Cytochalasin E
(Synonyms: 细胞松弛素E) 目录号 : GC43359Inhibitor of actin polymerization
Cas No.:36011-19-5
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
Cytochalasin E, an epoxide containing Aspergillus-derived fungal metabolite, inhibits angiogenesis and tumor growth. Cytochalasin E is a potent actin depolymerization agent, and it binds and caps the barbed end of actin filaments to prevent actin elongation[1][2].
Cytochalasin E prominently inhibits the growth of A549 cells in a dose-dependent manner[3].Cytochalasin E could induce the up-regulation of autophagy-related protein (LC3-II) and SQSTM1/p62[3].
References:
[1]. Udagawa T, et al. Cytochalasin E, an epoxide containing Aspergillus-derived fungal metabolite, inhibits angiogenesisand tumor growth. J Pharmacol Exp Ther. 2000 Aug;294(2):421-7.
[2]. Lu QY, et al. Green tea extract modulates actin remodeling via Rho activity in an in vitro multistep carcinogenicmodel. Clin Cancer Res. 2005 Feb 15;11(4):1675-83.
[3]. Takanezawa Y, et al. Variation in the activity of distinct cytochalasins as autophagy inhibitiors in human lung A549 cells. Biochem Biophys Res Commun. 2017 Dec 16;494(3-4):641-647.
| Cas No. | 36011-19-5 | SDF | |
| 别名 | 细胞松弛素E | ||
| Canonical SMILES | O=C(OC12[C@@]([C@H]3[C@](C)(O3)[C@@H](C)[C@@]1([H])[C@H](CC4=CC=CC=C4)NC2=O)([H])/C=C/C[C@]5([H])C)O/C=C/[C@](O)(C)C5=O | ||
| 分子式 | C28H33NO7 | 分子量 | 495.6 |
| 溶解度 | DMF: 11 mg/ml,DMF:PBS (pH7.2) (1:30): 0.03 mg/ml,DMSO: 10 mg/ml,Ethanol: 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 | 2.0178 mL | 10.0888 mL | 20.1776 mL |
| 5 mM | 0.4036 mL | 2.0178 mL | 4.0355 mL |
| 10 mM | 0.2018 mL | 1.0089 mL | 2.0178 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。
Effects of Cytochalasin E on Paracoccidioides brasiliensis
J Appl Microbiol 2018 Nov;125(5):1296-1307.PMID:30053334DOI:10.1111/jam.14053.
Aims: To determine the effects of Cytochalasin E, isolated from the extremophile fungus Aspergillus felis, on the cells of Paracoccidioides brasiliensis Pb18. Methods and results: Cytochalasin E showed a minimal inhibitory concentration of 3·6 μmol l-1 and minimum fungicidal concentration of 7·2 μmol l-1 on P. brasiliensis by in vitro microdilution and IC50 >964·0 μmol l-1 on murine macrophages. Its selectivity index (>263) indicated that this compound has selectivity for fungal cells. Morphological alterations were determined by optical and fluorescence microscopy, as well as scanning and transmission electron microscopy. Cytochalasin E affected P. brasiliensis bud-forming pseudohyphae, cell morphology, cell walls and cell membranes; caused the release of cellular material; and resulted in the production of reactive oxygen species. In murine macrophages, it affected cytoskeletal actin and inhibited phagocytosis. Conclusion: Cytochalasin E may be useful as an antifungal prototype against P. brasiliensis and in studies on phagocytosis. Significance and impact of the study: Paracoccidioides spp. are the etiological agents of paracoccidioidomycosis (PCM). Treatment is prolonged to control the clinical manifestations and prevent relapse. The study on the effects of Cytochalasin E in P. brasiliensis is important because it can be used as a prototype for new antifungal drugs and consequently, broadens the treatment options for PCM.
Cytochalasin E alters the cytoskeleton and decreases ENaC activity in Xenopus 2F3 cells
Am J Physiol Renal Physiol 2014 Jul 1;307(1):F86-95.PMID:24829507DOI:10.1152/ajprenal.00251.2013.
