Clinical data
Pronunciation /əˌsɛtəlˈsɪstn/
Trade names Acetadote, Fluimucil, Mucomyst, Parvolex
AHFS/ Monograph
License data
  • AU: B2
  • US: B (No risk in non-human studies)
Routes of
By mouth, injection, inhalation
ATC code R05CB01 (WHO) S01XA08 (WHO) V03AB23 (WHO)
Legal status
Legal status
  • AU: S2 (Pharmacy only)
  • US: OTC (by mouth), Rx-only (IV, inhalation)
Pharmacokinetic data
Bioavailability 10% (Oral)[1]
Protein binding 50 to 83%[2]
Metabolism Liver[2]
Biological half-life 5.6 hours[3]
Excretion Renal (30%),[2] faecal (3%)
CAS Number 616-91-1 YesY
PubChem (CID) 581
DrugBank DB06151 YesY
ChemSpider 561 N
KEGG D00221 YesY
ChEBI CHEBI:28939 YesY
Chemical and physical data
Formula C5H9NO3S
Molar mass 163.195
3D model (Jmol) Interactive image
Specific rotation +5 ° (c = 3% in water)[5]
Melting point 109 to 110 °C (228 to 230 °F) [5]
 NYesY (what is this?)  (verify)

Acetylcysteine, also known as N-acetylcysteine or N-acetyl-L-cysteine (NAC), is a medication used to treat paracetamol (acetaminophen) overdose and to loosen thick mucus such as in cystic fibrosis or chronic obstructive pulmonary disease.[2] It can be taken intravenously, by mouth, or inhaled as a mist.[2]

Common side effects include nausea and vomiting when taken by mouth. The skin may occasionally become red and itchy with either form. A non immune type of anaphylaxis may also occur. It appears to be safe in pregnancy. It works by increasing glutathione levels and binding with the toxic breakdown products of paracetamol.[2]

Acetylcysteine was initially patented in 1960 and licensed for use in 1968.[6] It is on the World Health Organization's List of Essential Medicines, the medications needed in a basic health system.[7] It is available as a generic medication and is not very expensive.[8]


Paracetamol overdose

Main article: Paracetamol poisoning

Intravenous and oral formulations of acetylcysteine are available for the treatment of paracetamol (acetaminophen) overdose.[9] When paracetamol is taken in large quantities, a minor metabolite called N-acetyl-p-benzoquinone imine (NAPQI) accumulates within the body. It is normally conjugated by glutathione, but when taken in excess, the body's glutathione reserves are not sufficient to inactivate the toxic NAPQI. This metabolite is then free to react with key hepatic enzymes, thereby damaging liver cells. This may lead to severe liver damage and even death by acute liver failure.

In the treatment of acetaminophen overdose, acetylcysteine acts to maintain or replenish depleted glutathione reserves in the liver and enhance non-toxic metabolism of acetaminophen.[10] These actions serve to protect liver cells from NAPQI toxicity. It is most effective in preventing or lessening hepatic injury when administered within 8–10 hours after overdose.[10] Research suggests that the rate of liver toxicity is approximately 3% when acetylcysteine is administered within 10 hours of overdose.[9]

Although both IV and oral acetylcysteine are equally effective for this indication, oral administration is poorly tolerated because high oral doses are required due to low oral bioavailability,[11] because of its very unpleasant taste and odour, and because of adverse effects, particularly nausea and vomiting. Prior pharmacokinetic studies of acetylcysteine did not consider acetylation as a reason for the low bioavailability of acetylcysteine.[12] Oral acetylcysteine is identical in bioavailability to cysteine precursors.[12] However, 3% to 6% of people given intravenous acetylcysteine show a severe, anaphylaxis-like allergic reaction, which may include extreme breathing difficulty (due to bronchospasm), a decrease in blood pressure, rash, angioedema, and sometimes also nausea and vomiting.[13] Repeated doses of intravenous acetylcysteine will cause these allergic reactions to progressively worsen in these people.

