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N-Acetylcysteine

(別名: NAC L; NAC; N-アセチル-L-システイン; アセチルシステイン; LNAC)
666 Cited Publications
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Based on 666 publication(s) in Google Scholar

Acetylcysteine (N-Acetylcysteine) is a mucolytic agent that can cross the blood-brain barrier, which reduces the thickness of the mucus. Acetylcysteine is a ROS inhibitor. Acetylcysteine is a cysteine precursor, prevents hemin-induced ferroptosis by neutralizing toxic lipids generated by arachidonate-dependent activity of 5-lipoxygenases. Acetylcysteine induces cell apoptosis. Acetylcysteine also has anti-influenza virus activities. In addition, Acetylcysteine ​​is the most stable form of cysteine ​​during drug delivery and can be used in disulfidptosis studies.

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  • 純度: 99.86%
  • CAS 番号: 616-91-1
  • 分子式: C5H9NO3S
  • 分子量:163.20
  • 保管条件:

    4°C, protect from light

    * In solvent : -80°C, 6 months; -20°C, 1 month (protect from light)

  • Acetylcysteine Chemical Structure
  • Experimental Validation Results for Acetylcysteine
  • Experimental Validation Results for Acetylcysteine
  • Experimental Validation Results for Acetylcysteine
  • Experimental Validation Results for Acetylcysteine
  • Experimental Validation Results for Acetylcysteine
  • Experimental Validation Results for Acetylcysteine
  • Experimental Validation Results for Acetylcysteine
  • Experimental Validation Results for Acetylcysteine
  • Experimental Validation Results for Acetylcysteine
  • Acetylcysteine Chemical Structure
    Acetylcysteine 構造式
  • Experimental Validation Results for Acetylcysteine
  • Experimental Validation Results for Acetylcysteine
  • Experimental Validation Results for Acetylcysteine
  • Experimental Validation Results for Acetylcysteine
  • Experimental Validation Results for Acetylcysteine
  • Experimental Validation Results for Acetylcysteine
  • Experimental Validation Results for Acetylcysteine
  • Experimental Validation Results for Acetylcysteine
  • Experimental Validation Results for Acetylcysteine
CAS 番号: 616-91-1
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  • Acetylcysteine Chemical Structure
    Acetylcysteine Chemical Structure
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    Acetylcysteine purchased from MedChemExpress. Usage Cited in: Adv Sci (Weinh). 2025 Aug 7:e09208. [Abstract]

    Customer Validation
     Trolox (100 µM), a hydrophilic analogue of VE with potent antioxidant effect, was used as a control of VE. After a short incubation time of 6 h, cathepsin inhibitors (CA‐074, Pep‐A, and E‐64), Ca2+ chelator, and cellular ROS scavengers (NAC, VC, and Trolox) displayed a delayed effect of ipLNP cytotoxicity.

  • 1/16

    Acetylcysteine purchased from MedChemExpress. Usage Cited in: Sci Bull. 2024 Dec 15;69(23):3700-3716. [Abstract]

    Customer Validation
     Summary of cell viability measured for MCD-induced wild-type hepatocytes, hepatocytes treated with 2 mmol/L fatty acid (FA) for 24 h with the indicated concentrations of PAG together with 2 mmol/L N-acetylcysteine (NAC) or 5 μmol/L Fer-1.

  • 1/16

    Acetylcysteine purchased from MedChemExpress. Usage Cited in: Microb Pathog. 2024 Dec:197:107046. [Abstract]

    Customer Validation
     BMDMs pretreated with degarelix (1 μM), aminoguanidine hydrochloride (AGHS, 100 μM), BafA1 (100 nM), NAC (5 mM), Z-VAD (20 μM), or 3-MA (5 mM) were infected with H37Rv (MOI = 2). At different time points after infection, bacterial survival was calculated by dividing the CFU at 24 h by the CFU at 3 h.

  • 1/16

    Acetylcysteine purchased from MedChemExpress. Usage Cited in: Adv Funct Mater. 2023 May 14.

    Customer Validation
     The viability of MC38 cells treated with PAD@MS for 48 h in the presence or absence of 10 µM Ferr-1 (Ferrostatin-1), 20 µM Nec-1 (Necrostatin-1), 10 µM Z-VAD-FMK, and 1 mM N-Aetyl-L-cysteine (NAC).

  • 1/16

    Acetylcysteine purchased from MedChemExpress. Usage Cited in: Cell Death Discov. 2018 Apr 27:4:47. [Abstract]

    Customer Validation
     Wild-type, Prx1KO, and Prx1OE cells are each divided into three groups, which are control groups, groups treated with 100 ng/mL LPS, and groups treated with 100 ng/mL LPS and NAC. Western blot analysis is then performed with antibodies against Bax, Bcl-2, Cyto-c, caspase 3, and GAPDH, and band intensity is measured with densitometry.

  • 1/16

    Acetylcysteine purchased from MedChemExpress. Usage Cited in: Fundam Clin Pharmacol. 2017 Feb;31(1):64-74. [Abstract]

    Customer Validation
     Advanced oxidation production product (AOPP)-triggered apoptosis-related signals were triggered by ROS production. Human chondrocytes were pretreated with N-Acetylcysteine (NAC; 5 mM) for 60 min, and then, chondrocyte were co-incubated with AOPP and NAC for 24 h. Pretreatment of ROS scavenger NAC markedly alleviated AOPP-triggered mitochondria-mediated apoptosis proteins.

  • 1/16

    Acetylcysteine purchased from MedChemExpress. Usage Cited in: Fundam Clin Pharmacol. 2017 Feb;31(1):64-74. [Abstract]

    Customer Validation
     Effect of advanced oxidation production products (AOPPs) on ROS production in human chondrocyte. Human chondrocytes were treated with the indicated concentration of AOPPs (50–400 μg/mL) for 120 min, or 200 μg/mL of AOPPs for the 0–120 min. The intracellular ROS production was determined by measuring the fluorescence of DCFH. Inhibition experiments were carried out by pretreatment for 60 min with N-Acetylcysteine (NAC) (5 mM), and then, chondrocytes were co-incubated with AOPP and NAC for 24 h. Pretreatment of NAC suppressed AOPP-induced ROS production.

  • 1/16

    Acetylcysteine purchased from MedChemExpress. Usage Cited in: Fundam Clin Pharmacol. 2017 Feb;31(1):64-74. [Abstract]

    Customer Validation
     Advanced oxidation production product (AOPP)-triggered apoptosis-related signals were triggered by ROS production. Human chondrocytes were pretreated with N-Acetylcysteine (NAC; 5 mM) for 60 min, and then, chondrocyte were co-incubated with AOPP and NAC for 24 h. Pretreatment of chondrocyte with NAC abrogated the intracellular Ca2+ mobilization.

  • 1/16

    Acetylcysteine purchased from MedChemExpress. Usage Cited in: Sci Rep. 2016 Oct 27;6:35995. [Abstract]

    Customer Validation
     Pretreatment of NAC, a free radical scavenger, largely decreases the expression of caspase-3 and almost abolishes the H2O2 induced upregulation of PRX1. Western blot analysis shows the pretreatment of osteoblast cells with E2 partially abrogates the increased PRX1 and caspase-3 expressions induced by H2O2.

  • Acetylcysteine