Hinokiflavone
(Synonyms: 扁柏双黄酮) 目录号 : GC38488
Hinokiflavone, isolated from Selaginella P. Beauv, Juniperus phoenicea and Rhus succedanea, possesses excellent pharmacological activities, including anti-inflammatory, antioxidant and antitumor activity. Hinokiflavone induces apoptosis and inhibits migration of breast cancer cells via EMT signalling pathway.
Cas No.:19202-36-9
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
Hinokiflavone, isolated from Selaginella P. Beauv, Juniperus phoenicea and Rhus succedanea, possesses excellent pharmacological activities, including anti-inflammatory, antioxidant and antitumor activity. Hinokiflavone induces apoptosis and inhibits migration of breast cancer cells via EMT signalling pathway.
[1] Wenzhen Huang, et al. Cell Biochem Funct . 2020 Apr;38(3):249-256. [2]Yuting Chen, et al. J Pharm Biomed Anal . 2019 May 30;169:19-29.
| Cas No. | 19202-36-9 | SDF | |
| 别名 | 扁柏双黄酮 | ||
| Canonical SMILES | O=C1C=C(C2=CC=C(O)C=C2)OC3=CC(O)=C(OC4=CC=C(C5=CC(C6=C(O)C=C(O)C=C6O5)=O)C=C4)C(O)=C13 | ||
| 分子式 | C30H18O10 | 分子量 | 538.46 |
| 溶解度 | Soluble in DMSO | 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 | 1.8571 mL | 9.2857 mL | 18.5715 mL |
| 5 mM | 0.3714 mL | 1.8571 mL | 3.7143 mL |
| 10 mM | 0.1857 mL | 0.9286 mL | 1.8571 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。
Hinokiflavone Inhibits MDM2 Activity by Targeting the MDM2-MDMX RING Domain
Biomolecules 2022 Apr 27;12(5):643.PMID:35625571DOI:10.3390/biom12050643.
The proto-oncogene MDM2 is frequently amplified in many human cancers and its overexpression is clinically associated with a poor prognosis. The oncogenic activity of MDM2 is demonstrated by its negative regulation of tumor suppressor p53 and the substrate proteins involved in DNA repair, cell cycle control, and apoptosis pathways. Thus, inhibition of MDM2 activity has been pursued as an attractive direction for the development of anti-cancer therapeutics. Virtual screening was performed using the crystal structure of the MDM2-MDMX RING domain dimer against a natural product library and identified a biflavonoid Hinokiflavone as a promising candidate compound targeting MDM2. Hinokiflavone was shown to bind the MDM2-MDMX RING domain and inhibit MDM2-mediated ubiquitination in vitro. Hinokiflavone treatment resulted in the downregulation of MDM2 and MDMX and induction of apoptosis in various cancer cell lines. Hinokiflavone demonstrated p53-dependent and -independent tumor-suppressive activity. This report provides biochemical and cellular evidence demonstrating the anti-cancer effects of Hinokiflavone through targeting the MDM2-MDMX RING domain.
Hinokiflavone Attenuates the Virulence of Methicillin-Resistant Staphylococcus aureus by Targeting Caseinolytic Protease P
Antimicrob Agents Chemother 2022 Aug 16;66(8):e0024022.PMID:35862746DOI:10.1128/aac.00240-22.
Drug-resistant bacteria was the third leading cause of death worldwide in 2019, which sounds like a cautionary note for global public health. Therefore, developing novel strategies to combat Methicillin-resistant Staphylococcus aureus (MRSA) infections is the need of the hour. Caseinolytic protease P (ClpP) represents pivotal microbial degradation machinery in MRSA involved in bacterial homeostasis and pathogenicity, considered an ideal target for combating S. aureus infections. Herein, we identified a natural compound, Hinokiflavone, that inhibited the activity of ClpP of MRSA strain USA300 with an IC50 of 34.36 μg/mL. Further assays showed that Hinokiflavone reduced the virulence of S. aureus by inhibiting multiple virulence factors expression. Results obtained from cellular thermal transfer assay (CETSA), thermal shift assay (TSA), local surface plasmon resonance (LSPR) and molecular docking (MD) assay enunciated that Hinokiflavone directly bonded to ClpP with confirmed docking sites, including SER-22, LYS-26 and ARG-28. In vivo, the evaluation of anti-infective activity showed that Hinokiflavone in combination with vancomycin effectively protected mice from MRSA-induced fatal pneumonia, which was more potent than vancomycin alone. As mentioned above, Hinokiflavone, as an inhibitor of ClpP, could be further developed into a promising adjuvant against S. aureus infections.
