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Submit ReviewN-Acetylcysteine amide is a glutathione (GSH) precursor and cell-permeable antioxidant. N-Acetylcysteine amide replenishes intracellular Glutathione (GSH). N-Acetylcysteine amide directly reduces intracellular Glutathione disulfide (GSSG) to GSH without glutathione peroxidase. N-Acetylcysteine amide has anti-inflammatory activity through regulation of activation of NF-κB and HIF-1α, as well as modulation of reactive oxygen species. N-Acetylcysteine amide improves neuronal mitochondrial bioenergetics, reduces tissue damage and enhances functional recovery following spinal cord injury in rats. N-Acetylcysteine amide also enhances behavioral recovery in rats following traumatic brain injury. Neuroprotective.
For more information about how N-Acetylcysteine amide may be used, see our protocol: 3D Culture of Lung Alveolar Cells
M. Wt | 162.21 |
Formula | C5H10N2O2S |
Storage | Store at -20°C |
CAS Number | 38520-57-9 |
PubChem ID | 10176265 |
InChI Key | UJCHIZDEQZMODR-BYPYZUCNSA-N |
Smiles | SC[C@H](NC(C)=O)C(N)=O |
The technical data provided above is for guidance only. For batch specific data refer to the Certificate of Analysis.
Tocris products are intended for laboratory research use only, unless stated otherwise.
Solvent | Max Conc. mg/mL | Max Conc. mM | |
---|---|---|---|
Solubility | |||
water | 16.22 | 100 | |
DMSO | 16.22 | 100 |
The following data is based on the product molecular weight 162.21. Batch specific molecular weights may vary from batch to batch due to the degree of hydration, which will affect the solvent volumes required to prepare stock solutions.
Concentration / Solvent Volume / Mass | 1 mg | 5 mg | 10 mg |
---|---|---|---|
1 mM | 6.16 mL | 30.82 mL | 61.65 mL |
5 mM | 1.23 mL | 6.16 mL | 12.33 mL |
10 mM | 0.62 mL | 3.08 mL | 6.16 mL |
50 mM | 0.12 mL | 0.62 mL | 1.23 mL |
References are publications that support the biological activity of the product.
Patel et al (2014) N-acetylcysteine amide preserves mitochondrial bioenergetics and improves functional recovery following spinal trauma. Exp.Neurol. 257 95 PMID: 24805071
Pandya et al (2014) N-acetylcysteine amide confers neuroprotection, improves bioenergetics and behavioral outcome following TBI. Exp.Neurol. 257 106 PMID: 24792639
Tu et al (2019) The anti-inflammatory and anti-oxidant mechanisms of the Keap1/Nrf2/ARE signaling pathway in chronic diseases. Aging Dis 10 637 PMID: 31165007
If you know of a relevant reference for N-Acetylcysteine amide, please let us know.
Keywords: N-Acetylcysteine amide, N-Acetylcysteine amide supplier, cell, permeable, antioxidant, neuroprotective, glutathione, precursor, GSH, organoids, hematopoietic, haematopoietic, stem, cells, HSC, Antioxidants, Hematopoietic, Stem, Cells, 5619, Tocris Bioscience
Citations are publications that use Tocris products. Selected citations for N-Acetylcysteine amide include:
Christian et al (2021) NF-κB determines Paneth versus goblet cell fate decision in the small intestine. Development 148 PMID: 34751748
Craig et al (2022) Liver X receptor-agonist treatment rescues degeneration in a Drosophila model of hereditary spastic paraplegia. Acta Neuropathol Commun 10 40 PMID: 35346366
Young-Min et al (2020) Nanosphere Loaded with Curcumin Inhibits the Gastrointestinal Cell Death Signaling Pathway Induced by the Foodborne Pathogen Vibrio vulnificus. Cells 9 PMID: 32151068
Tao et al (2021) Microengineered multi-organoid system from hiPSCs to recapitulate human liver-islet axis in normal and type 2 diabetes. Adv.Sci. 9 e2103495 PMID: 34951149
Gutierrez et al (2014) The anticancer agent di-2-pyridylketone 4,4-dimethyl-3-thiosemicarbazone (Dp44mT) overcomes prosurvival autophagy by two mechanisms: persistent induction of autophagosome synthesis and impairment of lysosomal integrity. J Biol Chem 289 33568 PMID: 25301941
Do you know of a great paper that uses N-Acetylcysteine amide from Tocris? Please let us know.
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HL-1 cardiomyocytes were pre-treated with Pyrrolidinedithiocarbamate (PDTC, 1 mM), Tempol (1 mM) or N-Acetylcysteine (NAC, 1 mM) for 30 min and stimulated with HOCl-LDL (200 µg/ml) for 2 h to follow CaMKII oxidation using Western blot.