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  • Brand : BIOFRON

  • Catalogue Number : BD-P0494

  • Specification : 95.0%(HPLC)

  • CAS number : 151870-74-5

  • Formula : C10H16O8

  • Molecular Weight : 264.23

  • PUBCHEM ID : 10422896

  • Volume : 25mg

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Catalogue Number


Analysis Method






Molecular Weight




Botanical Source

Anoectochilus roxburghii (Wall.) Lindl

Structure Type



Standards;Natural Pytochemical;API




2(3H)-Furanone, 4-(β-D-glucopyranosyloxy)dihydro-, (4R)-/goodyeroside/(4R)-4-[(2R,3R,4S,5S,6R)-3,4,5-trihydroxy-6-(hydroxymethyl)oxan-2-yl]oxyoxolan-2-one/(3R)-5-Oxotetrahydro-3-furanyl β-D-glucopyranoside





1.6±0.1 g/cm3


Methanol; Water

Flash Point

226.2±23.6 °C

Boiling Point

570.2±50.0 °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#:151870-74-5) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate

No Technical Documents Available For This Product.




The objective was to investigate the effect of kinsenoside (Kin) treatments on macrophage polarity and evaluate the resulting protection of chondrocytes to attenuate osteoarthritis (OA) progression. RAW264.7 macrophages were polarized to M1/M2 subtypes then administered with different concentrations of Kin. The polarization transitions were evaluated with quantitative real-time polymerase chain reaction (qRT-PCR), confocal observation and flow cytometry analysis. The mechanism of Kin repolarizing M1 macrophages was evaluated by Western blot. Further, macrophage conditioned medium (CM) and IL-1β were administered to chondrocytes. Micro-CT scanning and histological observations were conducted in vivo on anterior cruciate ligament transection (ACLT) mice with or without Kin treatment. We found that Kin repolarized M1 macrophages to the M2 phenotype. Mechanistically, Kin inhibited the phosphorylation of IκBα, which further reduced the downstream phosphorylation of P65 in nuclear factor-κB (NF-κB) signaling. Moreover, Kin inhibited mitogen-activated protein kinases (MAPK) signaling molecules p-JNK, p-ERK and p-P38. Additionally, Kin attenuated macrophage CM and IL-1β-induced chondrocyte damage. In vivo, Kin reduced the infiltration of M1 macrophages, promoted M2 macrophages in the synovium, inhibited subchondral bone destruction and reduced articular cartilage damage induced by ACLT. All the results indicated that Kin is an effective therapeutic candidate for OA treatment.

© 2019 Chinese Pharmaceutical Association and Institute of Materia Medica, Chinese Academy of Medical Sciences. Production and hosting by Elsevier B.V.


AP-1, activator protein-1; Arg-1, arginase-1; BV, bone volume; BV/TV, bone volume/total tissue volume; C/EBP β, CCAAT/enhancer-binding protein β; CM, conditioned medium; Chondrocytes; DMEM, Dulbecco׳s minimum essential medium; GA, gouty arthritis; H&E, hematoxylin & eosin; HUVECs, human umbilical vein endothelial cells; IFN-γ, interferon-γ; IRF4, interferon regulatory factor 4; Kin, kinsenoside; Kinsenoside; LPS, lipopolysaccharides; MAPK, mitogen-activated protein kinases; MSU, monosodium urate; Macrophages; NF-κB, nuclear factor-κB; NSAIDs, non-steroidal anti-inflammatory drugs; OA, osteoarthritis; OARSI, Osteoarthritis Research Society International; Osteoarthritis; PPARγ, peroxisome proliferator-activated receptor γ; Polarization; RA, rheumatoid arthritis; ROS, reactive oxygen species; S&F, safranin O-fast green; TLRs, toll-like receptors; TNF-α, tumor necrosis factor-α; Tb.N, trabecular number; Tb.Sp, trabecular separation; Tb.Th, trabecular thickness; iNOS, inducible nitric oxide synthase


Kinsenoside attenuates osteoarthritis by repolarizing macrophages through inactivating NF-κB/MAPK signaling and protecting chondrocytes.


