Acetylcysteine |
| (Synonyms: N-acetylcysteine; N-acetyl-L-cysteine; NAC; Acetadote) Catalog No.: GC11786 |
Acetylcysteine is the N-acetyl derivative of CYSTEINE.
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.:616-91-1
Sample solution is provided at 25 µL, 10mM.
Quality Control & SDS
- View current batch:
-
Purity: >99.00%
- COA (Certificate Of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
| Kinase experiment [1]: | |
|
Preparation Method |
PRP was preincubated at 37°C for 4 min with Acetylcysteine or with nitroglycerin, or first with Acetylcysteine and then nitroglycerin, and sodium nitroprusside, sodium azide, sodium nitrite, or S-nitroso-N-acetylcysteine for 1 min before addition of agonist. |
|
Reaction Conditions |
5.5 mM Acetylcysteine for 4 min |
|
Applications |
Millimolar concentrations of Acetylcysteine potentiated markedly the inhibitory effect of nitroglycerin on platelet aggregation induced by ADP, epinephrine, collagen, and arachidonate, decreasing the 50% inhibitory concentration (IC50) approximately 50-fold for each of these agents. |
| Cell experiment [2]: | |
|
Cell lines |
PC12 cell line |
|
Preparation Method |
Cells were treated with 100 ng/ml NGF or 60 mm Acetylcysteine in serum-containing medium for the indicated times. |
|
Reaction Conditions |
60 mm Acetylcysteine for 15min-4h |
|
Applications |
Acetylcysteine activates the Ras-ERK pathway |
| Animal experiment [3]: | |
|
Animal models |
Thirty-five male Wistar rats |
|
Preparation Method |
Group control underwent IIR without Acetylcysteine. In the other groups, Acetylcysteine was administered intraperitoneally with different regimens: 150 mg/kg before ischemia, 300 mg/kg before ischemia, and 150 mg/kg before ischemia plus 150 mg/kg 5 min before reperfusion. |
|
Dosage form |
150-300 mg/kg Acetylcysteine(Intraperitoneal administration) |
|
Applications |
Acetylcysteine exerts a significant protective role in liver injury following IIR, which seems to be independent of an intestinal protective effect. Additional administration of Acetylcysteine before reperfusion was of no further benefit. The most effective regimen among the compared regimens was that of 300 mg/kg before ischemia. |
|
References: [1]. Loscalzo J. N-Acetylcysteine potentiates inhibition of platelet aggregation by nitroglycerin. J Clin Invest. 1985 Aug;76(2):703-8. doi: 10.1172/JCI112024. PMID: 2863286; PMCID: PMC423881. [2]. Yan CY, Greene LA. Prevention of PC12 cell death by N-acetylcysteine requires activation of the Ras pathway. J Neurosci. 1998 Jun 1;18(11):4042-9. doi: 10.1523/JNEUROSCI.18-11-04042.1998. PMID: 9592085; PMCID: PMC6792807. [3]. Kalimeris K, Briassoulis P, et,al. N-acetylcysteine ameliorates liver injury in a rat model of intestinal ischemia reperfusion. J Surg Res. 2016 Dec;206(2):263-272. doi: 10.1016/j.jss.2016.08.049. Epub 2016 Aug 19. PMID: 27884318. |
|
Acetylcysteine is the N-acetyl derivative of CYSTEINE. NAC (N-acetyl-L-cysteine) is commonly used to identify and test ROS (reactive oxygen species) inducers, and to inhibit ROS.Acetylcysteine (N-Acetylcysteine) is a mucolytic agent which reduces the thickness of the mucus[1]. It has also been shown to have antiviral effects in patients with HIV due to inhibition of viral stimulation by reactive oxygen intermediates. Acetylcysteine also has anti-influenza virus activities[5].
