Eriocalyxin B
(Synonyms: 毛萼乙素) 目录号 : GC60153
EriocalyxinB是从中草药枇杷素中分离得到的一种二萜类化合物。EriocalyxinB具有抗癌、抗炎作用。EriocalyxinB诱导细胞凋亡(apoptosis)。
Cas No.:84745-95-9
Sample solution is provided at 25 µL, 10mM.
;)
,-1-7$$$37316672.jpg');)
;)
;)
$$$36806353.jpg');)
;33(7)%EF%BC%9A546-561$$$37156877.jpg');)
;)
;)
;)
%201124-1138.$$$35908550.jpg');)
%20766-780.$$$37100057.jpg');)
%20418-432.$$$36893736.jpg');)
%EF%BC%9A-240-255.$$$35108512.jpg');)
533-545$$$36543525.jpg');)
%201-13.$$$36600053.jpg');)
;)
Quality Control & SDS
- View current batch:
- Purity: >98.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Eriocalyxin B is an ent-Kaurene diterpenoid isolated from Chinese herb Isodon eriocalyx. Eriocalyxin B has anti-cancer and anti-infammatory activities. Eriocalyxin B induces cell apoptosis[1].
[1]. Rong-Fang Mu, et al. Eriocalyxin B Inhibits Adipogenesis in 3T3-L1 Adipocytes by Cell Cycle Arrest. Nat Prod Bioprospect. 2020 Jun;10(3):131-140.
| Cas No. | 84745-95-9 | SDF | |
| 别名 | 毛萼乙素 | ||
| Canonical SMILES | O[C@]1(OC2)[C@](C[C@]3([H])C4=C)(C4=O)[C@](CC3)([H])[C@]2(C(C=C5)=O)[C@](C5(C)C)([H])[C@@H]1O | ||
| 分子式 | C20H24O5 | 分子量 | 344.4 |
| 溶解度 | 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。 | ||
| 制备储备液 | |||
 |
1 mg | 5 mg | 10 mg |
| 1 mM | 2.9036 mL | 14.518 mL | 29.036 mL |
| 5 mM | 0.5807 mL | 2.9036 mL | 5.8072 mL |
| 10 mM | 0.2904 mL | 1.4518 mL | 2.9036 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。
Eriocalyxin B Inhibits Adipogenesis in 3T3-L1 Adipocytes by Cell Cycle Arrest
Nat Prod Bioprospect 2020 Jun;10(3):131-140.PMID:32314168DOI:10.1007/s13659-020-00240-6.
Eriocalyxin B, an ent-Kaurene diterpenoid extracted from a traditional Chinese herb Isodon eriocalyx, has been shown to possess multifunctional activities such as anti-cancer and anti-inflammatory. However, the function and mechanism of the compound in adipocyte differentiation is still unknown. Here we reported that Eriocalyxin B blunted adipogenesis remarkably by inhibiting the accumulation of lipid droplets, triglycerides and the expressions of adipogenesis-related factors, including C/EBPβ, C/EBPα, PPARγ, and FABP4. Moreover, we showed that the inhibition might be the consequence of cell cycle being arrested at the G2/M phase during the mitotic clonal expansion of adipocyte differentiation, most likely by suppressing mRNAs and proteins of CDK1, CDK2, Cyclin A and Cyclin B1. Overall, we conclude that Eriocalyxin B is capable of inhibiting adipocyte differentiation at the early stage through downregulating the proteins involved in cell cycle progression.
Eriocalyxin B Induces Apoptosis and Autophagy Involving Akt/Mammalian Target of Rapamycin (mTOR) Pathway in Prostate Cancer Cells
Med Sci Monit 2019 Nov 12;25:8534-8543.PMID:31714902DOI:10.12659/MSM.917333.
BACKGROUND Eriocalyxin B (EriB), a diterpenoid isolated from the plant Isodon eriocalyx, has been shown to possess anti-tumor properties. However, few systematic studies of the mechanism underlying the anti-tumor activity of Eriocalyxin B in prostate cancer cells have been published. The aim of this study was to investigate the effect of Eriocalyxin B on prostate cancer cells. MATERIAL AND METHODS In the present study, the PC-3 (androgen-independent) and 22RV1 (androgen-dependent) human prostate cancer cell lines were cultured with and without increasing doses of Eriocalyxin B. MTT assay was used to measure cell viability. Western blotting was performed to measure levels of proteins associated with apoptosis and autophagy. Flow cytometry was used to assess changes in cell apoptosis and cycle. Fluorescence microscopy was used to capture images of autophagy-related proteins. RESULTS Treatment of human prostate cancer cells with Eriocalyxin B resulted in apoptosis in a dose- and time-dependent manner. Eriocalyxin B also induced autophagy, with elevated LC3B-II protein expression and punctuate patterns. Additionally, autophagy protected prostate cancer cells from apoptosis induced by Eriocalyxin B, which was demonstrated by addition of chloroquine (CQ). Moreover, the results indicated that Eriocalyxin B could inhibit the phosphorylation of Akt and mTOR. Eriocalyxin B induced apoptosis and autophagy by inhibition of the Akt/mTOR pathway. CONCLUSIONS Eriocalyxin B induces apoptosis and autophagy involving the Akt/mTOR pathway in prostate cancer cells in vitro. These findings provide evidence for Eriocalyxin B as a potent therapeutic for the treatment of prostate cancer.
