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    Sophocarpine
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    CAS No. 145572-44-7 Price $30 / 20mg
    Catalog No.CFN99182Purity>=98%
    Molecular Weight246.35Type of CompoundAlkaloids
    FormulaC15H22N2OPhysical DescriptionPowder
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    Sophocarpine

    Sophocarpine
    Product Name Sophocarpine
    CAS No.: 145572-44-7
    Catalog No.: CFN99182
    Molecular Formula: C15H22N2O
    Molecular Weight: 246.35 g/mol
    Purity: >=98%
    Type of Compound: Alkaloids
    Physical Desc.: Powder
    Targets: TGF-尾/Smad | TLR | ERK | JNK | p38MAPK | IkB | AMPK | NF-kB | NOS | COX | TNF-伪 | IL Receptor | IKK
    Source: The herbs of Sophora alopecuroidos L.
    Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
    Price: $30 / 20mg
    Inquire / Order: manager@chemfaces.com
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  • Sci Rep.2019, 9(1):4342
  • Pharmacognosy Magazine2018, 14(56):418-424
  • PLoS One.2017, 12(3):e0173585
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  • Front Endocrinol (Lausanne).2020, 11:568436.
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  • JPC-Journal of Planar Chromatography 2017, 30(4)
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  • Biological Activity
    Description: Sophocarpine has anti-cachectic, anti-inflammatory, and neuroprotective effects. It has significant antivirus effects against coxsackievirus B3 and therapeutic effects for viral myocarditis in clinical, can ameliorate the ischemic injury induced by transient focal cerebral ischemia in rats, and may be a potential chemotherapeutic agent for chronic liver diseases. Sophocarpine inhibited the expression of TNF-alpha, IL-6, JNK, iNOS, COX-2, p38 MAPK, NF-κB, TLR4, and activated signaling pathway of AMPK.
    Targets: TGF-β/Smad | TLR | ERK | JNK | p38MAPK | IkB | AMPK | NF-kB | NOS | COX | TNF-α | IL Receptor | IKK
    In vitro:
    Toxicol In Vitro. 2013 Apr;27(3):1065-71.
    Sophocarpine alleviates hepatocyte steatosis through activating AMPK signaling pathway.[Pubmed: 23395669]
    Sophocarpine, an effective compound derived from foxtail-like sophora herb and seed, has been reported that it can alleviate non-alcoholic steatohepatitis (NASH) in rats and affect adipocytokine synthesis. Meanwhile, adipocytokines could adjust hepatic lipid metabolism through AMPK signaling pathway.
    METHODS AND RESULTS:
    In the work presented here, primary hepatocytes were isolated from specific pathogen-free male SD rats and incubated with 200 μmol/L oleic acid for 24h to induce steatotic model, then treated with Sophocarpine for 72 h. Oil red staining was performed to evaluate steatosis, total RNA and protein of primary hepatocytes were extracted for real-time RT-PCR and western blot analysis. A cluster of aberrances were observed in the model group, including hepatocyte steatosis, increased leptin and decreased adiponectin mRNA expressions. While Sophocarpine treatment resulted in: significant improvement of steatosis (>50% decrease), decrease of leptin expression (<0.57-fold) and increase of adiponectin expression (>1.48-fold). Moreover, compared with the model group, Sophocarpine could significantly increase P-AMPKα (>5.82-fold), AMPKα (>1.29-fold) and ACC (>3.27-fold) protein expressions, and reduce P-ACC (<0.30-fold) and HNF-4α (<0.20-fold) protein expression. The mRNA expression of Srebp-1c was downregulated significantly simultaneously (<0.68-fold).
    CONCLUSIONS:
    We concluded that Sophocarpine could alleviate hepatocyte steatosis and the potential mechanism might be the activated signaling pathway of AMPK.
    Toxicol In Vitro. 2012 Feb;26(1):1-6.
    Anti-inflammatory effects of sophocarpine in LPS-induced RAW 264.7 cells via NF-κB and MAPKs signaling pathways.[Pubmed: 21978812]
    Sophocarpine, a tetracyclic quinolizidine alkaloid, is one of the most abundant active ingredients in Sophora alopecuroides L. Our previous studies have showed that Sophocarpine exerts anti-inflammatory activity in animal models.
