Sophoridine
(Synonyms: 槐定碱) 目录号 : GC38425
A quinolizidine alkaloid with diverse biological activities
Cas No.:6882-68-4
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
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- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Sophoradin is a quinolizidine alkaloid that has been found in S. alopecuroides and has diverse biological activities.1,2,3 It reduces viral titers in primary neonatal rat cardiomyocytes infected with coxsackievirus B3 (CVB3) when used at concentrations of 1 and 5 ?g/ml.2 Sophoradin inhibits the growth of, and induces apoptosis in, SW480 colorectal cancer cells, as well as reduces tumor growth in an SW480 mouse xenograft model.1 It reduces increases in TNF-α, IL-8, and prostaglandin E2 levels in the inflammatory exudate in a mouse model of carrageenan-induced paw edema when administered at doses of 12.15 and 48.6 mg/kg.3
1.Liang, L., Wang, X.-Y., Zhang, X.-H., et al.Sophoridine exerts an anti-colorectal carcinoma effect through apoptosis induction in vitro and in vivoLife Sci.91(25-26)1295-1303(2012) 2.Zhang, Y., Zhu, H., Ye, G., et al.Antiviral effects of sophoridine against coxsackievirus B3 and its pharmacokinetics in ratsLife Sci.78(17)1998-2005(2006) 3.Huang, X., Li, B., and Shen, L.Studies on the anti-inflammatory effect and its mechanisms of sophoridineJ. Anal. Methods Chem.502626(2014)
| Cas No. | 6882-68-4 | SDF | |
| 别名 | 槐定碱 | ||
| Canonical SMILES | O=C1CCC[C@]2([H])[C@@]3([H])CCCN4[C@@]3([H])[C@@](CCC4)([H])CN21 | ||
| 分子式 | C15H24N2O | 分子量 | 248.36 |
| 溶解度 | DMSO: 50 mg/mL (201.32 mM) | 储存条件 | Store at -20°C |
| General tips | 请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。 储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。 为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。 |
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| Shipping Condition | 评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。 | ||
| 制备储备液 | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 4.0264 mL | 20.1321 mL | 40.2641 mL |
| 5 mM | 0.8053 mL | 4.0264 mL | 8.0528 mL |
| 10 mM | 0.4026 mL | 2.0132 mL | 4.0264 mL |
| 第一步：请输入基本实验信息（考虑到实验过程中的损耗，建议多配一只动物的药量） | ||||||||||
| 给药剂量 | mg/kg |  |
动物平均体重 | g | |
每只动物给药体积 | ul | |
动物数量 | 只 |
| 第二步：请输入动物体内配方组成（配方适用于不溶于水的药物；不同批次药物配方比例不同，请联系GLPBIO为您提供正确的澄清溶液配方） | ||||||||||
| % DMSO % % Tween 80 % saline | ||||||||||
| 计算重置 | ||||||||||
计算结果:
工作液浓度： mg/ml；
DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，
体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。
1. 首先保证母液是澄清的；
2.
一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。
Sophoridine: A review of its pharmacology, pharmacokinetics and toxicity
Phytomedicine 2022 Jan;95:153756.PMID:34615616DOI:10.1016/j.phymed.2021.153756.
