Acetylcysteine


CAS No. : 616-91-1

(Synonyms: N-Acetylcysteine; N-Acetyl-L-cysteine; NAC)

616-91-1
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Cat. No. : HY-B0215
M.Wt: 163.20
Formula: C5H9NO3S
Purity: >98 %
Solubility: H2O : 100 mg/mL (ultrasonic);DMSO : 100 mg/mL (ultrasonic)
Introduction of 616-91-1 :

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[1][2][3][4][5][6][7][8]. IC50 & Target:IC50: ROS; ferroptosis; apoptosis In Vitro:Acetylcysteine prevents apoptotic DNA fragmentation and maintains long-term survival in the absence of other trophic support in serum-deprived PC12 cells. Acetylcysteine also prevents death of PC12 cells and sympathetic neurons[2].
Acetylcysteine causes dose-dependent reductions in viability in rat and human aortic smooth muscle cells[3].
Acetylcysteine activates the Ras-extracellular signal-regulated kinase (ERK) pathway in PC12 cells. Acetylcysteine protects neuronal cells from death evoked by withdrawal of trophic support. Acetylcysteine increases nitric oxide (NO) release from protein-bound stores in vascular tissue. Acetylcysteine pretreatment of PC12 cells interferes with NGF-dependent signaling and neurite outgrowth, and it is suggested that Acetylcysteine interferes with redox-sensitive steps in the NGF mechanism[4].
In Vivo:Acetylcysteine (150, 300 mg/kg) treatment significantly reduces liver transaminases in all groups of treatment, mostly in group Acetylcysteine 300 mg/kg. Lung glutathione peroxidase is significantly increases in group Acetylcysteine 300 mg/kg(P=0.04), while the other oxidation biomarkers show no significant differences[6].
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].

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