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Purity: >99.00%

实验参考方法

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.

产品描述

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.

乙酰半胱氨酸是半胱氨酸的 N-乙酰基衍生物。 NAC（N-乙酰基-L-半胱氨酸）通常用于识别和测试 ROS（活性氧）诱导剂，并抑制 ROS。乙酰半胱氨酸（N-乙酰半胱氨酸）是一种粘液溶解剂，可降低粘液的厚度^[1]。由于活性氧中间体抑制病毒刺激，它还被证明对 HIV 患者具有抗病毒作用。乙酰半胱氨酸还具有抗流感病毒活性^[5]。

毫摩尔浓度的乙酰半胱氨酸显着增强硝酸甘油对 ADP、肾上腺素、胶原蛋白和花生四烯酸诱导的血小板聚集的抑制作用, 将这些药物中的每一种的 50% 抑制浓度 (IC50) 降低约 50 倍。在没有乙酰半胱氨酸的情况下，硝酸甘油会导致血小板还原谷胱甘肽含量显着降低，因为会产生 S-亚硝基-硫醇加合物。合成的 S-亚硝基硫醇，S-亚硝基-N-乙酰半胱氨酸显着抑制血小板聚集，IC50 为 6 nM^[7]。乙酰半胱氨酸在 15 分钟后增加 PC12 细胞中的 ERK-1 活性治疗和最大刺激活动 60 分钟。我们还观察到乙酰半胱氨酸在用该化合物处理 30 分钟的细胞中引起 ERK-1 的酪氨酸磷酸化^[4]。乙酰半胱氨酸诱导细胞凋亡。当使用剥夺血清的 PC12 细胞、剥夺血清和 NGF 的神经元分化 PC12 细胞以及剥夺 NGF 的新生儿交感神经元时。在每种情况下，L-乙酰半胱氨酸都可以防止凋亡的 DNA 片段化，并在没有其他营养支持的情况下维持长期存活^[3]。乙酰半胱氨酸通过中和花生四烯酸依赖性活动产生的有毒脂质来防止血红素诱导的铁死亡5-脂氧合酶^[2]。

在小鼠中，乙酰半胱氨酸在 IIR 后的肝损伤中发挥重要的保护作用，这似乎与肠道保护作用无关。再灌注前额外给予乙酰半胱氨酸没有进一步的益处。比较方案中最有效的方案是缺血前300 mg/kg^[6]。

Chemical Properties

Cas No.	616-91-1	SDF
别名	乙酰半胱氨酸; N-Acetylcysteine; N-Acetyl-L-cysteine; NAC
化学名	(2R)-2-acetamido-3-sulfanylpropanoic acid
Canonical SMILES	CC(=O)NC(CS)C(=O)O
分子式	C₅H₉NO₃S	分子量	163.19
溶解度	DMF: 50 mg/mL,DMSO: 50 mg/mL,Ethanol: 50 mg/mL,PBS (pH 7.2): 30 mg/mL	储存条件	4°C, protect from light
General tips	请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。储备液的保存方式和期限：-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。为了提高溶解度，请将管子加热至37℃，然后在超声波浴中震荡一段时间。
Shipping Condition	评估样品解决方案：配备蓝冰进行发货。所有其他可用尺寸：配备RT，或根据请求配备蓝冰。

溶解性数据

制备储备液
		1 mg	5 mg	10 mg
	1 mM	6.1278 mL	30.6391 mL	61.2783 mL
	5 mM	1.2256 mL	6.1278 mL	12.2557 mL
	10 mM	0.6128 mL	3.0639 mL	6.1278 mL

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DMSO母液配制方法： mg 药物溶于 μL DMSO溶液（母液浓度 mg/mL，注：如该浓度超过该批次药物DMSO溶解度，请先联系GLPBIO）；

