Home>>Signaling Pathways>> Immunology/Inflammation>> NF-κB>>Eurycomalactone

Eurycomalactone Sale

(Synonyms: 东革内酯) 目录号 : GC38548

Eurycomalactone 是一种天然产物,为有效的 NF-κB 抑制剂,IC50 值为 0.5 μM。Eurycomalactone 可抑制蛋白合成,降低 cyclin D1 蛋白水平,但对 TNFα 诱导的 IκBα 降解或 IKKα/β 和 IκBα 的磷酸化水平没有作用。

Eurycomalactone Chemical Structure

Cas No.:23062-24-0

规格 价格 库存 购买数量
1mg
¥1,368.00
现货
5mg
¥4,113.00
现货

电话:400-920-5774 Email: sales@glpbio.cn

Customer Reviews

Based on customer reviews.

Sample solution is provided at 25 µL, 10mM.

产品文档

Quality Control & SDS

View current batch:

产品描述

Eurycomalactone is a natural product found in Eurycoma longifolia Jack., acts as a potent NF-κB inhibitor, with an IC50 of 0.5 μM. Eurycomalactone inhibits protein synthesis, depletes cyclin D1, but does not affect TNFα-induced degradation of IκBα or the phosphorylation of IKKα/β and IκBα[1].

[1]. Malainer C, et al. Eurycomalactone Inhibits Expression of Endothelial Adhesion Molecules at a Post-Transcriptional Level. J Nat Prod. 2017 Dec 22;80(12):3186-3193.

Chemical Properties

Cas No. 23062-24-0 SDF
别名 东革内酯
Canonical SMILES C[C@]12[C@@]([C@H]([C@@](O3)([H])[C@@](C)([H])[C@]2([H])C3=O)O)([H])[C@]([C@@](C(C)=CC4=O)([H])CC1=O)([C@@H]4O)C
分子式 C19H24O6 分子量 348.39
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。
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。

溶解性数据

制备储备液
1 mg 5 mg 10 mg
1 mM 2.8703 mL 14.3517 mL 28.7035 mL
5 mM 0.5741 mL 2.8703 mL 5.7407 mL
10 mM 0.287 mL 1.4352 mL 2.8703 mL
  • 摩尔浓度计算器

  • 稀释计算器

  • 分子量计算器

质量
=
浓度
x
体积
x
分子量
 
 
 
*在配置溶液时,请务必参考产品标签上、MSDS / COA(可在Glpbio的产品页面获得)批次特异的分子量使用本工具。

计算

动物体内配方计算器 (澄清溶液)

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
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

Research Update

Review on a Traditional Herbal Medicine, Eurycoma longifolia Jack (Tongkat Ali): Its Traditional Uses, Chemistry, Evidence-Based Pharmacology and Toxicology

Molecules 2016 Mar 10;21(3):331.PMID:26978330DOI:10.3390/molecules21030331.

Eurycoma longifolia Jack (known as tongkat ali), a popular traditional herbal medicine, is a flowering plant of the family Simaroubaceae, native to Indonesia, Malaysia, Vietnam and also Cambodia, Myanmar, Laos and Thailand. E. longifolia, is one of the well-known folk medicines for aphrodisiac effects as well as intermittent fever (malaria) in Asia. Decoctions of E. longifolia leaves are used for washing itches, while its fruits are used in curing dysentery. Its bark is mostly used as a vermifuge, while the taproots are used to treat high blood pressure, and the root bark is used for the treatment of diarrhea and fever. Mostly, the roots extract of E. longifolia are used as folk medicine for sexual dysfunction, aging, malaria, cancer, diabetes, anxiety, aches, constipation, exercise recovery, fever, increased energy, increased strength, leukemia, osteoporosis, stress, syphilis and glandular swelling. The roots are also used as an aphrodisiac, antibiotic, appetite stimulant and health supplement. The plant is reported to be rich in various classes of bioactive compounds such as quassinoids, canthin-6-one alkaloids, β-carboline alkaloids, triterpene tirucallane type, squalene derivatives and biphenyl neolignan, eurycolactone, laurycolactone, and Eurycomalactone, and bioactive steroids. Among these phytoconstituents, quassinoids account for a major portion of the E. longifolia root phytochemicals. An acute toxicity study has found that the oral Lethal Dose 50 (LD50) of the alcoholic extract of E. longifolia in mice is between 1500-2000 mg/kg, while the oral LD50 of the aqueous extract form is more than 3000 mg/kg. Liver and renal function tests showed no adverse changes at normal daily dose and chronic use of E. longifolia. Based on established literature on health benefits of E. longifolia, it is important to focus attention on its more active constituents and the constituents' identification, determination, further development and most importantly, the standardization. Besides the available data, more evidence is required regarding its therapeutic efficacy and safety, so it can be considered a rich herbal source of new drug candidates. It is very important to conserve this valuable medicinal plant for the health benefit of future generations.

