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  • Brand : BIOFRON

  • Catalogue Number : BF-S3015

  • Specification : 98%

  • CAS number : 115-53-7

  • Formula : C19H23NO4

  • Molecular Weight : 329.39

  • PUBCHEM ID : 5459308

  • Volume : 25mg

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Catalogue Number


Analysis Method






Molecular Weight



White crystalline powder

Botanical Source

Chaenomeles speciosa,Menispermum dauricum,Sinomenium acutum,Stephania dentifolia,Stephania micrantha

Structure Type



Standards;Natural Pytochemical;API







1.3±0.1 g/cm3



Flash Point

264.4±30.1 °C

Boiling Point

513.6±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#:115-53-7) MSDS, density, melting point, boiling point, structure, formula, molecular weight etc. Articles of coniferyl ferulate are included as well.>> amp version: coniferyl ferulate




Sinomenine, an alkaloid originally isolated from the roots of Sinomeniumacutum, is used as a traditional Chinese medicine for rheumatic arthritis. However, little is known about the neuronal mechanisms underlying the analgesic effects of sinomenine in animals with chronic inflammatory pain. In this study, we investigated the persistent inflammatory pain induced by hind paw injection of complete Freund’s adjuvant (CFA) in mice, which was reversed by sinomenine administration. In the anterior cingulate cortex (ACC), a region highly associated with chronic pain processing, the upregulation of GluN2B-containing N-methyl-D-aspartate (NMDA) receptors and Ca2+/calmodulin-dependent protein kinase II, total levels of GluA1, and phosphorylation of GluA1 at Ser831 (p-GluA1-Ser831) were reversed by systemically administrating sinomenine. Furthermore, sinomenine treatment downregulated the mammalian target of rapamycin (mTOR) pathway. Increases in p-mTOR, p-p70S6k, p-S6, and p-4EBP, which were induced by chronic inflammation, were all changed. However, sinomenine did not affect the levels of GluN2A-containing NMDA receptors and p-GluA1-Ser845, as well as the total levels of mTOR, p70S6k, S6, and 4EBP. In conclusion, results indicated that sinomenine reduced the chronic inflammatory pain induced by CFA, at least partially by regulating the GluN2B receptors and mTOR signals in the ACC.


Anterior cingulate cortex; Chronic pain; NMDA receptor; Sinomenine; mTOR.


Sinomenine Attenuates Chronic Inflammatory Pain in Mice


Shuo Li 1 , Jing Han 1 , Dong-Sheng Wang 2 , Qi Yang 1 , Bin Feng 1 , Wen-Bo Kang 2 , Le Yang 1 , Gang Liu 3 , Ming-Gao Zhao 4

Publish date

2017 Feb




Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory arthropathy associated with articular damage and attendant comorbidities. Even although RA treatment has advanced remarkably over the last decade, a significant proportion of patients still do not achieve sustained remission. The cause of RA is not yet known despite the many potential mechanisms proposed. It has been confirmed that RA is associated with dysregulated immune system and persistent inflammation. Therefore, management of inflammation is always the target of therapy. Sinomenine (SIN) is the prescription drug approved by the Chinese government for RA treatment. A previous study found that SIN was a robust anti-inflammation drug. In this study, we screened the different secretory cytokines using inflammation antibody arrays and qRT-PCR in both LPS-induced and SIN-treated RAW264.7 cells followed by evaluation of the ability of SIN to modulate cytokine secretion in a cell model, collagen-induced arthritis (CIA) mouse model, and RA patients. Several clinical indexes affecting the 28-joint disease activity score (DAS28) were determined before and after SIN treatment. Clinical indexes, inflammatory cytokine secretion, and DAS28 were compared among RA patients treated with either SIN or methotrexate (MTX). To explore the mechanism of SIN anti-inflammatory function, RA-associated monocyte/macrophage subsets were determined using flow cytometry in CIA mouse model and RA patients, both treated with SIN. The results demonstrated that SIN regulated IL-6, GM-CSF, IL-12 p40, IL-1α, TNF-α, IL-1β, KC (CXCL1), Eotaxin-2, IL-10, M-CSF, RANTES, and MCP-1 secretion in vivo and in vitro and reduced RA activity and DAS28 in a clinical setting. Furthermore, SIN attenuated CD11b+F4/80+CD64+ resident macrophages in the synovial tissue, CD11b+Ly6C+CD43+ macrophages in the spleen and draining lymph nodes of CIA mice. The percentage of CD14+CD16+ peripheral blood mononuclear cells was reduced by SIN in RA patients. These data indicated that SIN regulates the secretion of multiple inflammatory cytokines and monocyte/macrophage subsets, thereby suppressing RA progression. Therefore, along with MTX, SIN could be an alternative cost-effective anti-inflammatory agent for treating RA.