Background: Sophoridine is a bioactive alkaloid found in many Chinese herbs, such as Sophora alopecuroides l, Euchresta japonica Benth and Sophora moocrorftinan. Sophoridine hydrochloride injection has been approved as an anticancer drug in China. Purpose: This review aims to provide a comprehensive summary on the pharmacological, molecular mechanism, pharmacokinetic and toxicity studies of Sophoridine. Method: PubMed, Web of Science and China National Knowledge Infrastructure were used for a systematic search with the keywords including "Sophoridine", "pharmacology", "pharmacokinetics", and "toxicity". Results: Emerging evidence suggests that Sophoridine exhibits a broad spectrum of pharmacological activities including antitumor, anti-inflammatory, antiviral, myocardialprotective and hepatoprotective activities. These pharmacological properties lay foundation for using the plants containing Sophoridine for the treatment of numerous diseases, such as cancer, colitis, injury of lungs, ischemia myocardial,etc. The mechanisms involved in the pharmacological actions of Sophoridine are regulation of NF-κB, TLR4/IRF3, JNK/ERK, Akt/mTOR signaling pathways, down-regulating the expression of HMG3B, bcl-2, MMP-2, MMP-9, TNF-α, IL-1β IL-6 and other cytokines or kinases. However, an increasing number of published reports indicated that Sophoridine has serious adverse effects. The primary toxic effects are neurotoxicity and acute toxicity, which are of wide concern in worldwide. Moreover, Sophoridine is reported to distribute in kidney, liver, uterus, lung and other organs. It undergoes glucuronidation and excreted in urine. Conclusion: Future studies should elucidate the detailed in vivo metabolism studies on Sophoridine. The effect of substituent functional groups on Sophoridine on metabolism, the enzymes involved in the metabolism and the chemistry of metabolites also should be studied. Either structural modification of Sophoridine or its combined with other drugs may play a pivotal role to enhance its pharmacological activities and reduce its toxicity.
Sophoridine suppresses lenvatinib-resistant hepatocellular carcinoma growth by inhibiting RAS/MEK/ERK axis via decreasing VEGFR2 expression
J Cell Mol Med 2021 Jan;25(1):549-560.PMID:33210432DOI:10.1111/jcmm.16108.
Hepatocellular carcinoma (HCC) is one of the most lethal cancer types with insufficient approved therapies, among which lenvatinib is a newly approved multi-targeted tyrosine kinase inhibitor for frontline advanced HCC treatment. However, resistance to lenvatinib has been reported in HCC treatment recently, which limits the clinical benefits of lenvatinib. This study aims to investigate the underlying mechanism of lenvatinib resistance and explore the potential drug to improve the treatment for lenvatinib-resistant (LR) HCC. Here, we developed two human LR HCC cell lines by culturing with long-term exposure to lenvatinib. Results showed that the vascular endothelial growth factor receptors (VEGFR)2 expression and its downstream RAS/MEK/ERK signalling were obviously up-regulated in LR HCC cells, whereas the expression of VEGFR1, VEGFR3, FGFR1-4 and PDGFRα/β showed no difference. Furthermore, ETS-1 was identified to be responsible for VEGFR2 mediated lenvatinib resistance. The cell models were further used to explore the potential strategies for restoration of sensitivity of lenvatinib. Sophoridine, an alkaloid extraction, inhibited the proliferation, colony formation, cell migration and increased apoptosis of LR HCC cells. In vivo and in vitro results showed Sophoridine could further sensitize the therapeutic of lenvatinib against LR HCC. Mechanism studies revealed that Sophoridine decreased ETS-1 expression to down-regulate VEGFR2 expression along with downstream RAS/MEK/ERK axis in LR HCC cells. Hence, our study revealed that up-regulated VEGFR2 expression could be a predicator of the resistance of lenvatinib treatment against HCC and provided a potential candidate to restore the sensitivity of lenvatinib for HCC treatment.
Anti-cancer potential of Sophoridine and its derivatives: Recent progress and future perspectives
Bioorg Chem 2020 Jun;99:103863.PMID:32334197DOI:10.1016/j.bioorg.2020.103863.
Cancer is the second leading cause of mortality and has resulted in about 9.6 million deaths around the world in 2018. Cancer-caused deaths are expected to be 11.5 million by 2030 all over the world. Because of the fatal nature of cancer, substantial efforts are made all over the world to combat it. Phytoconstituents such as certain alkaloids, saponins, tannins, polyphenols, and terpenoids exhibit anticancer effects. Sophoridine is a tetracyclic quinolizidine alkaloid isolated from the stem and leaves of medicinal plants Sophora alopecuroides L., and Euchresta japonica Benth, and roots of Sophora alopecuroides Ait. Chinese Food and Drug Administration (CFDA) approved Sophoridine as an antitumor agent in 2005. This review covers the antitumor activities of Sophoridine and its derivatives. The efficacy of Sophoridine analogs is expressed with respect to their half-maximal inhibitory concentration (IC50 values). Structure-activity relationship (SAR) study for most of the Sophoridine derivatives has been explained. Moreover, the current market of anticancer drugs and its expected growth are discussed. Prospects provide suggestions and clues for novel sophoridine-based anticancer agents with enhanced expected efficacy and minimum toxicity.