Eurycomalactone Inhibits Expression of Endothelial Adhesion Molecules at a Post-Transcriptional Level

J Nat Prod 2017 Dec 22;80(12):3186-3193.PMID:29148754DOI:10.1021/acs.jnatprod.7b00503.

The C-19 quassinoid Eurycomalactone (1) has recently been shown to be a potent (IC50 = 0.5 μM) NF-κB inhibitor in a luciferase reporter model. In this study, we show that 1 with similar potency inhibited the expression of the NF-κB-dependent target genes ICAM-1, VCAM-1, and E-selectin in TNFα-activated human endothelial cells (HUVECtert) by flow cytometry experiments. Surprisingly, 1 (2 μM) did not inhibit TNFα-induced IKKα/β or IκBα phosphorylation significantly. Also, the TNFα-induced degradation of IκBα remained unchanged in response to 1 (2 μM). In addition, pretreatment of HUVECtert with 1 (2 μM) had no statistically significant effect on TNFα-mediated nuclear translocation of the NF-κB subunit p65 (RelA). Quantitative RT-PCR revealed that 1 (0.5-5 μM) exhibited diverse effects on the TNFα-induced transcription of ICAM-1, VCAM-1, and SELE genes since the mRNA level either remained unchanged (ICAM-1, E-selectin, and VCAM-1 at 0.5 μM 1), was reduced (VCAM-1 at 5 μM 1), or even increased (E-selectin at 5 μM 1). Finally, the time-dependent depletion of a short-lived protein (cyclin D1) as well as the measurement of de novo protein synthesis in the presence of 1 (2-5 μM) suggested that 1 might act as a protein synthesis inhibitor rather than an inhibitor of early NF-κB signaling.

Enhancement of Radiosensitivity by Eurycomalactone in Human NSCLC Cells Through G₂/M Cell Cycle Arrest and Delayed DNA Double-Strand Break Repair

Oncol Res 2020 Mar 27;28(2):161-175.PMID:31727206DOI:10.3727/096504019X15736439848765.

Radiotherapy (RT) is an important treatment for non-small cell lung cancer (NSCLC). However, the major obstacles to successful RT include the low radiosensitivity of cancer cells and the restricted radiation dose, which is given without damaging normal tissues. Therefore, the sensitizer that increases RT efficacy without dose escalation will be beneficial for NSCLC treatment. Eurycomalactone (ECL), an active quassinoid isolated from Eurycoma longifolia Jack, has been demonstrated to possess anticancer activity. In this study, we aimed to investigate the effect of ECL on sensitizing NSCLC cells to X-radiation (X-ray) as well as the underlying mechanisms. The results showed that ECL exhibited selective cytotoxicity against the NSCLC cells A549 and COR-L23 compared to the normal lung fibroblast. Clonogenic survival results indicated that ECL treatment prior to irradiation synergistically decreased the A549 and COR-L23 colony number. ECL treatment reduced the expression of cyclin B1 and CDK1/2 leading to induce cell cycle arrest at the radiosensitive G₂/M phase. Moreover, ECL markedly delayed the repair of radiation-induced DNA double-strand breaks (DSBs). In A549 cells, pretreatment with ECL not only delayed the resolving of radiation-induced γ-H2AX foci but also blocked the formation of 53BP1 foci at the DSB sites. In addition, ECL pretreatment attenuated the expression of DNA repair proteins Ku-80 and KDM4D in both NSCLC cells. Consequently, these effects led to an increase in apoptosis in irradiated cells. Thus, ECL radiosensitized the NSCLC cells to X-ray via G₂/M arrest induction and delayed the repair of X-ray-induced DSBs. This study offers a great potential for ECL as an alternative safer radiosensitizer for increasing the RT efficiency against NSCLC.