Millimolar concentrations of Acetylcysteine potentiated markedly the inhibitory effect of nitroglycerin on platelet aggregation induced by ADP, epinephrine, collagen, and arachidonate, decreasing the 50% inhibitory concentration (IC50) approximately 50-fold for each of these agents.In the absence of Acetylcysteine, nitroglycerin induced a marked decrease in platelet-reduced glutathione content as S-nitroso-thiol adducts were produced. The synthetic S-nitroso-thiol, S-nitroso-N-acetylcysteine, markedly inhibited platelet aggregation with an IC50 of 6 nM[7].Acetylcysteine increased ERK-1 activity in PC12 cells after 15 min of treatment and maximal stimulatory activity for 60 min. We also observed that Acetylcysteine caused tyrosine phosphorylation of ERK-1 in cells treated with this compound for 30 min[4].Acetylcysteine induces cell apoptosis. When used serum-deprived PC12 cells, neuronally differentiated PC12 cells deprived of serum and NGF, and NGF-deprived neonatal sympathetic neurons. In each case L-Acetylcysteine prevents apoptotic DNA fragmentation and maintains long-term survival in the absence of other trophic support[3].Acetylcysteine prevents hemin-induced ferroptosis by neutralizing toxic lipids generated by arachidonate-dependent activity of 5-lipoxygenases[2].
In mice, Acetylcysteine exerts a significant protective role in liver injury following IIR, which seems to be independent of an intestinal protective effect. Additional administration of Acetylcysteine before reperfusion was of no further benefit. The most effective regimen among the compared regimens was that of 300 mg/kg before ischemia[6].
References:
[1]: Halasi M, Wang M, et,al. ROS inhibitor N-acetyl-L-cysteine antagonizes the activity of proteasome inhibitors. Biochem J. 2013 Sep 1;454(2):201-8. doi: 10.1042/BJ20130282. PMID: 23772801; PMCID: PMC4322432.
[2]: Farr SA, Poon HF, et,al. The antioxidants alpha-lipoic acid and N-acetylcysteine reverse memory impairment and brain oxidative stress in aged SAMP8 mice. J Neurochem. 2003 Mar;84(5):1173-83. doi: 10.1046/j.1471-4159.2003.01580.x. PMID: 12603840.
[3]: Ferrari G, Yan CY, et,al. N-acetylcysteine (D-and L-stereoisomers) prevents apoptotic death of neuronal cells. J Neurosci. 1995 Apr;15(4):2857-66. doi: 10.1523/JNEUROSCI.15-04-02857.1995. PMID: 7722634; PMCID: PMC6577755.
[4]: Yan CY, Greene LA. Prevention of PC12 cell death by N-acetylcysteine requires activation of the Ras pathway. J Neurosci. 1998 Jun 1;18(11):4042-9. doi: 10.1523/JNEUROSCI.18-11-04042.1998. PMID: 9592085; PMCID: PMC6792807.
[5]: Garigliany MM, Desmecht DJ. N-acetylcysteine lacks universal inhibitory activity against influenza A viruses. J Negat Results Biomed. 2011 May 9;10:5. doi: 10.1186/1477-5751-10-5. PMID: 21554703; PMCID: PMC3104374.
[6]: Kalimeris K, Briassoulis P, et,al. N-acetylcysteine ameliorates liver injury in a rat model of intestinal ischemia reperfusion. J Surg Res. 2016 Dec;206(2):263-272. doi: 10.1016/j.jss.2016.08.049. Epub 2016 Aug 19. PMID: 27884318.
[7]: Loscalzo J. N-Acetylcysteine potentiates inhibition of platelet aggregation by nitroglycerin. J Clin Invest. 1985 Aug;76(2):703-8. doi: 10.1172/JCI112024. PMID: 2863286; PMCID: PMC423881.