cytokine; inflammatory; macrophages; monocytes; rheumatoid arthritis; sinomenine.


Sinomenine Inhibits the Progression of Rheumatoid Arthritis by Regulating the Secretion of Inflammatory Cytokines and Monocyte/Macrophage Subsets


Weiwei Liu 1 , Yajie Zhang 2 3 , Weina Zhu 2 3 , Chunhua Ma 2 3 , Jie Ruan 2 3 , Hongyan Long 2 3 4 , Yue Wang 1 5

Publish date

2018 Sep 26




Sinomenine is a nonaddictive alkaloid used to prevent morphine dependence, even thoughits mechanism isnot fully understood. Astrocytes aggravate the pathological process in their neighboring cellsthrough exosomes in central nervous system diseases. However, the effect of sinomenine on astrocyte-derived exosomes for the amelioration of morphine dependence has not been reported yet. In this study, we found that sinomenine prevented the morphine-induced conditionedplace preference in mice. Sinomenine reduced the levels of cAMP and intracellular Ca2+ in morphine-treated SH-SY5Y cells. Moreover, sinomenine inhibited the expressions of p-NMDAR1/NMDAR1, p-CAMKII/CAMKII, and p-CREB/CREB in the hippocampusof morphine-dependent mice and SH-SY5Y cells. Furthermore, we found that sinomenine inhibitedthe morphine-induced activation of astrocytesin vivo and in vitro. Afterwards, exosomes were isolated from cultured primary astrocytes treated with phosphate buffer saline (PBS, ctl-exo), morphine (mor-exo), or morphine and sinomenine (Sino-exo). Subsequently, morphine-treated SH-SY5Y cells were treated with ctl-exo, mor-exo, and Sino-exo. Results showed that Sino-exo reduced the level of cAMP, intracellular Ca2+, and the expression of p-CAMKII/CAMKII and p-CREB/CREB in morphine-treated SH-SY5Y cells. In conclusion, we demonstrated that sinomenine exhibited protective effects against morphine dependencein vivo and in vitro through theNMDAR1/CAMKII/CREB pathway. Sinomenine-induced alterationof the function of astrocyte-derived exosomes may contribute to the antidependence effects of sinomenine in morphine dependence


CAMKII; CREB; NMDAR1; exosomes; morphine; sinomenine.


Sinomenine Protects Against Morphine Dependence Through the NMDAR1/CAMKII/CREB Pathway: A Possible Role of Astrocyte-Derived Exosomes


Jinying Ou 1 , Yuting Zhou 2 , Chan Li 3 , Zhijie Chen 4 , Hancheng Li 5 , Miao Fang 6 , Chen Zhu 7 , Chuying Huo 8 , Ken Kin-Lam Yung 9 , Jing Li 10 , Chaohua Luo 11 , Zhixian Mo 12

Publish date

2018 Sep 17

Description :

