Anisomycin-Flagecidin-DataSheet-生命科学试剂-MedChemExpress

1、Hotline: 400-820-3792Inhibitors Agonists Screening Librarieswww.MedChemEAnisomycinCat. No.: HY-18982CAS No.: 22862-76-6Synonyms: Flagecidin; Wuningmeisu C分式: CHNO分量: 265.31作靶点: DNA/RNA Synthesis; JNK作通路: Cell Cycle/DNA Damage; MAPK/ERK Pathway储存式: Powder -20C 3 years4C 2 yearsIn solvent -80C 6 month

2、s-20C 1 month溶解性数据体外实验 DMSO : 50 mg/mL (188.46 mM)* means soluble, but saturation unknown.Mass Solvent1 mg 5 mg 10 mg Concentration制备储备液1 mM 3.7692 mL 18.8459 mL 37.6918 mL5 mM 0.7538 mL 3.7692 mL 7.5384 mL10 mM 0.3769 mL 1.8846 mL 3.7692 mL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，并请注意储备液的保存式和期限。体内实验请根据您的实验动物和给

3、药式选择适当的溶解案，配制前请先配制澄清的储备液，再依次添加助溶剂(为保证实验结果的可靠性，体内实验的作液，建议您现现配，当天使；澄清的储备液可以根据储存条件，适当保存；以下溶剂前的百分 指该溶剂在您配制终溶液中的体积占)：1. 请依序添加每种溶剂： 10% DMSO 40% PEG300 5% Tween-80 45% salineSolubility: 2.5 mg/mL (9.42 mM); Clear solution2. 请依序添加每种溶剂： 10% DMSO 90% (20% SBE-CD in saline)Solubility: 2.5 mg/mL (9.42 mM); Cle

4、ar solution1/3 Master of Small Molecules 您边的抑制剂师www.MedChemE3. 请依序添加每种溶剂： 10% DMSO 90% corn oilSolubility: 2.5 mg/mL (9.42 mM); Clear solutionBIOLOGICAL ACTIVITY物活性 Anisomycin种有效的蛋质合成抑制剂，它通过抑制肽 转移酶或80S核糖体系统扰蛋质和DNA合成。Anisomycin 种 JNK 激活剂，可增强磷酸化 JNK 。IC50 & Target JNK DNA synthesis体外研究 To examine whet

5、her JNK has a core role in colistin-induced neurotoxicity in PC-12 cells, an SP600125 (ahighly selective inhibitor of JNK) and Anisomycin (a potent activator) are used in this study. In order to selectan appropriate concentration, PC-12 cells are treated with a range of SP600125 (0-80 M) and Anisomy

6、cin(0-20 M) respectively for 24 h. The results show that the cells viability significantly decreases by SP600125treatment in a concentration-dependent manner, observed at the concentrations greater than 20 M (p 1.体内研究 Disruption of TNFRp55/p75 attenuates Anisomycin-induced ventricular functional imp

7、rovements. Anisomycinresults in an improvement in left ventricular developed pressure (LVDP), which disappears in animals withdisruption of TNFR p55/p75. In addition, the Anisomycin-induced improvement in LVEDP in wild-type animalsis eliminated by deletion of TNFR p55/p75. Likewise, disruption of TN

8、FR p55/p75 abrogates the recovery ofrate pressure product (RPP) elicited by pretreatment of Anisomycin. TNFR p55/p75-/- mice withoutAnisomycin treatment do not show differences in cardiac functional recovery compared with the control wild-type mice. There are no significant differences in heart rate

9、 between wild-type and TNFR p55/p75-deficientmice. To see whether Nox2 is involved in Anisomycin-induced myocardial protection, Nox2-deficient mice aretreated with Anisomycin. The improvement in the LVEDP in Anisomycin-treated mice is eliminated in Nox2-/-mice compared with wild-type mice. In additi

10、on, recovery of RPP in wild-type mice treated with Anisomycin ismitigated in Nox2-/- mice. Nox2-/- mice without Anisomycin treatment do not show the difference in cardiacfunctional recovery compared with wild-type control mice 2.PROTOCOLCell Assay 1 PC-12 cells are seeded in 96-well plates at a conc

11、entration of 1104 cells/well and cultured in an incubator at37C with 5% CO2 for at least 12 h prior to exposure to different concentrations of SP600125 (0-80 M) orAnisomycin (0-20 M) for 24 h. Subsequently, the culture medium is added to 20 L of 5 mg/mL MTTworking solution and the plate is incubated

12、 for 2 h at 37C. The culture supernatant is removed and theformazan crystals are dissolved in 150 L DMSO. Finally, the absorbance of each well is measured at 490nm by a microplate reader. Cell viability is expressed as the percentage of the control group, which is set to100% 1.MCE has not independen

13、tly confirmed the accuracy of these methods. They are for reference only.Animal Mice 2Administration 2 Adult male TNFRp55/p75 mice, adult male wild-type C57/BL and homozygous Nox2-/- mice are used in this2/3 Master of Small Molecules 您边的抑制剂师www.MedChemEstudy. Mice are randomized into six experimenta

14、l groups that undergo the following treatments,. Animals aredivided into six groups: group 1: control ischemia/reperfusion, wild-type mice are injected with DMSO (0.1mL); group 2: Anisomycin+wild-type mice, wild-type mice are injected with Anisomycin (0.1 mg/kg ip); group3: Anisomycin+TNFR p55/p75-/

15、- mice, TNFR p55/75-/- mice are injected with Anisomycin (0.1 mg/kg ip);group 4: TNFR p55/p75-/- mice, TNFR p55/75-/- mice are not injected with Anisomycin; group 5:Anisomycin+Nox2-/- mice, Nox2-/- mice are injected with Anisomycin (0.1 mg/kg ip); and group 6: Nox2-/-mice, Nox2-/- mice are not injec

16、ted with Anisomycin. Later (24 h), the hearts are subjected to 30 min ofischemia followed by 30 min of reperfusion 2.MCE has not independently confirmed the accuracy of these methods. They are for reference only.户使本产品发表的科研献 Am J Physiol Cell Physiol. 2018 Aug 1;315(2):C225-C235. Sci Rep. 2018 Apr 23

17、;8(1):6379. Sci Rep. 2017 Oct 19;7(1):13571. Front Mol Neurosci. 2017 Aug 28;10:269. Chem Biol Interact. 2017 Nov 1;277:62-73.See more customer validations on HYPERLINK / www.MedChemEREFERENCES1. Lu Z, et al. Colistin-induced autophagy and apoptosis involves the JNK-Bcl2-Bax signaling pathway and JN

18、K-p53-ROS positivefeedback loop in PC-12 cells.2. Zhao TC, et al. Disruption of Nox2 and TNFRp55/p75 eliminates cardioprotection induced by Anisomycin. Am J Physiol Heart CircPhysiol. 2012 Nov 15;303(10):H1263-72.3. Gao X, et al. Transcriptional regulation of stress kinase JNK2 in pro-arrhythmic CaMKII