| Cas No. | 616-91-1 | SDF | |
| Synonyms | N-acetylcysteine; N-acetyl-L-cysteine; NAC; Acetadote | ||
| Chemical Name | (2R)-2-acetamido-3-sulfanylpropanoic acid | ||
| Canonical SMILES | CC(=O)NC(CS)C(=O)O | ||
| Formula | C5H9NO3S | M.Wt | 163.19 |
| Solubility | DMF: 50 mg/mL,DMSO: 50 mg/mL,Ethanol: 50 mg/mL,PBS (pH 7.2): 30 mg/mL | Storage | 4°C, protect from light |
| General tips | For obtaining a higher solubility , please warm the tube at 37 ℃ and shake it in the ultrasonic bath for a while.Stock solution can be stored below -20℃ for several months. | ||
| Shipping Condition | Evaluation sample solution : ship with blue ice All other available size: ship with RT , or blue ice upon request |
||
Step 1: Enter information below (Recommended: An additional animal making an allowance for loss during the experiment)
g
μL
Step 2: Enter the in vivo formulation (This is only the calculator, not formulation. Please contact us first if there is no in vivo formulation at the solubility Section.)
Calculation results:
Working concentration: mg/ml;
Method for preparing DMSO master liquid: mg drug pre-dissolved in μL DMSO ( Master liquid concentration mg/mL, Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug. )
Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL saline, mix and clarify.
Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.
Note: 1. Please make sure the liquid is clear before adding the next solvent.
2. Be sure to add the solvent(s) in order. You must ensure that the solution obtained, in the previous addition, is a clear solution before proceeding to add the next solvent. Physical methods such as vortex, ultrasound or hot water bath can be used to aid dissolving.
3. All of the above co-solvents are available for purchase on the GlpBio website.
Clinical trials of N-acetylcysteine in psychiatry and neurology: A systematic review
N-acetylcysteine (NAC) is recognized for its role in acetaminophen overdose and as a mucolytic. Over the past decade, there has been growing evidence for the use of NAC in treating psychiatric and neurological disorders, considering its role in attenuating pathophysiological processes associated with these disorders, including oxidative stress, apoptosis, mitochondrial dysfunction, neuroinflammation and glutamate and dopamine dysregulation. In this systematic review we find favorable evidence for the use of NAC in several psychiatric and neurological disorders, particularly autism, Alzheimer's disease, cocaine and cannabis addiction, bipolar disorder, depression, trichotillomania, nail biting, skin picking, obsessive-compulsive disorder, schizophrenia, drug-induced neuropathy and progressive myoclonic epilepsy. Disorders such as anxiety, attention deficit hyperactivity disorder and mild traumatic brain injury have preliminary evidence and require larger confirmatory studies while current evidence does not support the use of NAC in gambling, methamphetamine and nicotine addictions and amyotrophic lateral sclerosis. Overall, NAC treatment appears to be safe and tolerable. Further well designed, larger controlled trials are needed for specific psychiatric and neurological disorders where the evidence is favorable.
Overview on the Effects of N-Acetylcysteine in Neurodegenerative Diseases
N-acetylcysteine (NAC), which is an acetylated cysteine compound, has aroused scientific interest for decades due to its important medical applications. It also represents a nutritional supplement in the human diet. NAC is a glutathione precursor and shows antioxidant and anti-inflammatory activities. In addition to the uses quoted in the literature, NAC may be considered helpful in therapies to counteract neurodegenerative and mental health diseases. Furthermore, this compound has been evaluated for its neuroprotective potential in the prevention of cognitive aging dementia. NAC is inexpensive, commercially available and no relevant side effects were observed after its administration. The purpose of this paper is to give an overview on the effects and applications of NAC in Parkinson's and Alzheimer's disorders and in neuropathic pain and stroke.
