AcetylcysteineAntioxidant;mucolytic agent CAS# 616-91-1 |
Quality Control & MSDS
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| Cas No. | 616-91-1 | SDF | Download SDF |
| PubChem ID | 12035 | Appearance | Powder |
| Formula | C5H9NO3S | M.Wt | 163.19 |
| Type of Compound | N/A | Storage | Desiccate at -20°C |
| Synonyms | N-Acetyl-L-cysteine; LNAC; NAC | ||
| Solubility | Soluble to 33 mg/mL (202.21 mM) in DMSO | ||
| Chemical Name | (2R)-2-acetamido-3-sulfanylpropanoic acid | ||
| SMILES | CC(=O)NC(CS)C(=O)O | ||
| Standard InChIKey | PWKSKIMOESPYIA-BYPYZUCNSA-N | ||
| Standard InChI | InChI=1S/C5H9NO3S/c1-3(7)6-4(2-10)5(8)9/h4,10H,2H2,1H3,(H,6,7)(H,8,9)/t4-/m0/s1 | ||
| 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. We recommend that you prepare and use the solution on the same day. However, if the test schedule requires, the stock solutions can be prepared in advance, and the stock solution must be sealed and stored below -20℃. In general, the stock solution can be kept for several months. Before use, we recommend that you leave the vial at room temperature for at least an hour before opening it. |
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| About Packaging | 1. The packaging of the product may be reversed during transportation, cause the high purity compounds to adhere to the neck or cap of the vial.Take the vail out of its packaging and shake gently until the compounds fall to the bottom of the vial. 2. For liquid products, please centrifuge at 500xg to gather the liquid to the bottom of the vial. 3. Try to avoid loss or contamination during the experiment. |
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| Shipping Condition | Packaging according to customer requirements(5mg, 10mg, 20mg and more). Ship via FedEx, DHL, UPS, EMS or other couriers with RT, or blue ice upon request. | ||
| Description | Acetylcysteine is used mainly as a mucolytic, which protects against acetaminophen overdose-induced hepatotoxicity by maintaining or restoring hepatic concentrations of glutathione.In Vitro:N-acetylcysteine prevents apoptotic DNA fragmentation and maintains long-term survival in the absence of other trophic support in serum-deprived PC12 cells. N-acetylcysteine also prevents death of PC12 cells and sympathetic neurons[2]. N-acetylcysteine causes dose-dependent reductions in viability in rat and human aortic smooth muscle cells[3]. N-acetylcysteine activates the Ras-extracellular signal-regulated kinase (ERK) pathway in PC12 cells. N-acetylcysteine protects neuronal cells from death evoked by withdrawal of trophic support. N-acetylcysteine increases nitric oxide (NO) release from protein-bound stores in vascular tissue. N-acetylcysteine pretreatment of PC12 cells interferes with NGF-dependent signaling and neurite outgrowth, and it is suggested that N-acetylcysteine interferes with redox-sensitive steps in the NGF mechanism[4].In Vivo:N-acetylcysteine (150, 300 mg/kg) treatment significantly reduces liver transaminases in all groups of treatment, mostly in group N-acetylcysteine 300. Lung glutathione peroxidase is significantly increases in group N-acetylcysteine 300 (P=0.04), while the other oxidation biomarkers show no significant differences[1]. N-acetylcysteine improves cognition of 12-month-old SAMP8 mice in both the T-maze footshock avoidance paradigm and the lever press appetitive task without inducing non-specific effects on motor activity, motivation to avoid shock, or body weight[5]. References: | |||||
Acetylcysteine Dilution Calculator
Acetylcysteine Molarity Calculator
| 1 mg | 5 mg | 10 mg | 20 mg | 25 mg | |
| 1 mM | 6.1278 mL | 30.6391 mL | 61.2783 mL | 122.5565 mL | 153.1957 mL |
| 5 mM | 1.2256 mL | 6.1278 mL | 12.2557 mL | 24.5113 mL | 30.6391 mL |
| 10 mM | 0.6128 mL | 3.0639 mL | 6.1278 mL | 12.2557 mL | 15.3196 mL |
| 50 mM | 0.1226 mL | 0.6128 mL | 1.2256 mL | 2.4511 mL | 3.0639 mL |
| 100 mM | 0.0613 mL | 0.3064 mL | 0.6128 mL | 1.2256 mL | 1.532 mL |
| * Note: If you are in the process of experiment, it's necessary to make the dilution ratios of the samples. The dilution data above is only for reference. Normally, it's can get a better solubility within lower of Concentrations. | |||||
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Acetylcysteine is a derivative of cysteine; an acetyl group that is attached to the nitrogen atom. This compound is sold as a dietary supplement commonly claiming antioxidant and liver protecting effects.
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Adjunctive N-acetylcysteine in depression: exploration of interleukin-6, C-reactive protein and brain-derived neurotrophic factor.[Pubmed:28318471]
Acta Neuropsychiatr. 2017 Dec;29(6):337-346.