Hinokiflavone and Related C-O-C-Type Biflavonoids as Anti-cancer Compounds: Properties and Mechanism of Action
Nat Prod Bioprospect 2021 Aug;11(4):365-377.PMID:33534099DOI:10.1007/s13659-021-00298-w.
Biflavonoids are divided in two classes: C-C type compounds represented by the dimeric compound amentoflavone and C-O-C-type compounds typified by Hinokiflavone (HNK) with an ether linkage between the two connected apigenin units. This later sub-group of bisflavonyl ethers includes HNK, ochnaflavone, delicaflavone and a few other dimeric compounds, found in a variety of plants, notably Selaginella species. A comprehensive review of the anticancer properties and mechanism of action of HNK is provided, to highlight the anti-proliferative and anti-metastatic activities of HNK and derivatives, and HNK-containing plant extracts. The anticancer effects rely on the capacity of HNK to interfere with the ERK1-2/p38/NFκB signaling pathway and the regulation of the expression of the matrix metalloproteinases MMP-2 and MMP-9 (with a potential direct binding to MMP-9). In addition, HNK was found to function as a potent modulator of pre-mRNA splicing, inhibiting the SUMO-specific protease SENP1. As such, HNK represents a rare SENP1 inhibitor of natural origin and a scaffold to design synthetic compounds. Oral formulations of HNK have been elaborated to enhance its solubility, to facilitate the compound delivery and to enhance its anticancer efficacy. The review shed light on the anticancer potential of C-O-C-type biflavonoids and specifically on the pharmacological profile of HNK. This compound deserves further attention as a regulator of pre-mRNA splicing, useful to treat cancers (in particular hepatocellular carcinoma) and other human pathologies.
Hinokiflavone induces apoptosis and inhibits migration of breast cancer cells via EMT signalling pathway
Cell Biochem Funct 2020 Apr;38(3):249-256.PMID:32107809DOI:10.1002/cbf.3443.
Hinokiflavone is a natural product, isolated from Selaginella P. Beauv, Juniperus phoenicea and Rhus succedanea. Even though Hinokiflavone was reported to possess cytotoxicity to many cancer cells, and has potential in cancer treatment, the anti-proliferation and anti-metastasis efficacy of Hinokiflavone on human breast cancer cells has not a further research. In this study, we investigated the anti-cancer activity of Hinokiflavone in human breast cancer cells in vitro and in vivo. Hinokiflavone exhibited a time- and dose-dependent manner apoptosis induction by upregulating expression of Bax and downregulating Bcl-2 in breast cancer cells. Furthermore, Hinokiflavone significantly inhibited the migration and invasion of breast cancer cells by impairing the process of epithelial-to-mesenchymal transition. In addition, the tumour growth was distinctly inhibited by treatment of Hinokiflavone in a xenograft tumour mouse model of MDA-MB-231 cells. Immunohistochemical analysis of tumour sections showed that MMP-2+ cells and Ki-67+ cells were remarkably decreased in tumour tissues of mice after treatment of Hinokiflavone, indicating that Hinokiflavone inhibits not only proliferation but also metastasis of breast cancer cells. Our study suggested that Hinokiflavone can be a potential drug to breast cancer. SIGNIFICANCE OF THE STUDY: Hinokiflavone significantly inhibited proliferation and induced apoptosis in breast cancer cells. In addition, Hinokiflavone remarkably inhibited migration and invasion of breast cancer cells via EMT signalling pathway. It is worth noting that Hinokiflavone possesses anti-tumour effect in tumour mouse xenograft model of breast cancer. Overall, our results indicated that Hinokiflavone may be a potential anticancer drug for breast cancer treatment.
Hinokiflavone, as a MDM2 inhibitor, activates p53 signaling pathway to induce apoptosis in human colon cancer HCT116 cells
Biochem Biophys Res Commun 2022 Feb 26;594:93-100.PMID:35078113DOI:10.1016/j.bbrc.2022.01.032.
Hinokiflavone (HF), a natural biflavonoid that possesses various biological activities, has reported that HF could be a pre-mRNA splicing modulator, whereas its underlying mechanisms remain elusive. In the present study, we identified HF as a potential MDM2 inhibitor. What's more, we found that HF suppressed mdm2 mRNA synthesis at the transcriptional level. Then, this MDM2 inhibition led in turn to increase p53 protein expression and activate p53 pathway, which could decrease the survival of HCT116 colon cells by G2/M phase arrest and apoptosis induction. Then, bioinformatics suggested that ESR1 was a predicted and potential target of HF. Finally, we used molecular docking and molecular dynamics simulation to demonstrate the binding patterns of HF and ESR1. To sum up, our study unearthed that HF was a feasible agent for MDM2 inhibitor through down-regulating mdm2 RNA level and activating p53 signaling pathway.