Fangchinoline
(Synonyms: 防己诺林碱) 目录号 : GC38437
An alkaloid with diverse biological activities
Cas No.:436-77-1
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >99.50%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Fangchinoline is an alkaloid that has been found in S. tetrandrae and has diverse biological activities, including anti-inflammatory, neuroprotective, and anticancer properties.1,2,3 It inhibits the activity of sheep COX and decreases IL-6-induced proliferation of MH60 mouse hybridoma cells with IC50 values of 129 and 3.7 ?M, respectively.1 Fangchinoline (1 and 10 ?M) reduces cyanide-induced increases in secreted glutamate levels and cell death in primary neonatal rat cerebellar granule neurons.2 It decreases proliferation of PC3 human prostate cancer cells by 63 and 86% when used at concentrations of 20 and 30 ?M, respectively.3 Fangchinoline reduces tumor growth in a PC3 mouse xenograft model when administered at a dose of 5 mg/kg per day for 12 days.
1.Choi, H.S., Kim, H.S., Min, K.R., et al.Anti-inflammatory effects of fangchinoline and tetrandrineJ. Ethnopharmacol.69(2)173-179(2000) 2.Cho, S.O., and Seong, Y.H.Protective effect of fangchinoline on cyanide-induced neurotoxicity in cultured rat cerebellar granule cellsArch. Pharm. Res.25(3)349-356(2002) 3.Wang, C.D., Huang, J.G., Gao, X., et al.Fangchinoline induced G1/S arrest by modulating expression of p27, PCNA, and cyclin D in human prostate carcinoma cancer PC3 cells and tumor xenograftBiosci. Biotechnol. Biochem.74(3)488-493(2010)
| Cas No. | 436-77-1 | SDF | |
| 别名 | 防己诺林碱 | ||
| Canonical SMILES | OC1=C(OC2=CC([C@]3([H])CC(C=C4)=CC=C4O5)=C(CCN3C)C=C2OC)C([C@](N6C)([H])CC7=CC=C(OC)C5=C7)=C(CC6)C=C1OC | ||
| 分子式 | C37H40N2O6 | 分子量 | 608.72 |
| 溶解度 | DMSO: 50 mg/mL (82.14 mM) | 储存条件 | 4°C, protect from light |
| 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 | 1.6428 mL | 8.214 mL | 16.4279 mL |
| 5 mM | 0.3286 mL | 1.6428 mL | 3.2856 mL |
| 10 mM | 0.1643 mL | 0.8214 mL | 1.6428 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。
Fangchinoline diminishes STAT3 activation by stimulating oxidative stress and targeting SHP-1 protein in multiple myeloma model
J Adv Res 2021 Mar 20;35:245-257.PMID:35024200DOI:10.1016/j.jare.2021.03.008.
Introduction: The development of cancer generally occurs as a result of various deregulated molecular mechanisms affecting the genes that can control normal cellular growth. Signal transducer and activator of transcription 3 (STAT3) pathway, once aberrantly activated can promote carcinogenesis by regulating the transcription of a number of oncogenic genes. Objectives: Here, we evaluated the impact of Fangchinoline (FCN) to attenuate tumor growth and survival through modulation of oncogenic STAT3 signaling pathway using diverse tumor cell lines and a xenograft mouse model. Methods: To evaluate the action of FCN on STAT3 cascade, protein levels were analyzed by Western blot analysis and electrophoretic mobility shift assay (EMSA). Translocation of STAT3 was detected by immunocytochemistry. Thereafter, FCN-induced ROS was measured by GSH/GSSG assay and H2DCF-DA. FCN-induced apoptosis was analyzed using Western blot analysis and flow cytometry for various assays. Finally, anti-cancer effects of FCN in vivo was evaluated in a myeloma model. Results: We noted that FCN abrogated protein expression levels of STAT3 and upstream signals (JAK1/2 and Src). In addition, FCN also attenuated DNA binding ability of STAT3 and its translocation into the nucleus. It altered the levels of upstream signaling proteins, increased SHP-1 levels, and induced substantial apoptosis in U266 cells. FCN also promoted an increased production of reactive oxygen species (ROS) and altered GSSG/GSH ratio in tumor cells. Moreover, FCN effectively abrogated tumor progression and STAT3 activation in a preclinical myeloma model. Conclusion: Overall, this study suggests that FCN may have a tremendous potential to alter abnormal STAT3 activation and induce cell death in malignant cells along with causing the suppression of pathogenesis and growth of cancer through a pro-oxidant dependent molecular mechanism.