Numerous reports have linked cytoskeleton-associated proteins with the regulation of epithelial Na(+) channel (ENaC) activity. The purpose of the present study was to determine the effect of actin cytoskeleton disruption by Cytochalasin E on ENaC activity in Xenopus 2F3 cells. Here, we show that Cytochalasin E treatment for 60 min can disrupt the integrity of the actin cytoskeleton in cultured Xenopus 2F3 cells. We show using single channel patch-clamp experiments and measurements of short-circuit current that ENaC activity, but not its density, is altered by cytochalasin E-induced disruption of the cytoskeleton. In nontreated cells, 8 of 33 patches (24%) had no measurable ENaC activity, whereas in cytochalasin E-treated cells, 17 of 32 patches (53%) had no activity. Analysis of those patches that did contain ENaC activity showed channel open probability significantly decreased from 0.081 ± 0.01 in nontreated cells to 0.043 ± 0.01 in cells treated with Cytochalasin E. Transepithelial current from mpkCCD cells treated with Cytochalasin E, cytochalasin D, or latrunculin B for 60 min was decreased compared with vehicle-treated cells. The subcellular expression of fodrin changed significantly, and several protein elements of the cytoskeleton decreased at least twofold after 60 min of Cytochalasin E treatment. Cytochalasin E treatment disrupted the association between ENaC and myristoylated alanine-rich C-kinase substrate. The results presented here suggest disruption of the actin cytoskeleton by different compounds can attenuate ENaC activity through a mechanism involving changes in the subcellular expression of fodrin, several elements of the cytoskeleton, and destabilization of the ENaC-myristoylated alanine-rich C-kinase substrate complex.
Cytochalasin E in the lichen Pleurosticta acetabulum. Anti-proliferative activity against human HT-29 colorectal cancer cells and quantitative variability
Fitoterapia 2017 Sep;121:146-151.PMID:28705509DOI:10.1016/j.fitote.2017.07.006.
A biological screening of sixteen lichen extracts on human HT-29 colorectal cancer cells, led to the selection of Pleurosticta acetabulum, a lichen widely present in tree barks in Europe. Bioguided purification of the acetonic extract resulted in the isolation of Cytochalasin E, a common fungal metabolite. This compound is responsible for the anti-proliferative activity of the extract. Its presence in lichens is reported here for the first time. LC-MS quantitation of Cytochalasin E in different samples of P. acetabulum demonstrated quantitative variations of Cytochalasin E production in the lichen and especially high concentrations in apothecia.
Cytochalasin E, an epoxide containing Aspergillus-derived fungal metabolite, inhibits angiogenesis and tumor growth
J Pharmacol Exp Ther 2000 Aug;294(2):421-7.PMID:10900214doi
Several previously identified inhibitors of angiogenesis have been epoxide-containing fungus-derived metabolites. We therefore hypothesized that novel epoxide-containing low molecular weight compounds structurally resembling known antiangiogenic agents may also exhibit antiangiogenic activity. Cytochalasin E was found to be a potent and selective inhibitor of bovine capillary endothelial (BCE) cell proliferation. Cytochalasin E differed from other cytochalasins by the presence of an epoxide. The epoxide was required for activity, because acid-catalyzed hydrolysis of the epoxide abrogated the specificity and potency of Cytochalasin E. Phalloidin staining indicated that disruption of actin stress fibers by Cytochalasin E occurred only at relatively high concentrations. Lower concentrations of Cytochalasin E preferentially inhibited BCE cell proliferation without disrupting actin stress fibers. In vivo, Cytochalasin E inhibited angiogenesis induced by basic fibroblast growth factor by 40% to 50% in the mouse cornea assay and inhibited the growth of Lewis lung tumors by approximately 72%. Cytochalasin E is a potent antiangiogenic agent that may hold promise for the treatment of cancer and other types of pathologic angiogenesis.
Cytochalasin E: inhibition of intestinal glucose absorption in the mouse
Toxicol Lett 1983 Mar;15(4):341-8.PMID:6836602DOI:10.1016/0378-4274(83)90154-6.
In situ glucose absorption in the mouse was significantly inhibited by Cytochalasin E. Cytochalasin E (5 micrograms/ml) also inhibited glucose absorption up to 55.5% in mouse jejunum in vitro. During its inhibition transmural potential difference (PD) was increased from -7.4 to -0.4 mV, together with a decrease in glucose accumulation in the intestinal tissues. Furthermore, it was also found that Cytochalasin E induced an alteration in Km value from 2.9 X 10(-3) to 4.0 X 10(-2) M and a constant Vmax value of 55.5 mumol/100 mg wet wt tissue/min. It is postulated that Cytochalasin E is a possible competitive inhibitor of glucose at the receptor sites of carriers on the microvillar membrane of the intestinal absorptive cells.