Endogenous Metabolite; ROS (reactive oxygen species)

In the absence of additional nutritional support, acetylcysteine prolongs the long-term mortality of PC12 cells under collagen by preventing DNA breakage. Acetylcysteine protects sympathetic neurons and PC12 cells from dying [2]. Human aortic smooth muscle cells become damaged and lose viability in a dose-dependent manner when exposed to acetylcysteine [3]. In PC12 cells, acetylcysteine stimulates the Ras extracellular signal regulator (ERK). Acetylcysteine prevents the death of neurons brought on by a lack of nourishment. Nitric oxide (NO) is released more readily from protein-bound reserves in vascular tissue when acetylcysteine is present. Acetylcysteine may disrupt neurite development and NGF-dependent signaling, indicating that it may disrupt oxidation-sensitive NGF mechanism steps [4].

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In the present study we tested whether N-acetyl-L-cysteine (LNAC) affects apoptotic death of neuronal cells caused by trophic factor deprivation. LNAC, an antioxidant, elevates intracellular levels of glutathione. We used serum-deprived PC12 cells, neuronally differentiated PC12 cells deprived of serum and NGF, and NGF-deprived neonatal sympathetic neurons. In each case LNAC prevents apoptotic DNA fragmentation and maintains long-term survival in the absence of other trophic support. Unlike NGF, LNAC does not induce or maintain neurite outgrowth or somatic hypertrophy. To rule out actions of LNAC metabolic derivatives, we assessed N-acetyl-D-cysteine (DNAC). DNAC also prevents death of PC12 cells and sympathetic neurons. However, other antioxidants were ineffective in this regard. Since it has been hypothesized that trophic factors prevent neuronal death by either preventing or coordinating cell cycle progression, we tested whether LNAC or DNAC treatment can affect cell cycle. We found that both (but not other antioxidants) suppress proliferation and DNA synthesis by PC12 cells and do so at concentrations similar to those at which they prevent apoptotic death. Although the abilities of LNAC and DNAC to rescue cells from apoptosis triggered by trophic factor deprivation could derive from their direct influences on cellular responsiveness to oxidative stress, our observations raise the possibility of a mechanism involving cell cycle regulation.[2]

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Pyrrolidinedithiocarbamate (PDTC) and N-acetylcysteine (NAC) have been used as antioxidants to prevent apoptosis in lymphocytes, neurons, and vascular endothelial cells. We report here that PDTC and NAC induce apoptosis in rat and human smooth muscle cells. In rat aortic smooth muscle cells, PDTC induced cell shrinkage, chromatin condensation, and DNA strand breaks consistent with apoptosis. In addition, overexpression of Bcl-2 suppressed vascular smooth muscle cell death caused by PDTC and NAC. The viability of rat aortic smooth muscle cells decreased within 3 h of treatment with PDTC and was reduced to 30% at 12 h. The effect of PDTC and NAC on smooth muscle cells was not species specific because PDTC and NAC both caused dose-dependent reductions in viability in rat and human aortic smooth muscle cells. In contrast, neither PDTC nor NAC reduced viability in human aortic endothelial cells. The use of antioxidants to induce apoptosis in vascular smooth muscle cells may help prevent their proliferation in arteriosclerotic lesions.[3]

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N-acetylcysteine (NAC) has been recently proposed as an adjuvant therapeutic drug for influenza pneumonia in humans. This proposal is based on its ability to restrict influenza virus replication in vitro and to attenuate the severity of the disease in mouse models. Although available studies were made with different viruses (human and avian), published information related to the anti-influenza spectrum of NAC is scarce. In this study, we show that NAC is unable to alter the course of a fatal influenza pneumonia caused by inoculation of a murinized swine H1N1 influenza virus. NAC was indeed able to inhibit the swine virus in vitro but far less than reported for other strains. Therefore, susceptibility of influenza viruses to NAC appears to be strain-dependent, suggesting that it cannot be considered as a universal treatment for influenza pneumonia.[7]

Acetylcysteine (150, 300 mg/kg) treatment significantly lowered hepatic transaminases in all treatment groups, notably in the acetylcysteine 300 mg/kg group. Lung glutathione peroxidase was considerably elevated in the acetylcysteine 300 mg/kg group (P= 0.04), whereas other oxidative indicators revealed no significant difference [6]. Acetylcysteine enhances cognition in 12-month-old SAMP8 models in a T-maze shock avoidance paradigm and a lever estimating test, but not motor production cue non-affecting activity, motivation to avoid shock, or body weight [5].

