N-Acetylcysteine-amide - Reactive Oxygen Species - MedChemExpress

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作靶點(diǎn): Reactive Oxygen Species作通路: Immunology/Inflammation; Metabolic Enzyme/Protease; NF-B儲(chǔ)存式: Powder -20C 3 years4C 2 yearsIn solvent -80C 6 months-2

2、0C 1 month溶解性數(shù)據(jù)體外實(shí)驗(yàn) DMSO : 100 mg/mL (616.48 mM)* means soluble, but saturation unknown.Mass Solvent1 mg 5 mg 10 mg Concentration制備儲(chǔ)備液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請(qǐng)根據(jù)產(chǎn)品在不同溶劑中的溶解度，選擇合適的溶劑配制儲(chǔ)備液，并請(qǐng)注意儲(chǔ)備液的保存式和期限。體內(nèi)實(shí)驗(yàn)請(qǐng)根據(jù)您的實(shí)驗(yàn)動(dòng)物和給藥

3、式選擇適當(dāng)?shù)娜芙獍?，配制前?qǐng)先配制澄清的儲(chǔ)備液，再依次添加助溶劑(為保證實(shí)驗(yàn)結(jié)果的可靠性，體內(nèi)實(shí)驗(yàn)的作液，建議您現(xiàn)現(xiàn)配，當(dāng)天使；澄清的儲(chǔ)備液可以根據(jù)儲(chǔ)存條件，適當(dāng)保存；以下溶劑前的百分 指該溶劑在您配制終溶液中的體積占)：1. 請(qǐng)依序添加每種溶劑： 10% DMSO 40% PEG300 5% Tween-80 45% salineSolubility: 2.5 mg/mL (15.41 mM); Clear solution2. 請(qǐng)依序添加每種溶劑： 10% DMSO 90% (20% SBE-CD in saline)Solubility: 2.5 mg/mL (15.41 mM); Cl

4、ear solution3. 請(qǐng)依序添加每種溶劑： 10% DMSO 90% corn oil1/3 Master of Small Molecules 您邊的抑制劑師www.MedChemESolubility: 2.5 mg/mL (15.41 mM); Clear solutionBIOLOGICAL ACTIVITY物活性 N-Acetylcysteine amide種能透過(guò)細(xì)胞膜和腦屏障的硫醇抗氧化劑和神經(jīng)保護(hù)劑，可降低 ROS 的產(chǎn)。體外研究 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.體內(nèi)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.戶使本產(chǎn)品發(fā)表的科研獻(xiàn) J Neurosci Res. 2019 Aug 16. Toxicology. 2019 Apr 15;418:22-31. J Funct Foods. 2019 Apr.2/3 Master of Small Molecules 您邊的抑制劑師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