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N-Acetylcysteine amide

MCE China：N-Acetylcysteine amide

Brand：MedChemExpress (MCE)

Cat. No.HY-110256

CAS：38520-57-9

Purity：99.78%

Storage：Powder -20°C 3 years 4°C 2 years In solvent -80°C 6 months -20°C 1 month

Shipping：Room temperature in continental US; may vary elsewhere.

Description：N-Acetylcysteine amide is a cell membranes and blood brain barrier permeant thiol antioxidant and neuroprotective agent, reduces ROS production.

In Vitro：N-Acetylcysteine amide shows no obvious effect on the viability of H9c2 cells treated with doxorubicin (DOX) at enzymes, such as catalase (CAT), gluthathione peroxidase (GPx), gluthathione reductase (GR)[1]. N-Acetylcysteine amide (1 mM) protects the human brain microvascular endothelial (HBMVEC) from methamphetamine (METH)- induced cell death[3].

In Vivo：N-Acetylcysteine amide has increased CNS bioavailability. N-Acetylcysteine amide (150 mg/kg, i.p.) improves cortical sparing and functional outcome, reduces oxidative stress, improves mitochondrial bioenergetics, and maintains mitochondrial glutathione content following traumatic brain injury (TBI) in rats[2].

Animal Administration：Rats[2] In order to assess mitochondrial respiration and glutathione content following traumatic brain injury (TBI), rats are randomly divided into three groups (n = 5 animals/group). (I.) N-Acetylcysteine amide group receives multiple bolus IP injections of N-Acetylcysteine amide (150 mg/kg) immediately after 5 minutes and then every 6 hours up to 24 hrs post-injury. (II.) Vehicle group receives equivalent v/v saline at 5 minutes and every 6 hours (6, 12, 18, 24 hrs) up to 24 hrs post-injury. (III.) Sham injured group animals do not receive any drug treatment. At 25 hrs post-injury, all animals are euthanized and mitochondria are isolated from the ipsilateral cortical hemisphere (6 mm punch) to carry out measurements of mitochondrial respiration and glutathione content[2].

Cell Assay：To choose a sublethal concentration of N-Acetylcysteine amide and N-acetylcysteine for the study on their ability to protect cells from doxorubicin (DOX)-induced toxicity, H9c2 cells are exposed with N-Acetylcysteine amide 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].

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References：

[1]. Shi R, et al. N-acetylcysteine amide decreases oxidative stress but not cell death induced by doxorubicin in H9c2 cardiomyocytes. BMC Pharmacol. 2009 Apr 15;9:7.  [Content Brief]

[2]. Pandya JD, et al. N-acetylcysteine amide confers neuroprotection, improves bioenergetics and behavioral outcome following TBI. Exp Neurol. 2014 Jul;257:106-13.  [Content Brief]

[3]. Zhang X, et al. N-Acetylcysteine amide protects against methamphetamine-induced oxidative stress and neurotoxicity in immortalized human brain endothelial cells. Brain Res. 2009 Jun 12;1275:87-95.  [Content Brief]