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Oxidative stress may play a crucial role in age-related neurodegenerative disorders. Here, we examined the ability of two antioxidants, alpha-lipoic acid (LA) and N-acetylcysteine (NAC), to reverse the cognitive deficits found in the SAMP8 mouse. By 12 months of age, this strain develops elevated levels of Abeta and severe deficits in learning and memory. We found that 12-month-old SAMP8 mice, in comparison with 4-month-old mice, had increased levels of protein carbonyls (an index of protein oxidation), increased TBARS (an index of lipid peroxidation) and a decrease in the weakly immobilized/strongly immobilized (W/S) ratio of the protein-specific spin label MAL-6 (an index of oxidation-induced conformational changes in synaptosomal membrane proteins). Chronic administration of either LA or NAC improved 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. These effects probably occurred directly within the brain, as NAC crossed the blood-brain barrier and accumulated in the brain. Furthermore, treatment of 12-month-old SAMP8 mice with LA reversed all three indexes of oxidative stress. These results support the hypothesis that oxidative stress can lead to cognitive dysfunction and provide evidence for a therapeutic role for antioxidants.[5]

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Histological score of the liver was significantly improved in NAC 300 compared with control (1.7 ± 0.5 versus 2.9 ± 1.1, respectively, P = 0.05). In addition, NAC treatment significantly reduced liver transaminases in all groups of treatment, mostly in group NAC 300. Plasma malondialdehyde levels were lower with NAC treatment, although not statistically significant. Lung glutathione peroxidase was significantly increased in group NAC 300 (P = 0.04), while the other oxidation biomarkers showed no significant differences.
Conclusions: NAC exerts a significant protective role in liver injury following IIR, which seems to be independent of an intestinal protective effect. Additional administration of NAC before reperfusion was of no further benefit. The most effective regimen among the compared regimens was that of 300 mg/kg before ischemia.[6]

NAC (N-acetyl-L-cysteine) is commonly used to identify and test ROS (reactive oxygen species) inducers, and to inhibit ROS. In the present study, we identified inhibition of proteasome inhibitors as a novel activity of NAC. Both NAC and catalase, another known scavenger of ROS, similarly inhibited ROS levels and apoptosis associated with H₂O₂. However, only NAC, and not catalase or another ROS scavenger Trolox, was able to prevent effects linked to proteasome inhibition, such as protein stabilization, apoptosis and accumulation of ubiquitin conjugates. These observations suggest that NAC has a dual activity as an inhibitor of ROS and proteasome inhibitors. Recently, NAC was used as a ROS inhibitor to functionally characterize a novel anticancer compound, piperlongumine, leading to its description as a ROS inducer. In contrast, our own experiments showed that this compound depicts features of proteasome inhibitors including suppression of FOXM1 (Forkhead box protein M1), stabilization of cellular proteins, induction of ROS-independent apoptosis and enhanced accumulation of ubiquitin conjugates. In addition, NAC, but not catalase or Trolox, interfered with the activity of piperlongumine, further supporting that piperlongumine is a proteasome inhibitor. Most importantly, we showed that NAC, but not other ROS scavengers, directly binds to proteasome inhibitors. To our knowledge, NAC is the first known compound that directly interacts with and antagonizes the activity of proteasome inhibitors. Taken together, the findings of the present study suggest that, as a result of the dual nature of NAC, data interpretation might not be straightforward when NAC is utilized as an antioxidant to demonstrate ROS involvement in drug-induced apoptosis.[1]