Inactivation of AKT/NF‑κB signaling by Eurycomalactone decreases human NSCLC cell viability and improves the chemosensitivity to cisplatin

Oncol Rep 2020 Oct;44(4):1441-1454.PMID:32945500DOI:10.3892/or.2020.7710.

The high activation of protein kinase B (AKT)/nuclear factor‑κB (NF‑κB) signaling has often been associated with the induction of non‑small cell lung cancer (NSCLC) cell survival and resistance to cisplatin, which is one of the most widely used chemotherapeutic drugs in the treatment of NSCLC. The inhibition of AKT/NF‑κB can potentially be used as a molecular target for cancer therapy. Eurycomalactone (ECL), a quassinoid from Eurycoma longifolia Jack, has previously been revealed to exhibit strong cytotoxic activity against the human NSCLC A549 cell line, and can inhibit NF‑κB activity in TNF‑α‑activated 293 cells stably transfected with an NF‑κB luciferase reporter. The present study was the first to investigate whether ECL inhibits the activation of AKT/NF‑κB signaling, induces apoptosis and enhances chemosensitivity to cisplatin in human NSCLC cells. The anticancer activity of ECL was evaluated in two NSCLC cell lines, A549 and Calu‑1. ECL decreased the viability and colony formation ability of both cell lines by inducing cell cycle arrest and apoptosis through the activation of pro‑apoptotic caspase‑3 and poly (ADP‑ribose) polymerase, as well as the reduction of anti‑apoptotic proteins Bcl‑xL and survivin. In addition, ECL treatment suppressed the levels of AKT (phospho Ser473) and NF‑κB (phospho Ser536). Notably, ECL significantly enhanced cisplatin sensitivity in both assessed NSCLC cell lines. The combination treatment of cisplatin and ECL promoted cell apoptosis more effectively than cisplatin alone, as revealed by the increased cleaved caspase‑3, but decreased Bcl‑xL and survivin levels. Exposure to cisplatin alone induced the levels of phosphorylated‑AKT and phosphorylated‑NF‑κB, whereas co‑treatment with ECL inhibited the cisplatin‑induced phosphorylation of AKT and NF‑κB, leading to an increased sensitization effect on cisplatin‑induced apoptosis. In conclusion, ECL exhibited an anticancer effect and sensitized NSCLC cells to cisplatin through the inactivation of AKT/NF‑κB signaling. This finding provides a rationale for the combined use of chemotherapy drugs with ECL to improve their efficacy in NSCLC treatment.

Review Ergogenic Effect of Long Jack, Eurycoma Longifolia

Pharmacogn Rev 2016 Jul-Dec;10(20):139-142.PMID:28082797DOI:10.4103/0973-7847.194041.

Eurycoma longifolia (family: Simaroubaceae) is commonly distributed in the Southeast Asia and Indo-China. In particular, the aqueous extract and decoction of its root are a well-known folk medicine which enhances sexuality, fertility, and antiaging. Furthermore, it has been shown to possess anti-inflammatory, antimalarial, antimicrobial, and antioxidant properties. Its common phytochemical components include alkaloids, flavonoids, phenolics, saponins, tannins, and triterpenes. This plant is rich in various quassinoids including eurycolactone, Eurycomalactone, eurycomanol, eurycomanone, and eurycomaoside all of which has been reported to contribute to its remedial properties including increased muscle strength, endurance in cycling time, and reduced anxiety and stress. Based on established literature on the health benefits of E. longifolia, this review article has attempted to compile E. longifolia to be one of the choices of ergogenic plants.