Several studies have found this anaphylaxis-like reaction to occur more often in people given IV acetylcysteine despite serum levels of paracetamol not high enough to be considered toxic.[14][15][16][17]

Mucolytic therapy

Inhaled acetylcysteine has been used for mucolytic ("mucus-dissolving") therapy in addition to other therapies in respiratory conditions with excessive and/or thick mucus production. It is also used post-operatively, as a diagnostic aid, and in tracheotomy care. It may be considered ineffective in cystic fibrosis.[18] A 2013 Cochrane review in cystic fibrosis found no evidence of benefit.[19]

Nephroprotective agent

Oral acetylcysteine is used for the prevention of radiocontrast-induced nephropathy (a form of acute kidney failure). Some studies show that prior administration of acetylcysteine decreases radiocontrast nephropathy,[20] whereas others do not.[21][22] It has been concluded that

  1. "Intravenous and oral N-acetylcysteine may prevent contrast-medium–induced nephropathy with a dose-dependent effect in patients treated with primary angioplasty and may improve hospital outcome."[23]
  2. "Acetylcysteine protects patients with moderate chronic renal insufficiency from contrast-induced deterioration in renal function after coronary angiographic procedures, with minimal adverse effects and at a low cost"[24]

A clinical trial from 2010, however, found that acetylcysteine is ineffective for the prevention of contrast-induced nephropathy. This trial, involving 2,308 patients, found that acetylcysteine was no better than a placebo; whether acetylcysteine or the placebo was used, the incidence of nephropathy was the same — 13%.[25]

Despite the conflicting research outcomes, the 2012 Kidney Disease: Improving Global Outcomes Guidelines suggest the use of oral acetylcysteine for the prevention of contrast-induced nephropathy in high-risk individuals, given its potential for benefit, low likelihood of adverse effects, and low cost.[26]

Hemorrhagic cystitis

Acetylcysteine has been used for cyclophosphamide-induced hemorrhagic cystitis, although mesna is generally preferred due to the ability of acetylcysteine to diminish the effectiveness of cyclophosphamide.[27][28]

Obstructive lung disease

Acetylcysteine is used in the treatment of obstructive lung disease as an adjuvant treatment.[29][30][31]


N-acetylcysteine has been successfully tried as a treatment for a number of psychiatric disorders.[32][33][34] A systematic review from 2015, and several earlier medical reviews, indicated that there is favorable evidence for N-acetylcysteine efficacy in the treatment of autism, Alzheimer's disease, bipolar disorder, major depressive disorder, obsessive-compulsive disorder, schizophrenia, specific drug addictions (cocaine and cannabis), and a certain form of epilepsy (progressive myoclonic).[32][33][35][36][37][38][39] Evidence to date does not support the efficacy for N-acetylcysteine in treating addictions to gambling, methamphetamine, or nicotine, although pilot controlled data are encouraging.[35] GLT1 is theorized as the active target of NAC's mediation of drug addiction.[40]

Acetylcysteine has also been hypothesized to exert beneficial effects through its modulation of glutamate and dopamine neurotransmission as well as its antioxidant properties.[33]

Microbiological use

Acetylcysteine can be used in Petroff's method i.e. liquefaction and decontamination of sputum, in preparation for recovery of mycobacterium.[41] It also displays significant antiviral activity against the influenza A viruses.[42]

Acetylcysteine has bactericidal properties and breaks down bacterial biofilms of clinically relevant pathogens including Pseudomonas aeruginosa, Staphylococcus aureus, Enterococcus faecalis, Enterobacter cloacae, Staphylococcus epidermidis and Klebsiella pneumoniae.[43]

Other uses

Acetylcysteine is sold as a dietary supplement commonly claiming antioxidant and liver protecting effects.

Acetylcysteine has been used to complex palladium, to help it dissolve in water. This helps to remove palladium from drugs or precursors synthesized by palladium-catalyzed coupling reactions.[44]

Adverse effects

The most commonly reported adverse effects for IV formulations of acetylcysteine are rash, urticaria, and itchiness.[10] Up to 18% of patients have been reported to experience anaphylaxis reaction, which are defined as rash, hypotension, wheezing, and/or shortness of breath. Lower rates of anaphylactoid reactions have been reported with slower rates of infusion.

