Home Apoptosis TNF-alpha inhibitor - ROS inhibitor - NF-κB inhibitor - Apoptosis related activator - Ferroptosis inhibitor - Antiviral inhibitor Acetylcysteine (N-Acetylcysteine, NAC)

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Acetylcysteine (N-Acetylcysteine, NAC) ROS inhibitor

Cat.No.S1623

Acetylcysteine (N-acetyl-l-cysteine, NAC, N-acetylcysteine) is a ROS(reactive oxygen species) inhibitor that antagonizes the activity of proteasome inhibitors. It is also a tumor necrosis factor production inhibitor, suppresses TNF-induced NF-κB activation through inhibition of IκB kinases, induces apoptosis via the mitochondria-dependent pathway, and inhibits ferroptosis and virus replication.Solutions are unstable and should be fresh-prepared.
Acetylcysteine (N-Acetylcysteine, NAC) TNF-alpha inhibitor Chemical Structure

Chemical Structure

Molecular Weight: 163.19

Jump to Mechanism of Action Cell Culture & Working Concentration Solubility Chemical Information, Storage & Stability Specificity

Quality Control

Cell Culture, Treatment & Working Concentration

Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID
HUVEC cells Function assay 10μM 2h HUVECs were pretreated with 10 μM NAC for 2 hours, and then treated with 0.5 μM PCB 118. presentce of NAC for 48 hours. 28592194
HUVEC cells Function assay 2μM,4μM,8μM 90min HUVECs that were exposed with serum of P. falciparum and treated with NAC 2 µM，4 µM，8 µM. Supernatant from culture and lysed cells culture were measured for H2O2, GSH and MDA levels. 21602763
BL21 (DE3) Function assay 30 mins Inhibition of hexahistidine-tagged IMP-7 (unknown origin) expressed in Escherichia coli BL21 (DE3) cells using fluorocillin as substrate incubated for 30 mins by TECAN fluorescent plate reader analysis, IC50 = 20.7 μM. 25815530
PC12 Cytotoxicity assay 24 hrs Inhibition of 6-hydroxydopamine induced cytotoxicity in rat PC12 cells pretreated for 24 hrs assessed as elevation of intracellular glutathione level 17158454
PC12 Cytotoxicity assay 24 hrs Inhibition of hydrogen peroxide induced cytotoxicity in rat PC12 cells pretreated for 24 hrs assessed as elevation of intracellular glutathione level 17158454
NHBE Cytotoxicity assay 1 mM 18 hrs Cytoprotective activity in NHBE cells assessed as inhibition of tBHP-induced GSH depletion at 1 mM preincubated for 18 hrs followed by tBHP addition for 4 hrs by thiostar dye based fluorescence assay 27031670
HUVEC Antioxidant assay 5 mmol/L 4 hrs Antioxidant activity against H2O2-induced lipid accumulation in HUVEC cells assessed as reduction in MDA level at 5 mmol/L incubated 4 hrs prior to H2O2 challenge measured after 12 hrs 22841280
HUVEC Antioxidant assay 5 mmol/L 4 hrs Antioxidant activity in HUVEC cells assessed as reduction in H2O2-induced GSH activity at 5 mmol/L incubated 4 hrs prior to H2O2 challenge measured after 12 hrs 22841280
HUVEC Cytotoxicity assay 5 mmol/L 4 hrs Inhibition of H2O2-induced cytotoxicity in HUVEC cells assessed as cell viability at 5 mmol/L incubated 4 hrs prior to H2O2 challenge measured after 12 hrs by MTT assay 22841280
HUVEC Cytotoxicity assay 5 mmol/L 4 hrs Inhibition of H2O2-induced cytotoxicity in HUVEC cells assessed as LDH release at 5 mmol/L incubated 4 hrs prior to H2O2 challenge measured after 12 hrs by LDH assay 22841280
SH-SY5Y Neuroprotective assay 5 mM 4 hrs Neuroprotective activity in H2O2-stimulated human SH-SY5Y cells assessed as upregulation of Bax expression at 5 mM incubated for 4 hrs prior to H2O2 challenge measured after 12 hrs by Western blotting analysis 23403085
SH-SY5Y Neuroprotective assay 5 mM 4 hrs Neuroprotective activity in H2O2-stimulated human SH-SY5Y cells assessed as downregulation of Bcl2 expression at 5 mM incubated for 4 hrs prior to H2O2 challenge measured after 12 hrs by Western blotting analysis 23403085
HT22 Neuroprotective assay 5 mM 24 hrs Neuroprotective activity against glutamate-induced cell death in mouse HT22 cells assessed as increase in cell viability at 5 mM after 24 hrs by MTT assay 29122481
HT22 Neuroprotective assay 50 uM 10 to 12 hrs Neuroprotective activity against glutamate-induced cell death in mouse HT22 cells assessed as reduction in apoptotic cells at 50 uM after 10 to 12 hrs by Annexin V-alexa 488/propidium iodide staining based flow cytometry 29122481
HL-7702 Hepatoprotective assay 10 uM 24 hrs Hepatoprotective activity against APAP-induced cell injury in human HL-7702 cells assessed as increase in survival rate at 10 uM pre-incubated for 24 hrs before APAP addition and measured 6 hrs post APAP challenge by MTT assay 28729056
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Chemical Information, Storage & Stability

