Linderalactone
(Synonyms: 异乌药内酯) 目录号 : GC38086
Linderalactone inhibits human lung cancer growth by modulating the expression of apoptosis-related proteins (Bax and Bcl-2) with an IC50 of 15 ?M in A-549 cells. Linderalactone induces G2/M cell cycle arrest and could also suppress the JAK/STAT signalling pathway. Linderalactone can be isolated from Radix linderae.
Cas No.:728-61-0
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
Linderalactone inhibits human lung cancer growth by modulating the expression of apoptosis-related proteins (Bax and Bcl-2) with an IC50 of 15 ?M in A-549 cells. Linderalactone induces G2/M cell cycle arrest and could also suppress the JAK/STAT signalling pathway. Linderalactone can be isolated from Radix linderae.
[1] Yanglin Deng, et al. J BUON. Mar-Apr 2019;24(2):566-571. [2] Qinghua Sun, et al. Journal of Liquid Chromatography & Related Technologies Volume 29, 2006 - Issue 1.
| Cas No. | 728-61-0 | SDF | |
| 别名 | 异乌药内酯 | ||
| Canonical SMILES | O=C1C2=C[C@@](C3=C(OC=C3C)C/C(C)=C/CC2)([H])O1 | ||
| 分子式 | C15H16O3 | 分子量 | 244.29 |
| 溶解度 | DMSO: 50 mg/mL (204.67 mM) | 储存条件 | -20°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 | 4.0935 mL | 20.4675 mL | 40.935 mL |
| 5 mM | 0.8187 mL | 4.0935 mL | 8.187 mL |
| 10 mM | 0.4093 mL | 2.0467 mL | 4.0935 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。
Linderalactone Suppresses Pancreatic Cancer Development In Vitro and In Vivo via Negatively Regulating PI3K/AKT Signaling Pathway
J Oncol 2022 Aug 4;2022:8675096.PMID:35966890DOI:10.1155/2022/8675096.
Linderalactone is one of the main extracts of Linderae Radix, which is widely used in traditional Chinese medicine. There have been few studies on the antitumor effect of Linderalactone in the past. In this study, we explored the anti-pancreatic cancer activity of Linderalactone in vitro and in vivo. The results showed that Linderalactone inhibited the proliferation of pancreatic cancer cells in a time- and dose-dependent manner. Cell migration and invasion were significantly inhibited by Linderalactone. The cell cycle was arrested in the G2/M phase, and the expression levels of cell cycle-associated proteins changed significantly with Linderalactone treatment. In addition, Linderalactone induced cell apoptosis and altered the expression of apoptotic markers, such as caspase 3 and PARP1. Mechanistically, Linderalactone suppressed the PI3K/AKT signaling pathway by downregulating the phosphorylation of PI3K and AKT. The xenograft study results were consistent with the in vitro results, and there was no obvious chemical toxicity. Thus, our research demonstrated that Linderalactone exhibits antitumor activity against pancreatic cancer and may be developed as a potential anti-pancreatic cancer agent in the future.
Linderalactone inhibits human lung cancer growth by modulating the expression of apoptosis-related proteins, G2/M cell cycle arrest and inhibition of JAK/STAT signalling pathway
J BUON 2019 Mar-Apr;24(2):566-571.PMID:31128007doi
Purpose: The main purpose of the current research work was to evaluate the antitumor effects of Linderalactone in A-549 human lung carcinoma cell line along with the study its effects on apoptosis-related proteins, cell cycle phase distribution and JAK/STAT signalling pathway. Methods: The viability of lung cancer cell line was investigated by MTT assay at varying doses of Linderalactone. Apoptosis was detected by using fluorescence microscopy and flow cytometry. Cell cycle analysis was carried out by flow cytometery. The protein expression was examined by western blotting. Results: Linderalactone could inhibit the proliferation of the lung cancer A-549 cells with an IC50 of 15 µM. Further investigations indicated the antiproliferative effects of Linderalactone are due to apoptosis induction which was further confirmed by Bax and Bcl-2 expression. It also induced G2/M cell cycle arrest which was also associated with alteration of the expression of several important proteins. Furthermore, Linderalactone could also suppress the JAK/STAT signalling pathway. Conclusions: In conclusion, Linderalactone could be developed as a potential drug candidate against lung cancer provided that further in depth studies are carried out in this direction focusing on its in vivo efficacy.