体内配方配制方法：取 μL DMSO母液，加入 μL PEG300，混匀澄清后加入μL Tween 80，混匀澄清后加入 μL saline，混匀澄清。

注意：1. 首先保证母液是澄清的；
2. 一定要按照顺序依次将溶剂加入，进行下一步操作之前必须保证上一步操作得到的是澄清的溶液，可采用涡旋、超声或水浴加热等物理方法助溶。
3. 以上所有助溶剂都可在 GlpBio 网站选购。

Research Update

Clinical trials of N-acetylcysteine in psychiatry and neurology: A systematic review

Neurosci Biobehav Rev2015 Aug;55:294-321.PMID: 25957927DOI: 10.1016/j.neubiorev.2015.04.015

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

Molecules2018 Dec 13;23(12):3305.PMID: 30551603DOI: 10.3390/molecules23123305

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.

N-acetylcysteine as a new prominent approach for treating psychiatric disorders

Br J Pharmacol2021 Jul;178(13):2569-2594.PMID: 33760228DOI: 10.1111/bph.15456

N-acetylcysteine (NAC) is a well-known and safe mucolytic agent, also used in patients with paracetamol overdose. In addition to these effects, recent preclinical and clinical studies have shown that NAC exerts beneficial effects on different psychiatric disorders. Many potential mechanisms have been proposed to underlie the therapeutic effects of NAC, including the regulation of several neurotransmitters, oxidative homeostasis, and inflammatory mediators. In this paper, we summarize the current knowledge on the ability of NAC to ameliorate symptoms and neuropathologies related to different psychiatric disorders, including attention deficit hyperactivity disorder, anxiety, bipolar disorder, depression, obsessive-compulsive disorder, obsessive-compulsive-related disorder, posttraumatic stress disorder, and schizophrenia. Although preclinical studies have shown a positive effect of NAC on animal models of psychiatric disorders, the clinical efficacy of NAC is not fully established. NAC remains a strong candidate for adjunct treatment for many psychiatric disorders, but additional preclinical and clinical studies are needed.

The chemistry and biological activities of N-acetylcysteine

Biochim Biophys Acta2013 Aug;1830(8):4117-29.PMID: 23618697DOI: 10.1016/j.bbagen.2013.04.016

Background: N-acetylcysteine (NAC) has been in clinical practice for several decades. It has been used as a mucolytic agent and for the treatment of numerous disorders including paracetamol intoxication, doxorubicin cardiotoxicity, ischemia-reperfusion cardiac injury, acute respiratory distress syndrome, bronchitis, chemotherapy-induced toxicity, HIV/AIDS, heavy metal toxicity and psychiatric disorders.
Scope of review: The mechanisms underlying the therapeutic and clinical applications of NAC are complex and still unclear. The present review is focused on the chemistry of NAC and its interactions and functions at the organ, tissue and cellular levels in an attempt to bridge the gap between its recognized biological activities and chemistry.
Major conclusions: The antioxidative activity of NAC as of other thiols can be attributed to its fast reactions with OH, NO2, CO3(-) and thiyl radicals as well as to restitution of impaired targets in vital cellular components. NAC reacts relatively slowly with superoxide, hydrogen-peroxide and peroxynitrite, which cast some doubt on the importance of these reactions under physiological conditions. The uniqueness of NAC is most probably due to efficient reduction of disulfide bonds in proteins thus altering their structures and disrupting their ligand bonding, competition with larger reducing molecules in sterically less accessible spaces, and serving as a precursor of cysteine for GSH synthesis.
General significance: The outlined reactions only partially explain the diverse biological effects of NAC, and further studies are required for determining its ability to cross the cell membrane and the blood-brain barrier as well as elucidating its reactions with components of cell signaling pathways.

N-Acetylcysteine for the Treatment of Psychiatric Disorders: A Review of Current Evidence

Biomed Res Int2018 Oct 22;2018:2469486.PMID: 30426004DOI: 10.1155/2018/2469486

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.

Acetylcysteine

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