    METHODS AND RESULTS:
    In the present study, anti-inflammatory mechanisms of Sophocarpine were investigated in lipopolysaccharide (LPS)-induced responses in RAW 264.7 cells. Furthermore, the cytotoxicity of Sophocarpine was tested. The results indicated that Sophocarpine could increase the LDH level and inhibit cell viability up to 800μg/ml, and which was far higher than that of the plasma concentration of Sophocarpine in clinical effective dosage. The results also demonstrated that Sophocarpine (50 and 100μg/ml) suppressed LPS-stimulated NO production and pro-inflammatory cytokines secretion, including tumor necrosis factor alpha (TNF-α) and interleukin-6 (IL-6). These were associated with the decrease of the expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). Furthermore, Sophocarpine inhibited LPS-mediated nuclear factor-κB (NF-κB) activation via the prevention of inhibitor κB (IκB) phosphorylation. Sophocarpine had no effect on the LPS-induced phosphorylation of extracellular signal-regulated kinase 1/2 (Erk1/2), whereas it attenuated the phosphorylation of p38 mitogen-activated protein (MAP) kinase and c-Jun NH(2)-terminal kinase (JNK).
    CONCLUSIONS:
    Our data suggested that Sophocarpine exerted anti-inflammatory activity in vitro, and it might attribute to the inhibition of iNOS and COX-2 expressions via down-regulation of the JNK and p38 MAP kinase signal pathways and inhibition of NF-κB activation.
    In vivo:
    Brain Res. 2011 Mar 25;1382:245-51.
    Neuroprotective effect of sophocarpine against transient focal cerebral ischemia via down-regulation of the acid-sensing ion channel 1 in rats.[Pubmed: 21232529]
    Sophocarpine, one of the major alkaloid compounds isolated from Sophora pachycarpa, is highly valued and important in traditional Chinese medicine. In the present study, we aimed to explore the possible mechanisms underlying Sophocarpine-mediated neuroprotection against transient focal cerebral ischemia.
    METHODS AND RESULTS:
    Sophocarpine (5, 10, or 20mg/kg) was given 30min before focal ischemia was induced in rats by occlusion of the middle cerebral artery. After Sophocarpine treatment, the total infarct volume was significantly decreased in comparison to the ischemia-reperfusion values. The results of a neurological evaluation were significantly improved in the Sophocarpine treated group when compared to controls. The number of TUNEL-positive cells was significantly reduced compared to the untreated ischemic group. Results of Western blotting and immunohistochemical staining indicated that pretreatment with Sophocarpine down-regulated the expression of acid-sensing ion channel 1 (ASIC1) in the ischemic cortex.
    CONCLUSIONS:
    These results suggest that Sophocarpine ameliorated the ischemic injury induced by transient focal cerebral ischemia in rats and that this neuroprotective effect might be related to the anti-ASIC1 channel and anti-apoptotic action of Sophocarpine.
    Sophocarpine Description
    Source: The herbs of Sophora alopecuroidos L.
    Solvent: Chloroform, Dichloromethane, Ethyl Acetate, DMSO, Acetone, etc.
    Storage: Providing storage is as stated on the product vial and the vial is kept tightly sealed, the product can be stored for up to 24 months(2-8C).

    Wherever possible, you should prepare and use solutions on the same day. However, if you need to make up stock solutions in advance, we recommend that you store the solution as aliquots in tightly sealed vials at -20C. Generally, these will be useable for up to two weeks. Before use, and prior to opening the vial we recommend that you allow your product to equilibrate to room temperature for at least 1 hour.

    Need more advice on solubility, usage and handling? Please email to: service@chemfaces.com

    After receiving: The packaging of the product may have turned upside down during transportation, resulting in the natural compounds adhering to the neck or cap of the vial. take the vial out of its packaging and gently shake to let the compounds fall to the bottom of the vial. for liquid products, centrifuge at 200-500 RPM to gather the liquid at the bottom of the vial. try to avoid loss or contamination during handling.
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    Calculate Dilution Ratios(Only for Reference)
    1 mg 5 mg 10 mg 20 mg 25 mg
    1 mM 4.0593 mL 20.2963 mL 40.5927 mL 81.1853 mL 101.4816 mL
    5 mM 0.8119 mL 4.0593 mL 8.1185 mL 16.2371 mL 20.2963 mL
    10 mM 0.4059 mL 2.0296 mL 4.0593 mL 8.1185 mL 10.1482 mL
    50 mM 0.0812 mL 0.4059 mL 0.8119 mL 1.6237 mL 2.0296 mL
    100 mM 0.0406 mL 0.203 mL 0.4059 mL 0.8119 mL 1.0148 mL
    * Note: If you are in the process of experiment, it's need to make the dilution ratios of the samples. The dilution data of the sheet for your reference. Normally, it's can get a better solubility within lower of Concentrations.