Molecular Weight 163.19 Formula

C5H9NO3S

 Storage (From the date of receipt) 3 years -20°C powder
CAS No. 616-91-1 Download SDF Storage of Stock Solutions Solutions are unstable. Prepare fresh or purchase small, pre-packaged sizes. Repackage upon receipt.
Synonyms N-acetylcysteine Smiles CC(=O)NC(CS)C(=O)O

Solubility

In vitro
Batch:

DMSO : 33 mg/mL (202.21 mM)
(Moisture-contaminated DMSO may reduce solubility. Use fresh, anhydrous DMSO.)

Water : 33 mg/mL

Ethanol : 33 mg/mL

Molarity Calculator

Mass Concentration Volume Molecular Weight

In vivo
Batch:

In vivo Formulation Calculator (Clear solution)

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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 ddH2O, 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.

Mechanism of Action

Targets/IC50/Ki
NF-κB [8]
Ferroptosis [9]
ROS [6]
TNF-α [7]
In vitro

Acetylcysteine (N-Acetylcysteine, NAC) inhibits activation of c-Jun N-terminal kinase, p38 MAP kinase and redox-sensitive activating protein-1 and nuclear factor kappa B transcription factor activities regulating expression of numerous genes. It can also prevent apoptosis and promote cell survival by activating extracellular signal-regulated kinase pathway, a concept useful for treating certain degenerative diseases. This compound directly modifies the activity of several proteins by its reducing activity. [1]

It prevents apoptotic DNA fragmentation and maintains long-term survival in the absence of other trophic support in serum-deprived PC12 cells. It also prevents death of PC12 cells and sympathetic neurons. [2]

It causes dose-dependent reductions in viability in rat and human aortic smooth muscle cells. [3]

It activates the Ras-extracellular signal-regulated kinase (ERK) pathway in PC12 cells. This compound protects neuronal cells from death evoked by withdrawal of trophic support. It increases nitric oxide (NO) release from protein-bound stores in vascular tissue. Its pretreatment of PC12 cells interferes with NGF-dependent signaling and neurite outgrowth, and it was suggested that NAC interferes with redox-sensitive steps in the NGF mechanism. [4]
In vivo

In both the T-maze footshock avoidance paradigm and the lever press appetitive task, N-acetylcysteine (NAC) improves cognition of 12-month-old SAMP8 mice without inducing non-specific effects on motor activity, motivation to avoid shock, or body weight. [5]
References
  • [4] https://pubmed.ncbi.nlm.nih.gov/9592085/
  • [5] https://pubmed.ncbi.nlm.nih.gov/12603840/
  • [6] https://pubmed.ncbi.nlm.nih.gov/23772801/
  • [7] https://pubmed.ncbi.nlm.nih.gov/1544168/
  • [8] https://pubmed.ncbi.nlm.nih.gov/29426002/
  • [9] https://pubmed.ncbi.nlm.nih.gov/30294906/
  • [10] https://pubmed.ncbi.nlm.nih.gov/35023619/

Clinical Trial Information

(data from https://clinicaltrials.gov, updated on 2024-05-22)

NCT Number Recruitment Conditions Sponsor/Collaborators Start Date Phases
NCT04520139 Not yet recruiting
Ovarian Cancer|Cognitive Impairment
University of California Irvine|Jarrow Formulas Inc
 December 2024 Phase 1|Phase 2
NCT06112834 Not yet recruiting
Botulism
California Department of Public Health
 June 2024 Phase 2
NCT06260566 Not yet recruiting
Biliary Atresia
Sanjiv Harpavat|Baylor College of Medicine
 May 2024 Phase 1
NCT06377410 Not yet recruiting
Chronic Obstructive Pulmonary Disease
National University of Malaysia
 May 1 2024 Not Applicable
NCT06223568 Not yet recruiting
Squamous Cell Carcinoma of the Head and Neck|Oropharynx|Human Papillomavirus Viruses|Drug Therapy|Cancer Vaccine
National Cancer Institute (NCI)|National Institutes of Health Clinical Center (CC)
 May 15 2024 Phase 2

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