Furanodienone
(Synonyms: 呋喃二烯酮) 目录号 : GC62981
Furanodienone 是源自姜黄根茎 Rhizoma Curcumae 的主要生物活性成分之一。Furanodienone 诱导细胞凋亡 (apoptosis)。
Cas No.:24268-41-5
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
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- Purity: >98.00%
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- SDS (Safety Data Sheet)
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Furanodienone is one of the major bioactive constituents derived from Rhizoma Curcumae. Furanodienone induced apoptosis[1].
Furanodienone (0-573.8 μM; 24 hours) exhibits IC50 values : 56.4 μM (RKO), 73.7 μM (sw480), 251.1 μM (HT-29), 412.5 μM (sw620) and 573.8 μM (LoVo) at 24 hours, while that in 48 h are 51.8 μM (RKO), 44.18 μM (sw480), 168.9 μM (HT-29), 314.2 μM (sw620) and 502.1 μM (LoVo), respectively[1].Furanodienone (0-150 μM; 24 hours) induces apoptosis and shows increase in caspase-9 and -3 activity has been observed in both cells, whereas a relative minor effect on that of caspase-8 in RKO and HT-29 cells[1].Furanodienone (0-150 μM; 24 hours) increases the apoptotic rates from 2.34±0.45% to 19.45±2.37% and 27.34±0.79%, in RKO cells at 75 and 150 μM. whereas 12.4±1.08 and 20.64±3.02% apoptosis at the concentration of 75 and 150 μM are observed in HT-29 cells compared with 2.89±0.26%[1].
[1]. Li YW, et al. Furanodienone induces cell cycle arrest and apoptosis by suppressing EGFR/HER2 signaling in HER2-overexpressing human breast cancer cells. Cancer Chemother Pharmacol. 2011 Nov;68(5):1315-23.
| Cas No. | 24268-41-5 | SDF | |
| 别名 | 呋喃二烯酮 | ||
| 分子式 | C15H18O2 | 分子量 | 230.3 |
| 溶解度 | 储存条件 | ||
| 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 | 4.3422 mL | 21.7108 mL | 43.4216 mL |
| 5 mM | 0.8684 mL | 4.3422 mL | 8.6843 mL |
| 10 mM | 0.4342 mL | 2.1711 mL | 4.3422 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。
Furanodienone induces G0/G1 arrest and causes apoptosis via the ROS/MAPKs-mediated caspase-dependent pathway in human colorectal cancer cells: a study in vitro and in vivo
Cell Death Dis 2017 May 25;8(5):e2815.PMID:28542135DOI:10.1038/cddis.2017.220.
Furanodienone, a major bioactive constituents of sesquiterpene derived from Rhizoma Curcumae, has been proven to possess the potent anticancer efficacy on human breast cancer cells. Here, we investigated the cytotoxicity of Furanodienone on human colorectal carcinoma cell lines in vitro and in vivo, as well as its underlying molecular mechanisms in the induction of apoptosis. In this study, we found that Furanodienone significantly inhibited proliferation of RKO and HT-29 cells, induced mitochondrial dysfunction characterized by collapse of mitochondrial transmembrane potential and reduction of ATP level, and promoted the production of reactive oxygen species (ROS) that functions upstream of caspase-dependent apoptosis. The antioxidant N-acetyl cysteine, a ROS scavenger, abolished this apoptosis induced by Furanodienone. In addition, Furanodienone elevated the expression of p-p38, p-JNK, but decreased p-ERK, as a result of the produced ROS. The specific inhibitors U0126, SP600125 and SB202190 attenuated the expression of MAPKs, and regulated the expression of cleaved caspase-8, -9 and -3. Furthermore, the potential inhibitory effect of Furanodienone on CRC cells was also corroborated in mouse xenograft model. In conclusion, the results demonstrated that furanodienone-triggered ROS plays a pivotal role in apoptosis as an upstream molecule-modulating activity of caspases in mitochondrial pathway via stimulating MAPKs signaling pathway. Our finding may provide a novel candidate for development of antitumor drugs targeting on colorectal cancer.
Furanodienone inhibits cell proliferation and survival by suppressing ERα signaling in human breast cancer MCF-7 cells
J Cell Biochem 2011 Jan;112(1):217-24.PMID:21069738DOI:10.1002/jcb.22922.
Estrogen receptor alpha (ERα) plays an important role in the development and progression of breast cancer and thus the attenuation of ERα activities is a promising treatment strategy. Furanodienone is one of the main bioactive chemical components of Rhizoma Curcumae which is commonly used in Chinese medicine for the treatment of cancer. In this study, we investigated the effects of Furanodienone on human breast cancer MCF-7, T47D, and MDA-MB-231 cells. Our results showed that Furanodienone could inhibit MCF-7, T47D, and MDA-MB-231 cells proliferation in a dose (10-160 µM) dependent manner. ERα-negative MDA-MB-231 cells were less sensitive to Furanodienone than ERα-positive MCF-7 and T47D cells. Furanodienone could effectively block 17β-estradiol (E2)-stimulated MCF-7 cell proliferation and cell cycle progression and induce apoptosis evidenced by the flow cytometric detection of sub-G1 DNA content and the appearance of apoptotic nuclei after DAPI staining. Furanodienone specifically down-regulated ERα protein and mRNA expression levels without altering ERβ expression. Furanodienone treatment inhibited E2-stimulation of estrogen response element (ERE)-driven reporter plasmid activity and ablated E2-targeted gene (e.g., c-Myc, Bcl-2, and cyclin D1) expression which resulted in the inhibition of cell cycle progression and cell proliferation, and in the induction of apoptosis. Knockdown of ERα in MCF-7 cells by ERα-specific siRNA decreased the cell growth inhibitory effect of Furanodienone. These findings suggest that effects of Furanodienone on MCF-7 cells are mediated, at least in part, by inhibiting ERα signaling.