The Multifaceted Therapeutic Role of N-Acetylcysteine (NAC) in Disorders Characterized by Oxidative Stress
Oxidative stress, which results in the damage of diverse biological molecules, is a ubiquitous cellular process implicated in the etiology of many illnesses. The sulfhydryl-containing tripeptide glutathione (GSH), which is synthesized and maintained at high concentrations in all cells, is one of the mechanisms by which cells protect themselves from oxidative stress. N-acetylcysteine (NAC), a synthetic derivative of the endogenous amino acid L-cysteine and a precursor of GSH, has been used for several decades as a mucolytic and as an antidote to acetaminophen (paracetamol) poisoning. As a mucolytic, NAC breaks the disulfide bonds of heavily cross-linked mucins, thereby reducing mucus viscosity. In vitro, NAC has antifibrotic effects on lung fibroblasts. As an antidote to acetaminophen poisoning, NAC restores the hepatic GSH pool depleted in the drug detoxification process. More recently, improved knowledge of the mechanisms by which NAC acts has expanded its clinical applications. In particular, the discovery that NAC can modulate the homeostasis of glutamate has prompted studies of NAC in neuropsychiatric diseases characterized by impaired glutamate homeostasis. This narrative review provides an overview of the most relevant and recent evidence on the clinical application of NAC, with a focus on respiratory diseases, acetaminophen poisoning, disorders of the central nervous system (chronic neuropathic pain, depression, schizophrenia, bipolar disorder, and addiction), cardiovascular disease, contrast-induced nephropathy, and ophthalmology (retinitis pigmentosa).
N-acetylcysteine in the treatment of psychiatric disorders: current status and future prospects
N-acetylcysteine (NAC) is widely known for its role as a mucolytic and as an antidote to paracetamol overdose. There is increasing interest in the use of NAC in the treatment of several psychiatric disorders. The rationale for the administration of NAC in psychiatric conditions is based on its role as a precursor to the antioxidant glutathione, and its action as a modulating agent of glutamatergic, dopaminergic, neurotropic and inflammatory pathways. Areas covered: This study reviews the available data regarding the use of NAC in different psychiatric disorders including substance use disorders, autism, obsessive-compulsive spectrum disorders, schizophrenia, depression, bipolar disorder. Promising results were found in trials testing the use of NAC, mainly as an add-on treatment, in cannabis use disorder in young people, depression in bipolar disorder, negative symptoms in schizophrenia, and excoriation (skin-picking) disorder. Despite initial optimism, recent findings regarding NAC efficacy in autism have been disappointing. Expert opinion: These preliminary positive results require further confirmation in larger samples and with longer follow-ups. Given its high tolerability and wide availability, NAC represents an important target to investigate in the field of new adjunctive treatments for psychiatric conditions.
N-Acetylcysteine for the Treatment of Psychiatric Disorders: A Review of Current Evidence
N-acetylcysteine, a sulphur-containing amino acid for the treatment of paracetamol overdose and chronic obstructive pulmonary disease, is a widely available off-the-shelf oral antioxidant supplement in many countries. With the potential to modulate several neurological pathways, including glutamate dysregulation, oxidative stress, and inflammation that can be beneficial to the brain functions, N-acetylcysteine is being explored as an adjunctive therapy for many psychiatric conditions. This narrative review synthesises and presents the current evidence from systematic reviews, meta-analyses, and latest clinical trials on N-acetylcysteine for addiction and substance abuse, schizophrenia, obsessive-compulsive and related disorders, and mood disorders. Good evidence exists to support the use of N-acetylcysteine as an adjunct treatment to reduce the total and negative symptoms of schizophrenia. N-acetylcysteine also appears to be effective in reducing craving in substance use disorders, especially for the treatment of cocaine and cannabis use among young people, in addition to preventing relapse in already abstinent individuals. Effects of N-acetylcysteine on obsessive-compulsive and related disorders, as well as on mood disorders, remain unclear with mixed reviews, even though promising evidence does exist. Larger and better-designed studies are required to further investigate the clinical effectiveness of N-acetylcysteine in these areas. Oral N-acetylcysteine is safe and well tolerated without any considerable adverse effects. Current evidence supports its use as an adjunctive therapy clinically for psychiatric conditions, administered concomitantly with existing medications, with a recommended dosage between 2000 and 2400 mg/day.
Average Rating: 5 (Based on Reviews and 26 reference(s) in Google Scholar.)
GLPBIO products are for RESEARCH USE ONLY. Please make sure your review or question is research based.
Required fields are marked with *