Powder: -20°C for 3 years | In solvent: -80°C for 1 year
N-acetylcysteine amide [38520-57-9]
Katalog-Nummer T5518-50mg
Size : 50mg
Marke : TargetMol
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N-acetylcysteine amide
Catalog No. T5518 CAS 38520-57-9
N-Acetylcysteine amide is a thiol antioxidant and neuroprotective agent that can permeate cell membranes and the blood-brain barrier.
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N-acetylcysteine amide, CAS 38520-57-9
| Description | N-Acetylcysteine amide is a thiol antioxidant and neuroprotective agent that can permeate cell membranes and the blood-brain barrier. |
| In vitro | Although NACA effectively reduced oxidative stress in DOX-treated H9c2 cells, it had minimal effects on DOX-induced cell death.?NACA prevented oxidative stress by elevation of GSH and CYS, reduction of ROS and lipid peroxidation, and restoration of antioxidant enzyme activities[1]. |
| In vivo | N-acetylcysteine amide reduces cortical tissue damage and decreases the distance traveled to the platform in the Morris water maze in a rat model of traumatic brain injury[2].N-acetylcysteine amide (60 and 120 mg/kg) also inhibits ovalbumin-induced decreases in GSH, increases in nuclear NF-κB p65 and HIF-1α, and increases in IL-4, IL-5, and IL-13 levels in mouse lung tissue[3]. |
| Cell Research | To determine effectiveness of NACA and NAC in protection of H9c2 cells from DOX-induced toxicity, cells were treated with NACA or NAC at 0.75 mM for 2 h followed by exposure to freshly prepared cell culture medium with DOX in presence or absence of NACA or NAC at designated concentrations. The concentrations of DOX were 0.25 μM, 0.75 μM, 2 μM, 5 μM, 20 μM, and 100 μM. The exposure durations were 24 h, 48 h, or 48 h. Cells incubated with NACA or NAC alone were used as the control[1]. |
| Animal Research | rats were randomly divided into three groups (n=6-8 animals/group): N-acetylcysteine amide?loaded pump (18.5?mg/kg/hr) and a single 150 mg/kg bolus intraperitoneal (IP) injection of NACA given (30 min post-injury) ?N-acetylcysteine amide?(18.5 mg/kg/hr) loaded pump and a single 150 mg/kg bolus injection of N-acetylcysteine amide?given IP (30 min post-injury) ?Vehicle loaded pump and?single vehicle bolus injection given IP (30 min post-injury).?Following random distribution of all animals into one of the three previous groups, experimenters were blinded to treatment group.?The osmotic mini pumps were assembled and implanted immediately after injury and remained in the animals for 7 days[2] |
| Molecular Weight | 162.21 |
| Formula | C5H10N2O2S |
| CAS No. | 38520-57-9 |
Storage
Solubility Information
DMSO: 100 mg/mL (616.48 mM)
References and Literature
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. 2. Pandya J D , Readnower R D , Patel S P , et al. N-acetylcysteine amide confers neuroprotection, improves bioenergetics and behavioral outcome following TBI[J]. Experimental Neurology, 2014, 257:106-113. 3. Penugonda S , Mare S , Goldstein G , et al. Effects of N-acetylcysteine amide (NACA), a novel thiol antioxidant against glutamate-induced cytotoxicity in neuronal cell line PC12[J]. Brain Research, 2005, 1056(2):132-138. 4. Xue J, Gruber F, Tschachler E, et al. Crosstalk between oxidative stress, autophagy and apoptosis in Hemoporfin Photodynamic Therapy treated human umbilical vein endothelial cells[J]. Photodiagnosis and Photodynamic Therapy. 2020: 102137.
Citations
1. Xue J, Gruber F, Tschachler E, et al. Crosstalk between oxidative stress, autophagy and apoptosis in Hemoporfin Photodynamic Therapy treated human umbilical vein endothelial cells. Photodiagnosis and Photodynamic Therapy. 2020: 102137. 2. Zhang H, Gong J, Zhang S, et al.N-acetylcysteine attenuates the incidence of phlebitis induced by carbomer/vinorelbine gel.Heliyon.2023, 9(11): e21235. 3. Li D, Xu Z, Li Y, et al.Breviscapine attenuates lead‑induced myocardial injury by activating the Nrf2 signaling pathway.Experimental and Therapeutic Medicine.2024, 27(1): 1-8.