Furanodienone induces cell cycle arrest and apoptosis by suppressing EGFR/HER2 signaling in HER2-overexpressing human breast cancer cells
Cancer Chemother Pharmacol 2011 Nov;68(5):1315-23.PMID:21461888DOI:10.1007/s00280-011-1624-x.
Purpose: Overexpression of EGFR and HER2 is seen in breast cancers and results in poor prognosis and decreased patient survival. Clinically, EGFR and HER2 are effective therapeutic targets. The objective of this study is to investigate the in vitro effects of Furanodienone, an active chemical component isolated from Rhizoma Curcumae, on the activation of EGFR/HER2 signaling, cell cycle, and apoptosis in HER2-overexpressing BT474 and SKBR3 cells. Methods: Cell growth was assessed by SRB protein assay. Cell cycle analysis was carried out by flow cytometry, and apoptosis was observed by Annexin V and DAPI staining. Effects of Furanodienone on the activation of EGFR/HER2 signaling-related proteins were analyzed by western blotting. Results: Furanodienone inhibited cell growth in BT474 and SKBR3 cells. Furanodienone caused G1 arrest in BT474 cells and induced apoptosis in SKBR3 cells. Furanodienone interfered with EGFR/HER2 signaling in treated cells as shown by decreases in phosphorylated EGFR, HER2, Akt, Gsk3β and an increase in p27(kip1) protein. Accordingly, Furanodienone inhibited EGF-induced phosphorylation of EGFR, HER2, Akt, and Gsk3β. EGFR-specific siRNA knockdown did not affect the cell growth inhibitory effect of Furanodienone. On the contrary, specific siRNA knockdown of HER2 increased cellular resistance to Furanodienone toxicity. In HER-2-deficient MDA-MB-231 cells, the transfection and expression of HER2 increased the sensitivity of cells to Furanodienone toxicity. Conclusion: Furanodienone inhibited EGFR/HER2 signaling pathway in BT474 and SKBR3 cells. More importantly, the effect of Furanodienone was specifically dependent on HER2, but not EGFR, expression.
Furanodienone overcomes temozolomide resistance in glioblastoma through the downregulation of CSPG4-Akt-ERK signalling by inhibiting EGR1-dependent transcription
Phytother Res 2019 Jun;33(6):1736-1747.PMID:31006910DOI:10.1002/ptr.6363.
Glioblastoma multiforme (GBM) is a highly aggressive type of brain tumour. Patients with GBM respond poorly to chemotherapy and have poor survival outcomes. Neuron-glial antigen 2 (NG2), also known as chondroitin sulphate proteoglycan 4 (CSPG4), has been shown to contribute to critical processes, such as cell survival, proliferation, and chemotherapy resistance, during glioma progression. In this study, we found that Furanodienone (FUR), a diene-type sesquiterpene isolated from the rhizomes of Rhizoma curcumae, exhibited a potential cytotoxic effect on temozolomide (TMZ)-resistant GBM cells in vitro by inhibiting CSPG4 and related signalling pathways. Studies investigating the mechanism demonstrated that FUR suppressed CSPG4-Akt-ERK signalling, inflammatory responses, and cytokine levels but activated caspase-dependent pathways and mitochondrial dysfunction. Furthermore, an immunofluorescence assay and a dual-luciferase reporter assay revealed that inhibition of EGR1-mediated transcription might have contributed to the FUR-dependent blockade of CSPG4 signalling and glioma cell survival. These results established a link between FUR-induced CSPG4 inhibition and the suppression of EGR1-dependent transcription. Attenuation of ERK1/2 and cytokine signalling might have generated the EGR1-dependent negative feedback loop of the CSPG4 pathway during FUR-induced apoptosis. These findings suggested that FUR could be a therapeutic candidate for the treatment of malignant glioma via targeting CSPG4 signalling.
Validation and application of a novel UHPLC-MS/MS method for the measurement of Furanodienone in rat plasma
Biomed Chromatogr 2020 Jan;34(1):e4717.PMID:31634986DOI:10.1002/bmc.4717.
A sensitive ultra-high performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS) method was established to analyze Furanodienone in rat plasma. In the process of chromatographic separation, selected reaction monitoring transitions for Furanodienone and patchouli alcohol (internal standard, IS) were m/z 231.1 → 83.2 and m/z 205.1 → 95.1, respectively. Great linearity of Furanodienone in plasma samples was found in the corresponding concentration range (r > 0.995). Intra- and inter-day precisions (RSD, %) were <11.3% in plasma, and the accuracy (RE, %) was within ±10.7%. This method was used to the Furanodienone study on rat pharmacokinetics after a single oral dose of 10 mg/kg of furanodiene. The results indicated that the maximum observed plasma concentration was 52.4 ± 19.1 ng/ml at 1.2 ± 0.7 h with an elimination half-life of 2.2 ± 0.7 h. The obtained data indicated that Furanodienone could be moderately distributed and eliminated.