Demethylzeylasteral
(Synonyms: 去甲泽拉木醛) 目录号 : GC38160
A nortriterpenoid with diverse biological activities
Cas No.:107316-88-1
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
Demethylzeylasteral is a nortriterpenoid originally isolated from T. wilfordii that has diverse biological activities, including enzyme inhibitory, anti-angiogenic, antiproliferative, anti-inflammatory, and immunosuppressive properties.1,2,3,4 Demethylzeylasteral inhibits the UDP-glucuronosyltransferase (UGT) isoforms UGT1A6 and UGT2B7 (Kis = 0.6 and 17.3 μM, respectively).2 It inhibits growth of bovine aortic endothelial cells (BAEs) and U251 human glioma cancer cells in vitro (IC50s = 0.21 and ~6.2 μM, respectively), as well as inhibits tumor growth and neovascularization in vivo in a B16/F10 melanoma mouse allograft model when administered at a dose of 30 mg/kg per day.1 Demethylzeylasteral (0.12 mg/kg per day) decreases renal proteinuria, lesions, immune cell infiltration, and protein levels of TNF-α, COX-2, and ICAM-1 in lupus-prone MRL/lpr mice.3 Demethylzeylasteral (10 mg/kg per day) also increases survival of recipient rats in a model of kidney transplant.4
1.Ushiro, S., Ono, M., Nakayama, J., et al.New nortriterpenoid isolated from anti-rheumatoid arthritic plant, Tripterygium wilfordii, modulates tumor growth and neovascularizationInt. J. Cancer72(4)657-663(1997) 2.Zhao, J.-W., Wang, G.-H., Chen, M., et al.Demethylzeylasteral exhibits strong inhibition towards UDP-glucuronosyltransferase (UGT) 1A6 and 2B7Molecules17(8)9469-9475(2012) 3.Hu, Q., Yang, C., Wang, Q., et al.Demethylzeylasteral (T-96) Treatment Ameliorates Mice Lupus Nephritis Accompanied by Inhibiting Activation of NF-κB PathwayPLoS One10(7)e0133724(2015) 4.Xu, W., Lin, Z., Yang, C., et al.Immunosuppressive effects of demethylzeylasteral in a rat kidney transplantation modelInt. Immunopharmacol.9(7-8)996-1001(2009)
| Cas No. | 107316-88-1 | SDF | |
| 别名 | 去甲泽拉木醛 | ||
| Canonical SMILES | C[C@](C1=CC2=O)(CC[C@]3(C)[C@@]4([H])C[C@@](C(O)=O)(C)CC3)[C@]4(CC[C@]1(C5=C2C(C=O)=C(O)C(O)=C5)C)C | ||
| 分子式 | C29H36O6 | 分子量 | 480.59 |
| 溶解度 | DMSO: 250 mg/mL (520.19 mM) | 储存条件 | Store at 2-8°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 | 2.0808 mL | 10.4039 mL | 20.8078 mL |
| 5 mM | 0.4162 mL | 2.0808 mL | 4.1616 mL |
| 10 mM | 0.2081 mL | 1.0404 mL | 2.0808 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。
Demethylzeylasteral targets lactate by inhibiting histone lactylation to suppress the tumorigenicity of liver cancer stem cells
Pharmacol Res 2022 Jul;181:106270.PMID:35605812DOI:10.1016/j.phrs.2022.106270.
Cancer stem cells drive tumor initiation, progression, and recurrence, which compromise the effectiveness of anti-tumor drugs. Here, we report that Demethylzeylasteral (DML), a triterpene anti-tumor compound, suppressed tumorigenesis of liver cancer stem cells (LCSCs) by interfering with lactylation of a metabolic stress-related histone. Using RNA sequencing (RNA-seq) and gas chromatography-mass spectrometric (GC-MS) analysis, we showed that the glycolysis metabolic pathway contributed to the anti-tumor effects of DML, and then focused on lactate downstream regulation as the molecular target. Mechanistically, DML opposed the progress of hepatocellular carcinoma (HCC), which was efficiently facilitated by the increase in H3 histone lactylation. Two histone modification sites: H3K9la and H3K56la, which were found to promote tumorigenesis, were inhibited by DML. In addition, we used a nude mouse tumor xenograft model to confirm that the anti-liver cancer effects of DML are mediated by regulating H3 lactylation in vivo. Our findings demonstrate that DML suppresses the tumorigenicity induced by LCSCs by inhibiting H3 histone lactylation, thus implicating DML as a potential candidate for the supplementary treatment of hepatocellular carcinoma.
Therapeutic potential of Demethylzeylasteral, a triterpenoid of the genus Tripterygium wilfordii
Fitoterapia 2022 Nov;163:105333.PMID:36244595DOI:10.1016/j.fitote.2022.105333.