Sinomenine reduces iNOS expression via inhibiting the T-bet IFN-γ pathway in experimental autoimmune encephalomyelitis in rats. PUMID/DOI:2355478 J Biomed Res. 2012 Nov;26(6):448-55. In this study, we further investigated the mechanisms of Sinomenine treatment in EAE rats. In EAE rats, treatment with Sinomenine exerted an anti-inducible NO synthase (anti-iNOS) effect, which is related to the reductions of Th1 cytokine interferon-γ (IFN-γ) and its transcription factor, T-bet, in spinal cords. Moreover, Sinomenine treatment of splenocytes stimulated with anti-CD3 antibody and recombinant rat interleukin 12 reduced the expression of T-bet and IFN-γ in vitro and also reduced the capability of supernatants of splenocyte culture to induce iNOS expression by primary astrocytes. However, Sinomenine had no direct inhibitory effect on iNOS produced by astrocytes cultured with IFN-γ and tumor necrosis factor α in vitro. In conclusion, the anti-iNOS effect of Sinomenine on EAE is mediated via the suppression of T-bet /IFN-γ pathway. Sinomenine attenuates 2, 4, 6-trinitrobenzene sulfonic acid-induced colitis in mice. PUMID/DOI:17386408 Int Immunopharmacol. 2007 May;7(5):604-11. Sinomenine is a pure alkaloid extracted from the Chinese medical plant Sinomenium acutum. It was demonstrated that Sinomenine had anti-inflammatory and immunosuppressive effects in the previous studies. The aim of the present study was to evaluate therapeutic effects of Sinomenine on 2, 4, 6-trinitrobenzene sulfonic acid (TNBS) induced colitis in mice. Two hours following colonic instillation of TNBS, Sinomenine with several doses (30, 100, 200 mg/kg) was given by gastric gavage once daily for 7 days. Comparing with the saline-treated mice with TNBS-induced colitis, Sinomenine (100 mg/kg and 200 mg/kg)-treated mice with TNBS-induced colitis were shown improvements of weight loss, macroscopic score, histological score, and myeloperoxidase activity. Moreover, treatments with Sinomenine (100 mg/kg and 200 mg/kg) decreased the up-regulated mRNA and protein levels of tumour necrosis factor-alpha(TNF-alpha) and interferon-gamma (IFN-gamma) caused by TNBS. Our findings suggest that Sinomenine attenuates TNBS-induced colitis in mice and the therapeutic mechanism might be related to the reduction of up-regulated colonic TNF-alpha and IFN-gamma production caused by TNBS. Sinomenine, a natural dextrorotatory morphinan analog, is anti-inflammatory and neuroprotective through inhibition of microglial NADPH oxidase PUMID/DOI:17880684 J. Neuroinflamm., 2007, 4(1):23. Sinomenine showed equivalent efficacy in protecting against dopaminergic (DA) neuron death in rat midbrain neuron-glial cultures at both micro- and sub-picomolar concentrations, but no protection was seen at nanomolar concentrations. The neuroprotective effect of Sinomenine was attributed to inhibition of microglial activation, since SN significantly decreased tumor necrosis factor-α (TNF-α, prostaglandin E2 (PGE2) and reactive oxygen species (ROS) production by microglia. In addition, from the therapeutic point of view, we focused on sub-picomolar concentration of SN for further mechanistic studies. We found that 10-14 M of Sinomenine failed to protect DA neurons against MPP+-induced toxicity in the absence of microglia. More importantly, Sinomenine failed to show a protective effect in neuron-glia cultures from mice lacking functional NADPH oxidase (PHOX), a key enzyme for extracellular superoxide production in immune cells. Furthermore, we demonstrated that Sinomenine reduced LPS-induced extracellular ROS production through the inhibition of the PHOX cytosolic subunit p47phoxtranslocation to the cell membrane.Conclusion:Our findings strongly suggest that the protective effects of Sinomenine are most likely mediated through the inhibition of microglial PHOX activity. These findings suggest a novel therapy to treat inflammation-mediated neurodegenerative diseases.