Sophoridine inhibits endotoxin-induced acute lung injury by enhancing autophagy of macrophage and reducing inflammation
J Leukoc Biol 2022 Jul;112(1):115-125.PMID:35603481DOI:10.1002/JLB.3MA0322-428R.
Acute lung injury (ALI) is characterized by uncontrolled inflammation, which can lead to respiratory distress syndrome and cause patient death. In this study, we sought to determine the role of Sophoridine, a compound purified from sophora, in ALI. A mouse model of ALI was established by treating mice with LPS through nonexposed tracheal instillation. After LPS-induced mice were treated with Sophoridine, LPS-induced alveolar wall thickening, alveolar interstitial inflammatory exudation and thickening, and the degree of pulmonary edema were found to be inhibited. Macrophages play an important role in inflammation, and in vitro experiments have demonstrated that Sophoridine reduces the LPS-induced expression of inflammatory factors by macrophages, suggesting that Sophoridine may inhibit lung inflammation in LPS-treated mice through reduces the secretion of inflammatory factors. Further, treatment with Sophoridine up-regulated autophagy in macrophage cells in vitro and mouse lung tissues in vivo. LPS can bind to TLRs and activate the MyD88/NF-κB pathways, leading to increased inflammation in the pathogenesis of ALI. Our findings revealed that Sophoridine down-regulated the expression of TLR4/MyD88/NF-κB and mTOR mRNA and protein in mouse pulmonary tissue. Collectively, these findings indicate that Sophoridine may inhibit LPS-induced ALI by enhancing autophagy of macrophages and reducing inflammation.
Sophoridine exerts tumor-suppressive activities via promoting ESRRG-mediated β-catenin degradation in gastric cancer
BMC Cancer 2020 Jun 22;20(1):582.PMID:32571331DOI:10.1186/s12885-020-07067-x.
Background: As a natural alkaloid product isolated from Sophora alopecuroides. L, Sophoridine reshapes gastric cancer immune microenvironment via inhibiting chemotaxis and M2 polarization of tumor-associated macrophages (TAMs). However, the exact effects and underlying mechanism of Sophoridine on gastric cancer cells remains poorly known. Methods: The potential anti-tumor effects of Sophoridine on gastric cancer cell lines, including AGS and SGC7901 cells, were detected by CCK-8, EDU and colony forming assay, immunofluorescence, transwell assay, and flow cytometry. Molecular mechanisms of Sophoridine were investigated by siRNA transfection, nuclear/cytoplasmic extraction and western blot. The synergistic effects of Sophoridine with cisplatin on gastric cancer cells were further investigated in in vitro functional studies. Results: Sophoridine exhibited potent tumor-suppressive activities in gastric cancer cells, including inhibition of proliferation, colony formulation, migration and invasion, as well as induction of apoptosis. In addition, we further showed that Sophoridine induced G2/M cell cycle arrest via inhibiting double-stranded DNA breaks repair and enhanced the efficacy of cisplatin in gastric cancer cells. Molecular studies further revealed that Sophoridine promoted β-catenin degradation by enhancing Estrogen-related receptor gamma (ESRRG) expression, but not depended on ubiquitination-proteasome pathway, either TRIM33-mediated (GSK3β-independent) or altered GSK3β activity, and thus exerted potent tumor-suppressive activities. Conclusion: Sophoridine depends on targeting ESRRG/β-catenin pathway to exert tumor-suppressive activities in gastric cancer cells and enhances the anti-tumor effect of cisplatin. Our study provided the promising preclinical anti-tumor evidence for the potential application of Sophoridine against gastric cancer.