Identification of Linderalactone as a natural inhibitor of SHP2 to ameliorate CCl4-induced liver fibrosis
Front Pharmacol 2023 Feb 9;14:1098463.PMID:36843936DOI:10.3389/fphar.2023.1098463.
Liver fibrosis is characterised by the activation of hepatic stellate cells (HSCs) and matrix deposition. Accumulating evidence has revealed that the oncogenic protein tyrosine phosphatase Src homology 2 domain-containing phosphatase 2 (SHP2) acts as a therapeutic target of fibrosis. Although several SHP2 inhibitors have reached early clinical trials, there are currently no FDA-approved drugs that target SHP2. In this study, we aimed to identify novel SHP2 inhibitors from an in-house natural product library to treat liver fibrosis. Out of the screened 800 compounds, a furanogermacrane sesquiterpene, Linderalactone (LIN), significantly inhibited SHP2 dephosphorylation activity in vitro. Cross-validated enzymatic assays, bio-layer interferometry (BLI) assays, and site-directed mutagenesis were used to confirm that LIN directly binds to the catalytic PTP domain of SHP2. In vivo administration of LIN significantly ameliorated carbon tetrachloride (CCl4)-induced HSC activation and liver fibrosis by inhibiting the TGFβ/Smad3 pathway. Thus, LIN or its derivatives could be considered potential therapeutic agents against SHP2-related diseases, such as liver fibrosis or NASH.
New sesquiterpene dilactone and β-carboline alkaloid and the α-glucosidase inhibitory activity of selected phytochemicals from Neolitsea cassia (L.) Kosterm
Nat Prod Res 2022 Aug;36(16):4061-4069.PMID:34343060DOI:10.1080/14786419.2021.1961134.
One new sesquiterpene dilactone, coccinine (1) and one new β-carboline alkaloid, daibucarboline F (2) together with 10 known compounds; linderane (3), Linderalactone (4), pseudoneolinderane (5), linderanlide C (6), linderanine A (7), epicatechin (8), (-)-taxifolin (9), astilbin (10), L-quercitrin (11) and afzelin (12) were isolated from the stems and leaves of Neolitsea cassia (L.) Kosterm (Lauraceae). The structures of (1 and 2) were established by extensive spectroscopic methods and the known compounds were identified by comparisons with data reported in literature. The relative stereochemistry of compound (1) was assigned by X-ray diffraction analysis with Cu-Kα irradiation. Compounds (3-8) and (10) were evaluated for their α-glucosidase enzymatic inhibitory activity. Compounds (4-6), (8) and (10) exhibited inhibition towards α-glucosidase enzymatic activity with IC50 values ranging from 12.10 to 96.77 μM. This is the first report on the isolation of phytochemicals from N. cassia and their bioactivities.
Sesquiterpene lactones from the root tubers of Lindera aggregata
J Nat Prod 2009 Aug;72(8):1497-501.PMID:19639966DOI:10.1021/np900354q.
Phytochemical investigation of the root tubers of Lindera aggregata resulted in the isolation of five new sesquiterpene lactones, linderagalactones A-E (1-5), along with eight known sesquiterpenoids, 3-eudesmene-1beta,11-diol, hydroxylindestenolide, strychnistenolide, hydroxyisogermafurenolide, atractylenolide III, linderane, neolinderalactone, and Linderalactone. The structures and relative configurations of 1-5 were determined by spectroscopic methods, especially HRESIMS and 2D NMR techniques. The absolute configurations of 1-4 were defined by comparison of quantum chemical TDDFT calculated and experimental ECD spectra. Linderagalactone A (1) is a halogenated sesquiterpene lactone possessing a unique rearranged carbon skeleton. Linderagalactone E (5), linderane, hydroxylindestenolide, and Linderalactone showed hepatoprotective activity against H2O2-induced oxidative damages on HepG2 cells with EC(50) values of 67.5, 167.0, 42.4, and 98.0 microM, respectively.