Eriocalyxin B blocks human SW1116 colon cancer cell proliferation, migration, invasion, cell cycle progression and angiogenesis via the JAK2/STAT3 signaling pathway
Mol Med Rep 2016 Mar;13(3):2235-40.PMID:26795301DOI:10.3892/mmr.2016.4800.
Eriocalyxin B, a natural ent-kaurene diterpene compound, has been shown to prevent carcinogenesis and tumor development. However, little is known regarding the mechanism underlying the antitumor activity of Eriocalyxin B in human colon cancer. The aim of the present study was to examine the role of Eriocalyxin B in SW1116 cells, and to verify the hypothesis that the Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) signaling pathway may serve as a therapeutic target in human colon cancer treatment. Cell proliferation was measured with a Cell Counting kit‑8 assay, and the cell cycle was assessed by flow cytometry. Cell migration and invasion were measured by Transwell analysis. In addition, western blot analysis was performed to detect the protein expression levels in SW1116 cells treated with various concentrations of Eriocalyxin B. The results demonstrated that 1 µmol/l Eriocalyxin B was effective at inhibiting JAK2 and STAT3 phosphorylation, followed by the downregulation of JAK2 and STAT3 downstream target expression, which resulted in the inhibition of cell proliferation, migration, invasion and angiogenesis. Eriocalyxin B also suppressed the expression of proliferation‑associated protein (proliferating cell nuclear antigen) and angiogenesis‑associated proteins (vascular endothelial growth factor and vascular endothelial growth factor receptor 2), as well as that of migration- and invasion‑associated proteins (matrix metalloproteinase 2 and 9). These results suggested that Eriocalyxin B may suppress JAK2/STAT3 signaling, and thus act as a therapeutic or preventive agent in the treatment of human colon cancer.
Correction to: Eriocalyxin B Inhibits Adipogenesis in 3T3‑L1 Adipocytes by Cell Cycle Arrest
Nat Prod Bioprospect 2020 Aug;10(4):269.PMID:32548686DOI:10.1007/s13659-020-00251-3.
In the original publication of this article, we found an error under the section "Introduction". The first sentence of the fourth paragraph appears incorrectly. The corrected sentence is given below. Eriocalyxin B, isolated and identified in 1982 [1], is the major component in Chinese plant Isodon eriocalyx (Dunn.) Hara (family Lamiaceae) showing many pharmacological activities, such as inhibiting inflammatory response, regulating immune cell differentiation, inhibiting tumor cells proliferation, causing cell cycle arrest affecting angiogenesis and promoting cancer cells apoptosis.
Natural diterpenoid Eriocalyxin B covalently modifies glutathione and selectively inhibits thioredoxin reductase inducing potent oxidative stress-mediated apoptosis in colorectal carcinoma RKO cells
Free Radic Biol Med 2021 Dec;177:15-23.PMID:34656698DOI:10.1016/j.freeradbiomed.2021.10.013.
Increasing evidence suggests the significant contribution of high levels of thioredoxin reductase (TrxR) in various stages of tumorigenesis and resistance to tumor chemotherapy. Thus, inhibition of TrxR with small molecules is an attractive strategy for cancer therapy. Eriocalyxin B (EriB), a naturally occurring diterpenoid extracted from Isodon eriocalyx, has reflected potential anticancer activities through numerous pathways. Here, we describe that EriB covalently modifies GSH and selectively inhibits TrxR activity by targeting the Sec residue of the enzyme. Pharmacological inhibition of TrxR by EriB results in elevated ROS levels, reduced total GSH and thiols content, which ultimately induced potent RKO cell apoptosis mediated by oxidative stress. Importantly, EriB indicates potent synthetic lethality with GSH inhibitors, BSO, in RKO cells. In summary, our results highlight that targeting TrxR by EriB explores a novel mechanism for the biological action of EriB. This opened up a new therapeutic indication for using EriB to combat cancers.