Molecular Weight : 608.546

  • PUBCHEM ID : 155692

  • Volume : 20mg

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Catalogue Number


Analysis Method






Molecular Weight



White crystalline powder

Botanical Source

Ziziphus jujuba var. spinosa,Hovenia acerba

Structure Type



Standards;Natural Pytochemical;API




6-(2-O-β-D-Glucopyranosyl-β-D-glucopyranosyl)-5-hydroxy-2-(4-hydroxyphenyl)-7-methoxy-4H-1-benzopyran-4-one/Spinosin/X1238/6-[(2S,3R,4S,5S,6R)-4,5-dihydroxy-6-(hydroxymethyl)-3-[(2S,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxyoxan-2-yl]-5-hydroxy-2-(4-hydroxyphenyl)-7-methoxychromen-4-one/D-Glucitol, 1,5-anhydro-2-O-β-D-glucopyranosyl-1-C-[5-hydroxy-2-(4-hydroxyphenyl)-7-methoxy-4-oxo-4H-1-benzopyran-6-yl]-, (1S)-/4H-1-Benzopyran-4-one, 6-(2-O-β-D-glucopyranosyl-β-D-glucopyranosyl)-5-hydroxy-2-(4-hydroxyphenyl)-7-methoxy-/(1S)-1,5-Anhydro-2-O-β-D-glucopyranosyl-1-[5-hydroxy-2-(4-hydroxyphenyl)-7-methoxy-4-oxo-4H-chromen-6-yl]-D-glucitol




1.7±0.1 g/cm3


Methanol; DMF

Flash Point

296.7±27.8 °C

Boiling Point

901.4±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#:72063-39-9) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Investigating active compounds from Chinese herbal medicine that can rescue myocardial cells is a good approach to preserve cardiac function. Several herbal formulae that containing Semen Ziziphi Spinosae (SZS), also called Suanzaoren in Chinese, are clinically effective in the treatment of patients with acute myocardial infarction (AMI). The present study aimed to investigate the cardioprotective effects of spinosin and 6”’‑feruloylspinosin, two flavonoid glycosides from SZS, in a rat model of myocardial ischemia and reperfusion. The left anterior descending artery (LAD) was occluded to induce myocardial ischemia. Spinosin or 6”’‑feruloylspinosin (5 mg/kg) was intraperitoneally injected into rats 30 min before LAD ligation. The protein levels of myocardial enzymes in the serum, the extent of tissue injury and the rate of apoptosis were examined after AMI in rats with or without pretreatment with spinosin or 6”’‑feruloylspinosin. Western blotting was performed to investigate the potential mechanisms underlying the function of these two flavonoid glycosides. The present results suggested that pretreatment with spinosin or 6”’‑feruloylspinosin significantly attenuated myocardial tissue injury, and reduced myocardial enzyme release and cell apoptosis in AMI rats. In addition, spinosin treatment increased light chain 3B‑II and 6”’‑feruloylspinosin, and reduced p62, indicating that autophagy was promoted after drug treatments. Treatments of spinosin and 6”’‑feruloylspinosin led to the reduction of glycogen synthase kinase‑3β (GSK3β) phosphorylation at Tyr216, and the increase of peroxisome proliferator‑activated receptor γ coactivator (PGC)‑1α and its downstream signaling proteins, including nuclear factor (erythroid‑derived 2)‑like 2 (Nrf2) and hemeoxygenase1 (HO‑1). The present data suggested that SZS flavonoids could protect myocardial cells against acute heart ischemia‑reperfusion, probably via the inhibition of GSK3β, which increased autophagy and the activity of the PGC‑1α/Nrf2/HO‑1 pathway.


Spinosin and 6'''‑Feruloylspinosin protect the heart against acute myocardial ischemia and reperfusion in rats.


Gu M1, He P1, Lyu C2, Liu X1, Xu Y1, Cheng S1, Gu Y2, Jia Y1.

Publish date

2019 Nov




Hippocampal synaptic dysfunction is a hallmark of Alzheimer’s disease (AD). Many agents regulating hippocampal synaptic plasticity show an ameliorative effect on AD pathology, making them potential candidates for AD therapy. In the present study, we investigated spinosin as a regulating agent of synaptic plasticity in AD. Spinosin attenuated amyloid β (Aβ)-induced long-term potentiation (LTP) impairment, and improved plasmin activity and protein level in the hippocampi of 5XFAD mice, a transgenic AD mouse model. Moreover, the effect of spinosin on hippocampal LTP in 5XFAD mice was prevented by 6-aminocaproic acid, a plasmin inhibitor. These results suggest that spinosin improves synaptic function in the AD hippocampus by regulating plasmin activity.


5XFAD; Alzheimer’s disease; LTP; Plasmin; Spinosin


Spinosin Attenuates Alzheimer's Disease-Associated Synaptic Dysfunction via Regulation of Plasmin Activity.


Cai M1, Jung I1, Kwon H2, Cho E2, Jeon J2, Yun J3,4, Lee YC2,4, Kim DH2,4, Ryu JH1,5.