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We have shown that N-acetylcysteine (NAC) promotes survival of sympathetic neurons and pheochromocytoma (PC12) cells in the absence of trophic factors. This action of NAC was not related to its antioxidant properties or ability to increase intracellular glutathione levels but was instead dependent on ongoing transcription and seemed attributable to the action of NAC as a reducing agent. Here, we investigate the mechanism by which NAC promotes neuronal survival. We show that NAC activates the Ras-extracellular signal-regulated kinase (ERK) pathway in PC12 cells. Ras activation by NAC seems necessary for survival in that it is unable to sustain serum-deprived PC12 MM17-26 cells constitutively expressing a dominant-negative form of Ras. Promotion of PC12 cell survival by NAC is totally blocked by PD98059, an inhibitor of the ERK-activating MAP kinase/ERK kinase, suggesting a required role for ERK activation in the NAC mechanism. In contrast, LY294002 and wortmannin, inhibitors of phosphatidylinositol 3-kinase (PI3K) that partially block NGF-promoted PC12 cell survival, have no effect on prevention of death by NAC. We hypothesized previously that the ability of NAC to promote survival correlates with its antiproliferative properties. However, although NAC does not protect PC12 MM17-26 cells from loss of trophic support, it does inhibit their capacity to synthesize DNA. Thus, the antiproliferative effect of NAC does not require Ras activation, and inhibition of DNA synthesis is insufficient to mediate NAC-promoted survival. These findings highlight the role of Ras-ERK activation in the mechanism by which NAC prevents neuronal death after loss of trophic support.[4]

For survival experiments, washed cells are resuspended in RPM1 1640 medium and plated in 0.5 mL at a density of 8-10×105 per well in 24 well plastic culture dishes coated with rat tail collagen. To feed, but to avoid loss of floating cells, fresh medium (0.2 mL) is added to the cultures on days 1, 5, and 10. For experiments involving "primed" PC12 cells, cultures are pretreated for l-2 weeks with NGF in RPM1 1640 medium supplemented with 1% heat-iN-acetylcysteinetivated horse serum. The cells are then washed and passaged into serum-free RPM1 1640 medium[2].

Rats are randomLy allocated into five groups: sham group (n=5), control group with IIR (n=8) and three groups with IIR who are given Acetylcysteine in different dosages: 150 mg/kg intraperitoneally 5 min before ischemia (n=8, group Acetylcysteine 150), 300 mg/kg i.p 5 min before ischemia (n=7, group Acetylcysteine 300), and 150 mg/kg i.p 5 min before ischemia plus 150 mg/kg 5 min before reperfusion (n=7, group Acetylcysteine 150 + 150). After 4 h of reperfusion, the animals are euthanized by exsanguination from the abdominal aorta [6].

Absorption, Distribution and Excretion
An 11 g dose in the form of an effervescent tablet for solution reaches a mean Cmax of 26.5 µg/mL, with a Tmax of 2 hours, and an AUC of 186 µg\*h/mL.
An oral dose of radiolabelled acetylcysteine is 13-38% recovered in the urine in the first 24 hours, while 3% is recovered in the feces.
The volume of distribution of acetylcysteine is 0.47 L/kg.
Acetylcysteine has a mean clearance of 0.11 L/hr/kg.
Following oral administration (e.g., when used as an antidote for acetaminophen overdosage), acetylcysteine is absorbed from the GI tract.
Oral acetylcysteine is rapidly absorbed, but the bioavailability is low (10-30%) due to significant first-pass metabolism. Intact acetylcysteine has a relatively small volume of distribution (0.5 L/kg). Serum concentrations after intravenous administration of an initial loading dose of 150 mg/kg over 15 minutes are about 500 mg/L. A steady state plasma concentration of 35 mg/L (10-90 mg/L) was reached in about 12 hours following the loading dose with a continuous infusion of 50 mg/kg over 4 hours and 100 mg/kg over the next 16 hours.

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Metabolism / Metabolites
Acetylcysteine can be deacetylated by aminoacylase 1 or other undefined deacetylases before undergoing the normal metabolism of cysteine.
Following oral inhalation or intratracheal instillation, most of the administered drug appears to participate in the sulfhydryl-disulfide reaction; the remainder is absorbed from the pulmonary epithelium, deacetylated by the liver to cysteine, and subsequently metabolized.
Acetylcysteine undergoes rapid deacetylation in vivo to yield cysteine or oxidation to yield diacetylcystine.

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Biological Half-Life
The mean terminal half life of acetylcysteine in adults is 5.6 hours and in pre-term neonates is 11 hours.
Following IV administration of acetylcysteine, mean elimination half lives of 5.6 and 11 hours have been reported in adults and in neonates, respectively. The mean elimination half life was increased by 80% in patients with severe liver damage (i.e., alcoholic cirrhosis (Child-Pugh score of 7-13) or primary and/or secondary biliary cirrhosis (Child-Pugh score of 5-11)).

