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Description: 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. [PubChem]
Drug Type: Small Molecule; Approved
Pharmacology: Acetylcysteine has been shown to reduce the extent of liver injury following acetaminophen overdose. It is most effective when given early, with benefit seen principally in patients treated within 8-10 hours of the overdose. Acetylcysteine likely protects the liver by maintaining or restoring the glutathione levels, or by acting as an alternate substrate for conjugation with, and thus detoxification of, the reactive metabolite.
Mechanism of Action: Acetylcysteine may protect against acetaminophen overdose-induced hepatotoxicity by maintaining or restoring hepatic concentrations of glutathione. Glutathione is required to inactivate an intermediate metabolite of acetaminophen that is thought to be hepatotoxic. In acetaminophen overdose, excessive quantities of this metabolite are formed because the primary metabolic (glucuronide and sulfate conjugation) pathways become saturated. Acetylcysteine may act by reducing the metabolite to the parent compound and/or by providing sulfhydryl for conjugation of the metabolite. Experimental evidence also suggests that a sulfhydryl-containing compound such as acetylcysteine may also directly inactivate the metabolite. Inhalation - Acetylcysteine exerts its mucolytic action through its free sulfhydryl group, which opens the disulfide bonds and lowers mucus viscosity. This action increases with increasing pH and is most significant at pH 7 to 9. The mucolytic action of acetylcysteine is not affected by the presence of DNA.
Indication: Used mainly as a mucolytic and in the management of paracetamol (acetaminophen) overdose.
Half Life: 5.6 hours (adults), 11 hours (neonates)
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Data Correlations | 8 studies

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Genes category icon Genes
Score Help
RFX3 100 100
SLK 96 96
TRAF1 94 94
SERPINB6 91 91
USP48 89 89
CSPG5 89 89
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Biogroups category icon Biogroups
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Activation of cAMP-dependent Protei… 100 100
Regulation of Spermatogenesis by CR… 99 99
Notch Signaling Pathway 98 98
Oxidative Phosphorylation 98 98
Ubiquitin Mediated Proteolysis 97 97
Glyoxylate and Dicarboxylate Metabo… 97 97
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Individual Studies

  • β-adrenergic agonist isoproterenol-induced tachycardia and myocardial necrosis

    Rattus norvegicus Rattus norvegicus | RNA Expression   RNA Expression

    Gene expression was evaluated in the myocardium of male Wistar rats after a single sc administration of 0.5 mg of isoproterenol, a β-adrenergic agonist that causes acute tachycardia with subsequent myocardial necrosis.

    Authors: Mikaelian I, Kanwal C

    Organization: Hoffman-La Roche RIGG 340 Kingsland Stre…

  • RAW 264.7 cells treated with LPS, ISO, PGE2, LPS+ISO and LPS+PGE2

    Mus musculus Mus musculus | RNA Expression   RNA Expression

    Characterization of modulation of TLR ligands by non-TLR ligands using murine RAW 264.7 cells by treating with with LPS, IFN-gamma, 2-methyl-thio-ATP (2MA), PGE(2), and isoproterenol (ISO).

    Authors: Zhu Xiaocui, Chang MiSook, Hsueh Robert et al.

    Organization: California Institute of Technology Biolo…
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Associated Researchers

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Thought leaders and organizations working on research involving n-acetylcysteine.

View All Author iconAuthors
  • Peter W Kalivas
  • Haoqian Chen
  • M Foster Olive
  • Martin Posch
  • F Bendtsen
View All Clinical trial sponsors icon Clinical Trials Sponsors
  • Yale University
  • National Institute on Drug Abuse (NIDA)
  • Medical University of South Carolina
  • National Institute of Diabetes and Digestive and Kidney Diseases (NIDD…
  • Minneapolis Veterans Affairs Medical Center
View All Affiliations icon Organizations
  • Medical University of South Carolina
  • Baylor College of Medicine
  • Panjab University
  • University of Texas Southwestern Medical Center
  • Ewha Womans University 911-1 Mok-6-dong

Clinical Trials | 166 trials

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