Zhou F1, Mei J1, Han X1, Li H1, Yang S1, Wang M1, Chu L1, Qiao H1, Tang T1.

Publish date

2019 Sep




Intervertebral disc degeneration (IDD) is recognized as the major contributor to low back pain, which results in disability worldwide and heavy burdens on society and economy. Here we present evidence that the lower level of Nrf2 is closely associated with higher grade of IDD. The apoptosis and senescence of nucleus pulposus cells (NPCs) were exacerbated by Nrf2 knockdown, but suppressed by Nrf2 overexpression under oxidative stress. Based on findings that Kinsenoside could exert multiple pharmacological effects, we found that Kinsenosiderescued the NPC viability under oxidative stress and protected against apoptosis, senescence and mitochondrial dysfunction in a Nrf2-dependent way. Further experiments revealed that Kinsenoside activated a signaling pathway of AKT-ERK1/2-Nrf2 in NPCs. Moreover, in vivo study showed that Kinsenoside ameliorated IDD in a puncture-induced model. Together, the present work suggests that Nrf2 is involved in the pathogenesis of IDD and shows the protective effects as well as the underlying mechanism of Kinsenoside on Nrf2 activation in NPCs.


Nrf2; apoptosis; intervertebral disc degeneration; kinsenoside; oxidative stress; senescence


Kinsenoside ameliorates intervertebral disc degeneration through the activation of AKT-ERK1/2-Nrf2 signaling pathway.


Wang Y1, Zuo R1, Wang Z2, Luo L1, Wu J1, Zhang C1, Liu M1, Shi C2, Zhou Y1.

Publish date

2019 Sep 23




The central purpose of this study was to investigate therapeutic effects of the botanical derivative, kinsenoside (KD), in experimental autoimmune hepatitis (AIH). Treatment with KD substantially reduced hepatic histopathological damage, induced by lymphocyte infiltration and proinflammatory cytokines, in concanavalin A-induced T-cell-mediated hepatitis, and in dendritic cells (DCs) loaded with hepatocellular carcinoma cells (DC/Hepa1-6) induced murine AIH. Interactions between immune cells after KD treatment in AIH were detected by anti-CD8 antibody blocking, CD8+ T cell sorting, and vaccinated mice with KD-pretreated DCs in a DC/Hepa1-6 model. These results showed that KD inhibited the elevated expressions of CD86 and major histocompatibility complex II, densities of chemokine receptor C-C chemokine receptor type 7, and extensive migration to lymph nodes, and increased the programmed death ligand 1 level of DCs, followed by suppressing CD8+ T cells, characterized as low differentiation and cytotoxicity, and eliciting cytokines balance. Furthermore, biochemical analysis, two-dimensional fingerprint screen and three-dimensional molecular docking results showed that KD bound to the vascular endothelial growth factor receptor 2 (VEGFR2) kinase domain, which inhibited the metabolism-related phosphatidylinositol 3 kinase/protein kinase B (PI3K-AKT) pathway in DCs and DC-modulated CD8+ T cells to lower the mitochondrial membrane potential and glucose/lipid utilization ratio in both cells. KD reversed activation of the PI3K-AKT pathway by 740 Y-P (PI3K agonist), thereby impeding the translocation and dimerization of signal transducer and activators of transcription (STAT) 3 and synergistically blocking the inflammation-related Janus kinase (JAK) 2/STAT3 pathway in DCs and DC-modulated T cells.

KD treatment elicits immunosuppression against autoimmune liver injury by targeting VEGFR2, followed by diminishing the cross-talk of metabolism-related PI3K-AKT and inflammation-related JAK2-STAT3 pathways, and thereby disrupts DC-induced cross-priming of CD8+ T cell responses. (Hepatology 2016;64:2135-2150).

© 2016 by the American Association for the Study of Liver Diseases.


Effects of kinsenoside, a potential immunosuppressive drug for autoimmune hepatitis, on dendritic cells/CD8+ T cells communication in mice.


Xiang M1, Liu T1, Tan W2, Ren H3, Li H1, Liu J2, Cao H1, Cheng Q1, Liu X1, Zhu H2, Tuo Y1, Wang J2, Zhang Y2.

Publish date

2016 Dec