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Acetylcysteine

Catalog No. T0875 CAS 616-91-1

Synonyms: NAC, LNAC, N-Acetyl-L-cysteine

Acetylcysteine is the N-acetyl derivative of CYSTEINE. It is used as a mucolytic agent to reduce the viscosity of mucous secretions. It has also been shown to have antiviral effects in patients with HIV due to inhibition of viral stimulation by reactive oxygen intermediates.

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Acetylcysteine, CAS 616-91-1

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5 g	In stock	$ 33.00
10 g	In stock	$ 42.00

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Purity: 99.94%

Purity: 99.69%

Purity: 99.34%

Purity: 98.98%

Biological Description

Chemical Properties

Storage & Solubility Information

Description	Acetylcysteine is the N-acetyl derivative of CYSTEINE. It is used as a mucolytic agent to reduce the viscosity of mucous secretions. It has also been shown to have antiviral effects in patients with HIV due to inhibition of viral stimulation by reactive oxygen intermediates.
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 the death of PC12 cells and sympathetic neurons[2]. N-acetylcysteine activates the Ras-extracellular signal-regulated kinase (ERK) pathway in PC12 cells. N-acetylcysteine protects neuronal cells from death evoked by the 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[3].
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 increased in group N-acetylcysteine 300 (P=0.04), while the other oxidation biomarkers show no significant differences[1].
Cell Research	For survival experiments, washed cells are resuspended in RPM1 1640 medium and plated in 0.5 mL at a density of 8-10×105 per well in 24 well plastic culture dishes coated with rat tail collagen. To feed, but to avoid loss of floating cells, fresh medium (0.2 mL) is added to the cultures on days 1, 5, and 10. For experiments involving "primed" PC12 cells, cultures are pretreated for l-2 weeks with NGF in RPM1 1640 medium supplemented with 1% heat-iN-acetylcysteinetivated horse serum. The cells are then washed and passaged into serum-free RPM1 1640 medium.
Animal Research	Rats are randomly allocated into five groups: sham group (n=5), control group with IIR (n=8) and three groups with IIR who are given N-acetylcysteine in different dosages: 150 mg/kg intraperitoneally 5 min before ischemia (n=8, group N-acetylcysteine 150), 300 mg/kg i.p 5 min before ischemia (n=7, group N-acetylcysteine 300), and 150 mg/kg i.p 5 min before ischemia plus 150 mg/kg 5 min before reperfusion (n=7, group N-acetylcysteine 150 + 150). After 4 h of reperfusion, the animals are euthanized by exsanguination from the abdominal aorta.[1]

Synonyms	NAC, LNAC, N-Acetyl-L-cysteine
Molecular Weight	163.19
Formula	C5H9NO3S
CAS No.	616-91-1

Storage

Powder: -20°C for 3 years | In solvent: -80°C for 2 years

Solubility Information

DMSO: 31 mg/mL (190 mM)

Ethanol: 31 mg/mL (190 mM)

H2O: 30 mg/mL (183.8 mM)

( < 1 mg/ml refers to the product slightly soluble or insoluble )

References and Literature

1. Alvirez-Freites EJ, et al. Antimicrob Agents Chemother, 2002, 46(4), 1022-1025. 2. Ferrari G, et al. N-acetylcysteine (D- and L-stereoisomers) prevents apoptotic death of neuronal cells. J Neurosci. 1995 Apr;15(4):2857-66. 3. Tsai JC, et al. J Biol Chem, 1996, 271(7), 3667-3670. 4. Yan CY, et al. Prevention of PC12 cell death by N-acetylcysteine requires activation of the Ras pathway. J Neurosci. 1998 Jun 1;18(11):4042-9. 5. Farr SA, et al. J Neurochem, 2003, 84(5), 1173-1183. 6. Kalimeris K, et al. N-acetylcysteine ameliorates liver injury in a rat model of intestinal ischemia reperfusion. J Surg Res. 2016 Dec;206(2):263-272. 7. Xu B, Xu J, Cai N, et al. Roflumilast prevents ischemic stroke-induced neuronal damage by restricting GSK3β-mediated oxidative stress and IRE1α/TRAF2/JNK pathway[J]. Free Radical Biology and Medicine. 2020 8. Xu B, Qin Y, Li D, et al. Inhibition of PDE4 protects neurons against oxygen-glucose deprivation-induced endoplasmic reticulum stress through activation of the Nrf-2/HO-1 pathway[J]. Redox Biology. 2020, 28: 101342.

Citations

1. Tang Y, Song H, Wang Z, et al.Repurposing antiparasitic antimonials to noncovalently rescue temperature-sensitive p53 mutations.Cell Reports.2022, 39(2): 110622. 2. Chen T, Leng J, Tan J, et al.Discovery of Novel Potent Covalent Glutathione Peroxidase 4 Inhibitors as Highly Selective Ferroptosis Inducers for the Treatment of Triple-Negative Breast Cancer.Journal of Medicinal Chemistry.2023 3. Liu X, Jin J, Wu Y, et al.Fluoroindole chalcone analogues targeting the colchicine binding site of tubulin for colorectal oncotherapy.European Journal of Medicinal Chemistry.2023: 115540. 4. Li Y, Bao Y, Li Y, et al.RSL3 Inhibits Porcine Epidemic Diarrhea Virus Replication by Activating Ferroptosis.Viruses.2023, 15(10): 2080. 5. Liu X, Sun W, Cao J, et al.Acrolein increases the concentration of intracellular Zn2⁺ by producing mitochondrial reactive oxygen species in A549 cells.Toxicology and Industrial Health.2023: 07482337231198350. 6. Zhu M, Tang X, Gong Z, et al. TAD1822-7 induces ROS-mediated apoptosis of HER2 positive breast cancer by decreasing E-cadherin in an EphB4 dependent manner. Life Sciences. 2021: 119954 7. Xu B, Qin Y, Li D, et al. Inhibition of PDE4 protects neurons against oxygen-glucose deprivation-induced endoplasmic reticulum stress through activation of the Nrf-2/HO-1 pathway. Redox Biology. 2020, 28: 101342 8. Xu B, Xu J, Cai N, et al. Roflumilast prevents ischemic stroke-induced neuronal damage by restricting GSK3β-mediated oxidative stress and IRE1α/TRAF2/JNK pathway. Free Radical Biology and Medicine. 2020 9. Xue J, Liao Q, Luo M, et al. Cigarette smoke-induced oxidative stress activates NRF2 to mediate fibronectin disorganization in vascular formation. Open Biology. 2022, 12(4): 210310 10. Yi Y, Gao K, Lin P, et al. Staphylococcus aureus-Induced Necroptosis Promotes Mitochondrial Damage in Goat Endometrial Epithelial Cells. Animals. 2022, 12(17): 2218.

Related compound libraries

This product is contained In the following compound libraries：

Human Endogenous Metabolite Library NMPA-Approved Drug Library Anti-Infection Compound Library Anti-Viral Compound Library Kinase Inhibitor Library Anti-Breast Cancer Compound Library Metabolism Compound Library Oxidation-Reduction Compound Library NF-κB Signaling Compound Library NO PAINS Compound Library

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Keywords

Acetylcysteine 616-91-1 Apoptosis Immunology/Inflammation Metabolism Microbiology/Virology NF-Κb Ferroptosis TNF Endogenous Metabolite Influenza Virus Reactive Oxygen Species ROS NAC LNAC Inhibitor inhibit N-Acetylcysteine N-Acetyl-L-cysteine inhibitor

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