Helenalin
(Synonyms: 心菊内酯) 目录号 : GC43810
An anti-inflammatory sesquiterpene lactone
Cas No.:6754-13-8
Sample solution is provided at 25 µL, 10mM.
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Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Helenalin is a sesquiterpene lactone first isolated from various species of Arnica. It has anti-inflammatory effects, most notably by inhibiting gene expression mediated by NF-κB at doses from 1 to 20 µM. Like other sesquiterpene lactones, helenalin can modify sulfhydryl groups of cysteine residues and it alkylates these groups on the p65 subunit of NF-κB. It also suppresses the proliferation of cancer cells through multiple mechanisms, including the prevention of signaling through NF-κB. Helenalin has antibacterial and anti-protozoal activities.
| Cas No. | 6754-13-8 | SDF | |
| 别名 | 心菊内酯 | ||
| Canonical SMILES | O[C@H]1[C@@](C(C(O2)=O)=C)([H])[C@@]2([H])C[C@@H](C)[C@@](C=C3)([H])[C@@]1(C)C3=O | ||
| 分子式 | C15H18O4 | 分子量 | 262.3 |
| 溶解度 | DMF: 20 mg/ml,DMSO: 20 mg/ml,Ethanol: 20 mg/ml,PBS (pH 7.2): 0.2 mg/ml | 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 | 3.8124 mL | 19.0621 mL | 38.1243 mL |
| 5 mM | 0.7625 mL | 3.8124 mL | 7.6249 mL |
| 10 mM | 0.3812 mL | 1.9062 mL | 3.8124 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。
Helenalin - A Sesquiterpene Lactone with Multidirectional Activity
Curr Drug Targets 2019;20(4):444-452.PMID:30317996DOI:10.2174/1389450119666181012125230.
Sesquiterpene lactones, secondary metabolites of plants, present in a large number of species mostly from the Asteracea family, are used in the traditional medicine of many countries for the treatment of various pathological conditions. They exert a broad range of activities, including antiinflammatory, anti-bacterial and anti-cancer properties. The best-known sesquiterpene lactones which are already used as drugs or are used in clinical trials are artemisinin, thapsigargin and parthenolide. Yet another sesquiterpene lactone, Helenalin, an active component of Arnica montana, known for its strong anti-inflammatory activity, has been used for centuries in folk medicine to treat minor injuries. Unfortunately, Helenalin's ability to cause allergic reactions and its toxicity to healthy tissues prevented so far the development of this sesquiterpene lactone as an anticancer or anti-inflammatory drug. Recently, the new interest in the biological properties, as well as in the synthesis of Helenalin analogs has been observed. This review describes Helenalin's major biological activities, molecular mechanisms of action, its toxicity and potential for further research.
Recent Patents on Anti-Cancer Potential of Helenalin
Recent Pat Anticancer Drug Discov 2020;15(2):132-142.PMID:32614752DOI:10.2174/1574892815666200702142601.
Background: Arnica montana, containing Helenalin as its principal active constituent, is the most widely used plant to treat various ailments. Recent studies indicate that Arnica and Helenalin provide significant health benefits, including anti-inflammatory, neuroprotective, antioxidant, cholesterol-lowering, immunomodulatory, and most important, anti-cancer properties. Objective: The objective of the present study is to overview the recent patents of Arnica and its principal constituent Helenalin, including new methods of isolation, and their use in the prevention of cancer and other ailments. Methods: Current prose and patents emphasizing the anti-cancer potential of Helenalin and Arnica, incorporated as anti-inflammary agents in anti-cancer preparations, have been identified and reviewed with particular emphasis on their scientific impact and novelty. Results: Helenalin has shown its anti-cancer potential to treat multiple types of tumors, both in vitro and in vivo. It has also portrayed synergistic effects when given in combination with other anti- cancer drugs or natural compounds. New purification/isolation techniques are also developing with novel Helenalin formulations and its synthetic derivatives have been developed to increase its solubility and bioavailability. Conclusion: The promising anti-cancer potential of Helenalin in various preclinical studies may open new avenues for therapeutic interventions in different tumors. Thus clinical trials validating its tumor suppressing and chemopreventive activities, particularly in conjunction with standard therapies, are immediately required.
Helenalin Facilitates Reactive Oxygen Species-Mediated Apoptosis and Cell Cycle Arrest by Targeting Thioredoxin Reductase-1 in Human Prostate Cancer Cells
Med Sci Monit 2021 Jun 14;27:e930083.PMID:34125740DOI:10.12659/MSM.930083.