Fangchinoline inhibits non-small cell lung cancer metastasis by reversing epithelial-mesenchymal transition and suppressing the cytosolic ROS-related Akt-mTOR signaling pathway
Cancer Lett 2022 Sep 1;543:215783.PMID:35700820DOI:10.1016/j.canlet.2022.215783.
Few drugs alleviate non-small cell lung cancer (NSCLC) metastasis effectively. Small molecular screening demonstrated that Fangchinoline (Fan) reversed epithelial-mesenchymal transition (EMT) in NSCLC cells, inhibiting cell invasion and migration. RNA sequencing (RNA-seq) of Fan-treated NSCLC cells revealed that Fan potently quenched the NADP+ metabolic process. Molecular docking analysis revealed that Fan directly and specifically targeted NOX4. NOX4 was associated with poor prognosis in NSCLC in both The Cancer Genome Atlas (TCGA) and Hong Kong cohorts. In mitochondrial DNA-depleted ρ0 NSCLC cells, Fan decreased cytosolic reactive oxygen species (ROS) to inhibit the Akt-mTOR signaling pathway by directly promoting NOX4 degradation. In TCGA and Hong Kong cohorts, NOX4 upregulation acted as a driver event as it positively correlated with metastasis and oxidative stress. Single-cell RNA-seq indicated that NOX4 was overexpressed, especially in cancer cells, cancer stem cells, and endothelial cells. In mice, Fan significantly impeded subcutaneous xenograft formation and reduced metastatic nodule numbers in mouse lung and liver. Drug sensitivity testing demonstrated that Fan suppressed patient-derived organoid growth dose-dependently. Fan is a potent small molecule for alleviating NSCLC metastasis by directly targeting NOX4 and is a potential novel therapeutic agent.
Fangchinoline induces gallbladder cancer cell apoptosis by suppressing PI3K/Akt/XIAP axis
PLoS One 2022 Apr 21;17(4):e0266738.PMID:35446864DOI:10.1371/journal.pone.0266738.
Gallbladder cancer (GBC) is the most common biliary tract malignancy with a dismal prognosis. The development of new drugs may help to improve prognosis. This study found that Fangchinoline, a bisbenzylisoquinoline alkaloids, inhibited the proliferation and clone formation of GBC cells in a dose-dependent manner. Moreover, Hoechst staining, TUNEL assays, and flow cytometry demonstrated that Fangchinoline effectively induced apoptosis in GBC cells. Further studies found that an anti-apoptotic pathway, the PI3K/Akt/XIAP axis, was significantly inhibited in GBC cells after treating with Fangchinoline. Finally, we confirmed that Fangchinoline restrained xenograft tumor growth in vivo. Our findings indicate that Fangchinoline can be considered a potential drug for GBC treatment.
Fangchinoline Inhibited Proliferation of Neoplastic B-lymphoid Cells and Alleviated Sjögren's Syndrome-like Responses in NOD/Ltj Mice via the Akt/mTOR Pathway
Curr Mol Pharmacol 2022;15(7):969-979.PMID:35176991DOI:10.2174/1874467215666220217103233.