Publish date

2020 Mar 1




The present research work primarily investigated whether spinosin has the potential of improving the pathogenesis of Alzheimer’s disease (AD) driven by β-amyloid (Aβ) overproduction through impacting the procession of amyloid precursor protein (APP). Wild type mouse Neuro-2a cells (N2a/WT) and N2a stably expressing human APP695 (N2a/APP695) cells were treated with spinosin for 24 h. The levels of APP protein and secreted enzymes closely related to APP procession were examined by western blot analysis. Oxidative stress related proteins, such as nuclear factor-erythroid 2-related factor 2 (Nrf2), and heme oxygenase-1 (HO-1) were detected by immunofluorescence assay and western blot analysis, respectively. The intracellular reactive oxygen species (ROS) level was analyzed by flow cytometry, the levels of Aβ1-42 were determined by ELISA kit, and Thioflavin T (ThT) assay was used to detect the effect of spinosin on Aβ1-42 aggregation. The results showed that ROS induced the expression of ADAM10 and reduced the expression of BACE1, while spinosin inhibited ROS production by activating Nrf2 and up-regulating the expression of HO-1. Additionally, spinosin reduced Aβ1-42 production by impacting the procession of APP. In addition, spinosin inhibited the aggregation of Aβ1-42. In conclusion, spinosin reduced Aβ1-42 production by activating the Nrf2/HO-1 pathway in N2a/WT and N2a/ APP695 cells. Therefore, spinosin is expected to be a promising treatment of AD.


Alzheimer's disease; Neuroprotection; Nrf2/HO-1; Spinosin


Spinosin Inhibits Aβ1-42 Production and Aggregation via Activating Nrf2/HO-1 Pathway.


Zhang X1, Wang J1, Gong G2, Ma R1, Xu F3, Yan T4, Wu B4, Jia Y4.

Publish date

2019 Dec 3

Description :

Spinosin, a C-Glucosylflavone, from Zizyphus jujuba var. spinosa Ameliorates Aβ1-42 Oligomer-Induced Memory Impairment in Mice. PUMID/DOI:25767684 Biomol Ther (Seoul). 2015 Mar;23(2):156-64. Alzheimer's disease (AD) is a neurodegenerative disorder associated with progressive memory loss and neuronal cell death. Although numerous previous studies have been focused on disease progression or reverse pathological symptoms, therapeutic strategies for AD are limited. Alternatively, the identification of traditional herbal medicines or their active compounds has received much attention. The aims of the present study were to characterize the ameliorating effects of Spinosin, a C-glucosylflavone isolated from Zizyphus jujuba var. spinosa, on memory impairment or the pathological changes induced through amyloid-β1-42 oligomer (AβO) in mice. Memory impairment was induced by intracerebroventricular injection of AβO (50 μM) and Spinosin (5, 10, and 20 mg/kg) was administered for 7 days. In the behavioral tasks, the subchronic administration of Spinosin (20 mg/kg, p.o.) significantly ameliorated AβO-induced cognitive impairment in the passive avoidance task or the Y-maze task. To identify the effects of Spinosin on the pathological changes induced through AβO, immunohistochemistry and Western blot analyses were performed. Spinosin treatment also reduced the number of activated microglia and astrocytes observed after AβO injection. In addition, Spinosin rescued the AβO-induced decrease in choline acetyltransferase expression levels. These results suggest that Spinosin ameliorated memory impairment induced through AβO, and these effects were regulated, in part, through neuroprotective activity via the anti-inflammatory effects of Spinosin. Therefore, Spinosin might be a useful agent against the amyloid b protein-induced cognitive dysfunction observed in AD patients. GABA and 5-HT systems are implicated in the anxiolytic-like effect of spinosin in mice. PUMID/DOI:25449359 Pharmacol Biochem Behav. 2015 Jan;128:41-9. The present study investigated the anxiolytic-like effects of Spinosin, one of the major flavonoids in Ziziphi Spinosae Semen (ZSS), in experimental models of anxiety compared with a known anxiolytic, diazepam. Repeated treatment with Spinosin (2.5 and 5mg/kg/day, p.o.) significantly increased the percentage of entries into and time spent on the open arms of the elevated plus maze compared with the control group. In the light/dark box test, Spinosin exerted an anxiolytic-like effect at 5mg/kg. In the open-field test, 5mg/kg Spinosin increased the number of central entries. Spinosin did not affect spontaneous activity. The anxiolytic-like effects of Spinosin in the elevated plus maze, light/dark box test, and open field test were blocked by the γ-aminobutyric acid-A (GABAA) receptor antagonist flumazenil (3mg/kg, i.p.) and 5-hydroxytryptamine-1A (5-HT1A) receptor antagonist WAY-100635 (1mg/kg, i.p.). These results suggest that Spinosin exerts anxiolytic-like effects, and its mechanism of action appears to be modulated by GABAA and 5-HT1A receptors.