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1、Hotline: 400-820-3792Inhibitors Agonists Screening Librarieswww.MedChemEN-Acetylcysteine amideCat. No.: HY-110256CAS No.: 38520-57-9分式: CHNOS分量: 162.21作靶点: Reactive Oxygen Species作通路: Immunology/Inflammation; Metabolic Enzyme/Protease; NF-B储存式: Powder -20C 3 years4C 2 yearsIn solvent -80C 6 months-2
2、0C 1 month溶解性数据体外实验 DMSO : 100 mg/mL (616.48 mM)* means soluble, but saturation unknown.Mass Solvent1 mg 5 mg 10 mg Concentration制备储备液1 mM 6.1648 mL 30.8242 mL 61.6485 mL5 mM 1.2330 mL 6.1648 mL 12.3297 mL10 mM 0.6165 mL 3.0824 mL 6.1648 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药
3、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 (15.41 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 (15.41 mM); Cl
4、ear solution3. 请依序添加每种溶剂: 10% DMSO 90% corn oil1/3 Master of Small Molecules 您边的抑制剂师www.MedChemESolubility: 2.5 mg/mL (15.41 mM); Clear solutionBIOLOGICAL ACTIVITY物活性 N-Acetylcysteine amide种能透过细胞膜和脑屏障的硫醇抗氧化剂和神经保护剂,可降低 ROS 的产。体外研究 N-Acetylcysteine amide shows no obvious effect on the viability of H9c
5、2 cells treated with doxorubicin (DOX)at 1 mM, but causes significant cytotoxicity at 10-20 mM. N-Acetylcysteine amide (750 M) reduces theROS levle and lipid peroxidation induced by DOX, and restores GSH/GSSG ratio and activities of antioxidantenzymes, such as catalase (CAT), gluthathione peroxidase
6、 (GPx), gluthathione reductase (GR) 1. N-Acetylcysteine amide (1 mM) protects the human brain microvascular endothelial (HBMVEC) frommethamphetamine (METH)- induced cell death 3.体内研究 N-Acetylcysteine amide has increased CNS bioavailability. N-Acetylcysteine amide (150 mg/kg, i.p.)improves cortical s
7、paring and functional outcome, reduces oxidative stress, improves mitochondrialbioenergetics, and maintains mitochondrial glutathione content following traumatic brain injury (TBI) in rats2.PROTOCOLCell Assay 1 To choose a sublethal concentration of N-Acetylcysteine amide and N-acetylcysteine for th
8、e study on theirability to protect cells from doxorubicin (DOX)-induced toxicity, H9c2 cells are exposed with N-Acetylcysteineamide or N-acetylcysteine at 0.25 mM, 0.50 mM, 0.75 mM, 1 mM, 2 mM, 5 mM, 10 mM, and 20 mM for 24 h.Untreated cells are used as the control for each experiment 1.MCE has not
9、independently confirmed the accuracy of these methods. They are for reference only.Animal Rats 2Administration 2 In order to assess mitochondrial respiration and glutathione content following traumatic brain injury (TBI), ratsare randomly divided into three groups (n = 5 animals/group). (I.) N-Acety
10、lcysteine amide group receivesmultiple bolus IP injections of N-Acetylcysteine amide (150 mg/kg) immediately after 5 minutes and thenevery 6 hours up to 24 hrs post-injury. (II.) Vehicle group receives equivalent v/v saline at 5 minutes andevery 6 hours (6, 12, 18, 24 hrs) up to 24 hrs post-injury.
11、(III.) Sham injured group animals do not receive anydrug treatment. At 25 hrs post-injury, all animals are euthanized and mitochondria are isolated from theipsilateral cortical hemisphere (6 mm punch) to carry out measurements of mitochondrial respiration andglutathione content 2.MCE has not indepen
12、dently confirmed the accuracy of these methods. They are for reference only.户使本产品发表的科研献 J Neurosci Res. 2019 Aug 16. Toxicology. 2019 Apr 15;418:22-31. J Funct Foods. 2019 Apr.2/3 Master of Small Molecules 您边的抑制剂师www.MedChemE Toxicol In Vitro. 2017 Oct;44:57-65. Int J Mol Med. 2019 May.See more cust
13、omer validations on HYPERLINK / www.MedChemEREFERENCES1. Shi R, et al. N-acetylcysteine amide decreases oxidative stress but not cell death induced by doxorubicin in H9c2 cardiomyocytes. BMCPharmacol. 2009 Apr 15;9:7.2. Pandya JD, et al. N-acetylcysteine amide confers neuroprotection, improves bioenergetics and behavioral outcome following TBI. ExpNeurol. 2014 Jul;257:106-13.3. Zhang X, et al. N-Acetylcysteine amide protects against methamphetamine-induced oxidative stress and neurotoxicity in immortalizedhuman brain endothelial cells. Brain Res. 2009 Jun 12;1275
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