Background: Fangchinoline is a bisbenzylisoquinoline alkaloid extracted from Stephania tetrandra S. Moore that is conventionally used as an analgesic, antirheumatic, and antihypertensive drug in China. However, the application of Fanchinoline in Sjögren syndrome (SS) remains unreported. Objective: This study aimed to identify the potential role of Fangchinoline in the treatment of SS via altering Akt/mTOR signaling. Methods: First, we examined levels of p-Akt and p-mTOR in infiltrating lymphocytes of labial glands from SS patients by immunohistochemistry. Then, the effects of Fangchinoline on Raji cells and Daudi cells were investigated using the CCK-8 assay, propidium iodide (PI)/RNase, and Annexin V/PI staining. Western blotting was used to identify the levels of Akt, p-Akt(ser473), mTOR, and p-mTOR. For in vivo analyses, NOD/Ltj and wild-type ICR mice were treated with a Fangchinoline solution, an LY294002 solution (an inhibitor of the PI3K/Akt/mTOR pathway), or their solvent for 28 days. Then, salivary flow assays and hematoxylin and eosin staining of submandibular glands were performed to determine the severity of SS-like responses in the mice. Results: Immunohistochemical staining of labial glands from SS patients showed that activation of p-Akt and p-mTOR in infiltrating lymphocytes might be correlated with SS development. In vitro, Fangchinoline and LY294002 inhibited proliferation, induced cell cycle arrest, and promoted apoptosis in Raji and Daudi cells by altering Akt/mTOR signaling. In vivo, Fangchinoline and LY294002 significantly improved the salivary secretion by NOD/Ltj mice and reduced the number of lymphocytic foci in the submandibular glands. Conclusion: These results indicated that Fangchinoline could effectively inhibit the proliferation of neoplastic B-lymphoid cells and reduce SS-like responses in NOD/Ltj mice. Our study highlights the potential value of the clinical application of Fangchinoline for SS treatment.
Fangchinoline supplementation attenuates inflammatory markers in experimental rheumatoid arthritis-induced rats
Biomed Pharmacother 2019 Mar;111:142-150.PMID:30579253DOI:10.1016/j.biopha.2018.12.043.
The present study evaluated the anti-inflammatory activity of Fangchinoline in rheumatoid arthritis-induced rats. Rats were grouped into sham (group I), rheumatoid arthritis (group II, control), Fangchinoline (2 μM, group III), and Fangchinoline (4 μM, group IV) groups. The serum levels of lipid peroxidation, superoxide dismutase (SOD), glutathione peroxidase (Gpx), catalase, reduced glutathione (GSH), interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α), matrix metalloproteinases (MMPs), prostaglandin-E2 (PGE2), nitric oxide (NO), zinc, ceruloplasmin, uric acid, and copper were determined. Chondrocyte cell proliferation, reactive oxygen species (ROS), and cellular levels of TNF-α and IL-6 were assessed. Lipid peroxidation, GSH, SOD, catalase, and Gpx levels recovered to near normal levels by Fangchinoline treatment. Fangchinoline treatment significantly reduced the TNF-α level by 17.8% and 40.8% in groups III and IV respectively, whereas IL-6 was significantly decreased by 23.2% and 45%, respectively. Fangchinoline treatment significantly decreased the MMP-3 level by 23.1% and 65.1% in groups III and IV respectively, whereas PGE2 was significantly decreased by 31.8% and 63.8%, respectively. Fangchinoline treatment decreased NO, uric acid, ceruloplasmin, and copper levels, whereas the zinc content was increased. Chondrocyte proliferation was significantly reduced to 73.3%, 51.3%, and 42.4% at 2 μM, 4 μM, and 6 μM Fangchinoline treatment respectively. Intracellular ROS, TNF-α, and IL-6 levels were significantly reduced in the chondrocytes. Protein expression of TNF-α was significantly decreased by 0.27-, 0.53-, and 0.67-fold at 2 μM, 4 μM, and 6 μM Fangchinoline treatment respectively. In conclusion, Fangchinoline is effective as an anti-inflammatory agent in rheumatoid arthritis-induced rats.