Adverse effects for inhalational formulations of acetylcysteine include nausea, vomiting, stomatitis, fever, rhinorrhea, drowsiness, clamminess, chest tightness, and bronchoconstriction. Though infrequent, bronchospasm has been reported to occur unpredictably in some patients.[45]

Adverse effects for oral formulations of acetylcysteine have been reported to include nausea, vomiting, rash, and fever.[45]

Antioxidants are widely used to protect cells from damage induced by reactive oxygen species (ROS). The concept that antioxidants can help fight cancer is deeply rooted in the general population, promoted by the food supplement industry. However, clinical trials have reported inconsistent results.[46] High levels of ROS or prolonged stress upregulates p53 and provokes a pro-oxidant response to further increase ROS, which subsequently elicits the p53-dependent apoptotic processes to eliminate damaged cells.[47][48][49] Thus, antioxidants can accelerate tumor growth by disrupting the ROS-p53 axis apoptosis, and autophagy, processes. Because somatic mutations in p53 occur late in tumor progression, antioxidants may accelerate the growth of early tumors or precancerous lesions in high-risk populations such as smokers and patients with chronic obstructive pulmonary disease who receive NAC to relieve mucus production.[50] It is not clear what dose(s) induced these effects. Additionally, it is important to reiterate that NAC does not cause cancer, it counteracts ROS accumulation caused by p53 and down-regulates p53, which in turn prevents p53-induced apoptosis and promotes autophagy.[51] in all cells; it is a dose dependent response, and the ability to manipulate cellular apoptosis and autophagy has many therapeutic benefits.[52][53][54][55]

Large doses in a mouse model showed that acetylcysteine could potentially cause damage to the heart and lungs.[56] They found that acetylcysteine was metabolized to S-nitroso-N-acetylcysteine (SNOAC), which increased blood pressure in the lungs and right ventricle of the heart (pulmonary artery hypertension) in mice treated with acetylcysteine. The effect was similar to that observed following a 3-week exposure to an oxygen-deprived environment (chronic hypoxia). The authors also found that SNOAC induced a hypoxia-like response in the expression of several important genes both in vitro and in vivo.

The implications of these findings for long-term treatment with acetylcysteine have not yet been investigated. The dose used by Palmer and colleagues was dramatically higher than that used in humans, the equivalent of about 20 grams per day.[56][57] Nonetheless, positive effects on age-diminished control of respiration (the hypoxic ventilatory response) have been observed previously in human subjects at more moderate doses.[58]

Although N-acetylcysteine prevented liver damage when taken before alcohol, when taken 4 hours after alcohol it actually made liver damage worse in a dose-dependent fashion.[59]



Acetylcysteine serves as a prodrug to L-cysteine.

L-cysteine is a precursor to the biologic antioxidant glutathione. Hence administration of acetylcysteine replenishes glutathione stores.[60]

– Glutathione, along with oxidized glutathione (GSSG) and S-nitrosoglutathione (GSNO), have been found to bind to the glutamate recognition site of the NMDA and AMPA receptors (via their γ-glutamyl moieties), and may be endogenous neuromodulators.[61][62] At millimolar concentrations, they may also modulate the redox state of the NMDA receptor complex.[62] In addition, glutathione has been found to bind to and activate ionotropic receptors that are different from any other excitatory amino acid receptor, and which may constitute glutathione receptors, potentially making it a neurotransmitter.[63] As such, since N-acetylcysteine is a prodrug of glutathione, it may modulate all of the aforementioned receptors as well.

– Glutathione also modulates the NMDA receptor by acting at the redox site.[33][64]

L-cysteine also serves as a precursor to cystine which in turn serves as a substrate for the cystine-glutamate antiporter on astrocytes hence increasing glutamate release into the extracellular space. This glutamate in turn acts on mGluR2/3 receptors, and at higher doses of acetylcysteine, mGluR5.[65][66]

Acetylcysteine also possesses some anti-inflammatory effects possibly via inhibiting NF-κB and modulating cytokine synthesis.[33]


Extensively liver metabolized; CYP450 minimal. Urine excretion 22-30% with a half-life of 5.6 hours in adults and 11 hours in neonates.


Acetylcysteine is the N-acetyl derivative of the amino acid L-cysteine, and is a precursor in the formation of the antioxidant glutathione in the body. The thiol (sulfhydryl) group confers antioxidant effects and is able to reduce free radicals.

N-acetyl-L-cysteine is soluble in water and alcohol, and practically insoluble in chloroform and ether.[67]

It is a white to white with light yellow cast powder, and has a pKa of 9.5 at 30 °C.[68]

Dosage forms

Acetylcysteine is available in different dosage forms for different indications:

The IV injection and inhalation preparations are, in general, prescription only, whereas the oral solution and the effervescent tablets are available over the counter in many countries. Acetylcysteine is available as a health supplement in the United States, typically in capsule form.



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