Pentacyclic triterpenoids are important natural products widely presenting in nature with rich bioactivities. Tripterygium wilfordii Hook. f., a precious Chinese medicinal material, is used to cure rheumatoid arthritis, nephrotic syndrome, systemic lupus erythematosus. Triterpenoids are one of the important active components of Tripterygium wilfordii Hook. f. Demethylzeylasteral extracted from Tripterygium wilfordii Hook. f. had numerous pharmacological effects, including anticancer, anti-inflammatory, immune suppression, anti-fertility, antivirus, antimicrobial. In this paper, we summarized comprehensively pharmacological activities of Demethylzeylasteral for potential application as a therapeutic agent.
Demethylzeylasteral inhibits cell proliferation and enhances cell chemosensitivity to 5-fluorouracil in Colorectal Cancer cells
J Cancer 2020 Aug 19;11(20):6059-6069.PMID:32922546DOI:10.7150/jca.44375.
Malignant growth and chemotherapy resistance to 5-fluorouracil (5-FU) are the obstacles to the treatment of Colorectal cancer (CRC). There is need to develop effective therapeutic option. Demethylzeylasteral benefits to immune and anti-tumor function. However, the role Demethylzeylasteral played in colorectal cancer remains unclear. Here, our study confirmed that Demethylzeylasteral could inhibit the cell malignant capacity, such as proliferation, migration and invasion. And we also found Demethylzeylasteral could cause cell cycle arrest and apoptosis. Followed we verified that combination Demethylzeylasteral with 5-FU has a better curative effect in vitro. The two drugs function synergistically in SW480 and additionally in RKO. IC50 values of 5-FU decreased when combined with Demethylzeylasteral. Next, we used the network pharmacology approach to explore the the potential molecular mechanism of Demethylzeylasteral. We constructed the "Colorectal - targets - Demethylzeylasteral" and protein-protein interactions (PPI) networks. And 15 hub genes were found in PPI network. Then Gene Ontology (GO) enrichment analysis showed that Demethylzeylasteral may affect cell cycle, apoptosis, invasion and response to chemotherapy drugs. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis indicated Demethylzeylasteral may be involved in many cancer-related pathways. Taken together, the network pharmacology approach provided a potential mechanism of Demethylzeylasteral in colorectal cells. Our study indicated that Demethylzeylasteral could exert anti-tumor effects and enhance the sensitivity of the Colorectal cells to 5-FU, suggesting a promising ability to serve as an anti-cancer agent in Colorectal cancer.
Demethylzeylasteral inhibits proliferation, migration, and invasion through FBXW7/c-Myc axis in gastric cancer
MedComm (2020) 2021 Jun 3;2(3):467-480.PMID:34766156DOI:10.1002/mco2.73.
Gastric cancer (GC) is one of the most familiar malignancy in the digestive system. Demethylzeylasteral (Dem), a natural functional monomer extracted from Tripterygium wilfordii Hook F, shows anti-tumor effects in a variety of cancers, including GC, however, with the underlying mechanism poorly understood. In our study, we show that Dem inhibits the proliferation, migration, and invasion of GC cells, which are mediated by down-regulating c-Myc protein levels. Mechanistically, Dem reduces the stability of c-Myc by up-regulating FBXW7, an E3 ubiquitin ligase. Moreover, in xenograft tumor model experiment, Dem also inhibits GC, which depends on suppressing c-Myc expression. Finally, Dem enhances GC cell chemosensitivity to the combination treatment of 5-Fluorouracil (5-Fu) and doxorubicin (DOX) in vitro. Together, Dem exerts anti-neoplastic activities through destabilizing and suppressing c-Myc, establishing a theory foundation for using it in future treatment of GC.
Demethylzeylasteral inhibits cell proliferation and induces apoptosis through suppressing MCL1 in melanoma cells
Cell Death Dis 2017 Oct 26;8(10):e3133.PMID:29072681DOI:10.1038/cddis.2017.529.
Demethylzeylasteral is one of the extracts of Tripterygium wilfordii Hook F, which plays important roles in multiple biological processes such as inflammation inhibition, as well as immunosuppression. However, anti-cancer function and the underlying mechanisms of Demethylzeylasteral in melanoma cells remain unclear. In this study, we demonstrate that Demethylzeylasteral has an anti-tumor property in melanoma cells. Demethylzeylasteral not only inhibits cell proliferation through cell cycle arrest at S phase, but also induces cell apoptosis in melanoma cells. MCL1 is an anti-apoptotic protein in BCL2 family, and amplifies frequently in multiple human cancers. MCL1 is also known as a potential contributor for the resistance of BCL2 inhibitors, as well as various chemotherapeutic drugs. MCL1 is, therefore, regarded as a potential target for cancer therapy. Here, for the first time, we unveil that Demethylzeylasteral suppresses the expression of MCL1. Interestingly, MCL1 interacts with S phase-related protein CDK2, and thereby inhibits it's ubiquitin-dependent degradation. Together, Demethylzeylasteral is a promising anti-tumor compound in melanoma cells. Demethylzeylasteral is also a potential inhibitor of MCL1.