    Protocol
    Cell Research:
    Int Immunopharmacol. 2008 Dec 20;8(13-14):1767-72.
    Sophocarpine and matrine inhibit the production of TNF-alpha and IL-6 in murine macrophages and prevent cachexia-related symptoms induced by colon26 adenocarcinoma in mice.[Pubmed: 18775799 ]
    The present study aims to access the effects of sophora alkaloids on the production of pro-inflammatory cytokines and evaluate their therapeutic efficiency on cachexia.
    METHODS AND RESULTS:
    The comparative study showed that all sophora alkaloids tested here, including matrine, oxymatrine, Sophocarpine, sophoramine, and sophoridine, inhibited TNF-alpha and IL-6 production in both RAW264.7 cells and murine primary macrophages, and Sophocarpine showed the most potent inhibitory effect among them. Quantification of TNF-alpha and IL-6 mRNA in RAW264.7 cells by real-time RT-PCR revealed that both Sophocarpine and matrine suppressed TNF-alpha and IL-6 expression and Sophocarpine has stronger suppressing potency than matrine. Inoculation (s.c.) of colon26 adenocarcinoma cells into BALB/c mice induced cachexia, as evidenced by progressive weight loss, reduction in food intake, wasting of gastrocnemius muscle and epididymal fat, and increase in serum levels of TNF-alpha and IL-6. Administration of 50 mg/kg/d Sophocarpine or matrine for 5 days from the onset of cachexia did not inhibit the tumor growth but resulted in attenuation of cachexia symptoms. Furthermore, Sophocarpine and matrine decreased the serum levels of TNF-alpha and IL-6, and Sophocarpine showed a better therapeutic effect than matrine.
    CONCLUSIONS:
    These results suggest that Sophocarpine and matrine exert anti-cachectic effects probably through inhibition of TNF-alpha and IL-6.
    Animal Research:
    World J Gastroenterol. 2014 Feb 21;20(7):1822-32.
    Sophocarpine attenuates liver fibrosis by inhibiting the TLR4 signaling pathway in rats.[Pubmed: 24587659]
    To explore the effect of Sophocarpine on experimental liver fibrosis and the potential mechanism involved.
    METHODS AND RESULTS:
    Sophocarpine was injected intraperitoneally in two distinct rat hepatic fibrosis models induced either by dimethylnitrosamine or bile duct ligation. Masson's trichrome staining, Sirius red staining and hepatic hydroxyproline level were used for collagen determination. Primary hepatic stellate cells (HSCs) were isolated and treated with different concentrations of Sophocarpine. Real-time reverse transcription-polymerase chain reaction was used to detect the mRNA levels of fibrotic markers and cytokines. The expression of pathway proteins was measured by Western blot. The Cell Counting Kit-8 test was used to detect the proliferation rate of activated HSCs treated with a gradient concentration of Sophocarpine. Sophocarpine decreased serum levels of aminotransferases and total bilirubin in rats under chronic insult. Moreover, administration of Sophocarpine suppressed extracellular matrix deposition and prevented the development of hepatic fibrosis. Furthermore, Sophocarpine inhibited the expression of α-smooth muscle actin (SMA), interleukin (IL)-6, transforming growth factor-β1 (TGF-β1), Toll-like receptor 4 (TLR4), and extracellular-related kinase (ERK) in rats. Sophocarpine also down-regulated the mRNA expression of α-SMA, collagen I, collagen III, TGF-β1, IL-6, tumor necrosis factor-α and monocyte chemoattractant protein-1, and decreased protein levels of TLR4, p-ERK, p-JNK, p-P38 and p-IKK in vitro after Lipopolysaccharide induction. In addition, Sophocarpine inhibited the proliferation of HSCs accompanied by a decrease in the expression of Cyclin D1. The protein level of proliferating cell nuclear antigen was decreased in activated HSCs following a gradient concentration of Sophocarpine.
    CONCLUSIONS:
    Sophocarpine can alleviate liver fibrosis mainly by inhibiting the TLR4 pathway. Sophocarpine may be a potential chemotherapeutic agent for chronic liver diseases.
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