OBJECTIVE: This study aimed to explore effects of adjunctive N-Acetylcysteine (NAC) treatment on inflammatory and neurogenesis markers in unipolar depression. METHODS: We embarked on a 12-week clinical trial of NAC (2000 mg/day compared with placebo) as an adjunctive treatment for unipolar depression. A follow-up visit was conducted 4 weeks following the completion of treatment. We collected serum samples at baseline and the end of the treatment phase (week 12) to determine changes in interleukin-6 (IL6), C-reactive protein (CRP) and brain-derived neurotrophic factor (BDNF) following NAC treatment. RESULTS: NAC treatment significantly improved depressive symptoms on the Montgomery-Asberg Depression Rating Scale (MADRS) over 16 weeks of the trial. Serum levels of IL6 were associated with reductions of MADRS scores independent of treatment response. However, we found no significant changes in IL6, CRP and BDNF levels following NAC treatment. CONCLUSION: Overall, this suggests that our results failed to support the hypothesis that IL6, CRP and BDNF are directly involved in the therapeutic mechanism of NAC in depression. IL6 may be a useful marker for future exploration of treatment response.
[A girl with self-harm treated with N-acetylcysteine (NAC)].[Pubmed:28350146]
Tijdschr Psychiatr. 2017;59(3):181-184.
Deliberate and recurrent self-harm could be regarded as addictive behaviour that can be treated with medication. In addiction, the dopaminergic mesolimbic reward system is activated. Pain caused by cutting stimulates the reward system through the opioid system. Glutamatergic neurotransmission follows the same pathway and plays a role in addiction as well. In this case-study a 17-year-old girl was successfully treated with N-Acetylcysteine (nac) in order to reduce the frequency of self-cutting. In addition, in this case nac reduced the symptoms of attention deficit/hyperactivity disorder and depression. nac modulates the glutamatergic neurotransmission. This article provides possible explanations for the effect of nac in this case.
Synergistic protective effect of N-acetylcysteine and taurine against cisplatin-induced nephrotoxicity in rats.[Pubmed:28356716]
Drug Des Devel Ther. 2017 Mar 20;11:901-908.
Cisplatin (cis-diaminedichloroplatinum II; CDDP) is an effective anticancer drug, but it has limitations because of its nephrotoxicity. This study investigates the protective effect of N-Acetylcysteine (NAC) and taurine (TAU), both individually and in combination, against CDDP nephrotoxicity in rats. For this purpose, 48 male rats were assigned into eight groups (n=6) as follows: 1) control group, 2) NAC group, 3) TAU group, 4) NAC-TAU group, 5) CDDP group, 6) CDDP-NAC group, 7) CDDP-TAU group, and 8) CDDP-NAC-TAU group. Cisplatin was administered as a single intraperitoneal injection at a concentration of 6 mg/kg. Three days after CDDP administration, NAC (50 mg/kg) and/or TAU (50 mg/kg) were administered three times weekly for four consecutive weeks. Kidney function markers in serum, urinary glucose and protein, as well as oxidant and antioxidant parameters in renal tissue were assessed. Administration of CDDP significantly elevated urinary glucose and protein, as well as serum creatinine, urea, and uric acid. Moreover, CDDP enhanced lipid peroxidation and suppressed the major enzymatic antioxidants in the kidney tissue. Treatment with NAC or TAU protected against the alterations in the serum, urine, and renal tissue when used individually along with CDDP. Furthermore, a combined therapy of both was more effective in ameliorating CDDP-induced nephrotoxicity, which points out to their synergistic effect.
N-Acetylcysteine Prevents Low T3 Syndrome and Attenuates Cardiac Dysfunction in a Male Rat Model of Myocardial Infarction.[Pubmed:28323971]
Endocrinology. 2017 May 1;158(5):1502-1510.
Nonthyroidal illness syndrome (NTIS) affects patients with myocardial infarction (MI). Oxidative stress has been implicated as a causative factor of NTIS, and reversed via N-Acetylcysteine (NAC). Male Wistar rats submitted to left anterior coronary artery occlusion received NAC or placebo. Decreases in triiodothyronine (T3) levels were noted in MI-placebo at 10 and 28 days post-MI, but not in MI-NAC. Groups exhibited similar infarct areas whereas MI-NAC exhibited higher ejection fraction than did MI-placebo. Left ventricular systolic and diastolic diameters were also preserved in MI-NAC, but not in MI-placebo. Ejection fraction was positively correlated with T3 levels. Oxidative balance was deranged only in MI-placebo animals. Increased type 3 iodothyronine deiodinase expression was detected in the cardiomyocytes of MI-placebo compared with normal heart tissue. NAC was shown to diminish type 3 iodothyronine deiodinase expression and activity in MI-NAC. These results show that restoring redox balance by NAC treatment prevents NTIS- related thyroid hormone derangement and preserves heart function in rats subjected to MI.