BACKGROUND Helenalin is a pseudoguaianolide natural product with anti-cancer activities. This study investigated the underlying mechanism of the anti-prostate cancer effects of Helenalin in vitro. MATERIAL AND METHODS CCK-8 assay was performed to detect the optimal concentrations of Helenalin in DU145 and PC-3 cells. After exposure to Helenalin and/or reactive oxygen species (ROS) inhibitor, ROS production was assessed by DCFH-DA staining. Thioredoxin reductase-1 (TrxR1) expression was detected by RT-qPCR and western blot. Moreover, apoptosis and cell cycle were evaluated by flow cytometry. Following TrxR1 knockdown or overexpression, TrxR1 expression, ROS generation, apoptosis, cell cycle, migration, and invasion were examined in cells co-treated with Helenalin. RESULTS Helenalin distinctly repressed the viability of prostate cancer cells in a concentration-dependent manner. We chose 8 μM and 4 μM as the optimal concentrations of Helenalin for DU145 and PC-3 cells, respectively. Helenalin treatment markedly triggered ROS production and lowered TrxR1 expression, which was ameliorated by ROS inhibitor. Exposure to Helenalin facilitated apoptosis as well as G0/G1 cell cycle arrest, which was reversed by ROS inhibitor. Helenalin relieved the inhibitory effect of TrxR1 on ROS production. Furthermore, Helenalin ameliorated the decrease in apoptosis rate and the shortening of G0/G1 phase as well as the increase in migration and invasion induced by TrxR1 overexpression. CONCLUSIONS Our findings revealed that Helenalin accelerated ROS-mediated apoptosis and cell cycle arrest via targeting TrxR1 in human prostate cancer cells.
In vitro metabolism of Helenalin and its inhibitory effect on human cytochrome P450 activity
Arch Toxicol 2022 Mar;96(3):793-808.PMID:34989853DOI:10.1007/s00204-021-03218-6.
Sesquiterpene lactone Helenalin is used as an antiphlogistic in European and Chinese folk medicine. The pharmacological activities of Helenalin have been extensively investigated, yet insufficient information exists about its metabolic properties. The objectives of the present study were (1) to investigate the in vitro NADPH-dependent metabolism of Helenalin (5 and 100 µM) using human and rat liver microsomes and liver cytosol, (2) to elucidate the role of human cytochrome P450 (CYP) enzymes in its oxidative metabolism, and (3) to study the inhibition of human CYPs by Helenalin. Five oxidative metabolites were detected in NADPH-dependent human and rat liver microsomal incubations, while two reduced metabolites were detected only in NADPH-dependent human microsomal and cytosolic incubations. In human liver microsomes, the main oxidative metabolite was 14-hydroxyhelenalin, and in rat liver microsomes 9-hydroxyhelenalin. The overall oxidation of Helenalin was several times more efficient in rat than in human liver microsomes. In humans, CYP3A4 and CYP3A5 followed by CYP2B6 were the main enzymes responsible for the hepatic metabolism of Helenalin. The extrahepatic CYP2A13 oxidized Helenalin most efficiently among CYP enzymes, possessing the Km value of 0.6 µM. Helenalin inhibited CYP3A4 (IC50 = 18.7 µM) and CYP3A5 (IC50 = 62.6 µM), and acted as a mechanism-based inhibitor of CYP2A13 (IC50 = 1.1 µM, KI = 6.7 µM, and kinact = 0.58 ln(%)/min). It may be concluded that the metabolism of Helenalin differs between rats and humans, in the latter its oxidation is catalyzed by hepatic CYP2B6, CYP3A4, CYP3A5, and CYP3A7, and extrahepatic CYP2A13.
Helenalin Acetate, a Natural Sesquiterpene Lactone with Anti-inflammatory and Anti-cancer Activity, Disrupts the Cooperation of CCAAT Box/Enhancer-binding Protein β (C/EBPβ) and Co-activator p300
J Biol Chem 2016 Dec 9;291(50):26098-26108.PMID:27803164DOI:10.1074/jbc.M116.748129.
Recent work has demonstrated pro-oncogenic functions of the transcription factor CCAAT box/enhancer-binding protein β (C/EBPβ) in various tumors, implicating C/EBPβ as an interesting target for the development of small-molecule inhibitors. We have previously discovered that the sesquiterpene lactone Helenalin acetate, a natural compound known to inhibit NF-κB, is a potent C/EBPβ inhibitor. We have now examined the inhibitory mechanism of Helenalin acetate in more detail. We demonstrate that Helenalin acetate is a significantly more potent inhibitor of C/EBPβ than of NF-κB. Our work shows that Helenalin acetate inhibits C/EBPβ by binding to the N-terminal part of C/EBPβ, thereby disrupting the cooperation of C/EBPβ with the co-activator p300. C/EBPβ is expressed in several isoforms from alternative translational start codons. We have previously demonstrated that Helenalin acetate selectively inhibits only the full-length (liver-enriched activating protein* (LAP*)) isoform but not the slightly shorter (LAP) isoform. Consistent with this, Helenalin acetate binds to the LAP* but not to the LAP isoform, explaining why its inhibitory activity is selective for LAP*. Although Helenalin acetate contains reactive groups that are able to interact covalently with cysteine residues, as exemplified by its effect on NF-κB, the inhibition of C/EBPβ by Helenalin acetate is not due to irreversible reaction with cysteine residues of C/EBPβ. In summary, Helenalin acetate is the first highly active small-molecule C/EBPβ inhibitor that inhibits C/EBPβ by a direct binding mechanism. Its selectivity for the LAP* isoform also makes Helenalin acetate an interesting tool to dissect the functions of the LAP* and LAP isoforms.