Hepatotoxicity
Acetylcysteine is a simple modified amino acid and appears to be hepatoprotective. In the many studies of acetylcysteine use with acetaminophen overdose as well as with other conditions such as contrast media nephropathy, pulmonary fibrosis, cystic fibrosis and ulcerative colitis, it has not been associated with serum enzyme elevations during therapy or with episodes of clinically apparent liver injury. Since approval of the oral and intravenous forms of acetylcysteine, there have been no published reports of hepatotoxicity and the product label does not mention liver injury as an adverse event. Indeed, acetylcysteine may be beneficial in treating liver diseases in general, although its current indications are limited to acetaminophen overdose or acetaminophen related acute liver injury.
Likelihood score: E (unlikely cause of clinically apparent liver injury).

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Effects During Pregnancy and Lactation
◉ Summary of Use during Lactation
No information is available on the use of acetylcysteine during breastfeeding. To avoid infant exposure, nursing mothers may consider pumping and discarding their milk for 30 hours after administration. Acetylcysteine is very minimally absorbed after inhalation, so breastfeeding can be continued and no special precautions are required.
◉ Effects in Breastfed Infants
Relevant published information was not found as of the revision date.
◉ Effects on Lactation and Breastmilk
Relevant published information was not found as of the revision date.

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Protein Binding
Acetylcysteine is 66-97% protein bound in serum, usually to albumin.

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Interactions
Guinea pigs were treated with daily drug injections as follows: 1 group received 200 mg kanamycin/kg, sc, 1 group received n-acetylcysteine (300 mg/kg, ip) & the 3rd group received n-acetylcysteine followed by kanamycin 1 hr later. After 7-day recovery, thresholds for detection of the compound action potential were measured. N-acetylcysteine alone had no detectable effect on hearing thresholds. Kanamycin alone produced a moderate (10-20 db) hearing loss below 10 khz & a more severe loss above 10 khz. Animals receiving both n-acetylcysteine & kanamycin had severe hearing losses (40-60 db) at all frequencies between 3 & 30 khz. These data indicate that n-acetylcysteine exerts a strong synergistic effect on kanamycin in producing severe hearing loss & cochlear damage.
The major side effect of photodynamic therapy (PDT) using photofrin enhanced skin sensitivity for sunlight which persists for 3-8 weeks after injection. Formation of singlet oxygen and radicals is believed to be involved in the basic mechanism of inducing skin damage. Reducing this side effect would make PDT more widely acceptable particularly for palliative use. Hairless dorsal skin patches of mice injected with 10 mg/kg photofrin ip 24 hr before illumination were used to evaluate the effect of increasing light doses. The light was obtained from a halogen lamp and transmitted via a fiber optic to illuminate a field of 2.5 sq cm. After establishing a dose response relationship for single or fractionated light dose illumination of the skin, drugs known to scavenge radicals, quench singlet oxygen or interfere with histamine release were tested for their protective effect. N-Acetylcysteine, a radical scavenger admin ip (1,000 and 2,000 mg/kg) 1 hr before illumination produced a significant decr in skin damage at light doses > 50 J sq cm (protection factor of 1.3-1.8). When N-acetylcysteine was administered in a dose of 500 mg/kg no protection was observed. Fractionated illumination experiments in combination with multiple injections of N-acetylcysteine (1000 mg/kg) also failed to show any protection. The addition of ranitidine, a histamine blocking agent (25-100 mg/kg) given prior to illumination resulted in a limited protection at higher light doses. From this study /results suggest/ that N-acetylcysteine could be of value in amelioration of the photosensitivity in patients with PDT.
The influence of acetylcysteine on cisplatin nephrotoxicity was investigated in female Wistar rats. Admin of 0.6 mg cisplatin/100 mg bw was followed by oliguria and proteinuria, as well as a significant incr of blood urea nitrogen concn. The ip admin of 0.6 mg cisplatin/100 g body wt concomitantly with 100 mg acetylcysteine/100 g body wt sc completely abolished the nephrotoxic effects of cisplatin. However, following this, the platinum concn in the kidney was decr significantly by acetylcysteine treatment. This was caused by a enhanced urinary excretion of platinum. The same effect on cisplatin nephrotoxicity appeared when cisplatin and acetylcysteine were dissolved together in a soln prior to injection. It could be shown that in this soln a ligand exchange reaction of cisplatin by acetylcysteine started immediately, resulting in incr renal excretion and decr platinum concn in the kidney. ... /Results show/ that the protective effect of acetylcysteine on cisplatin nephrotoxicity is based on the formation of a complex unsuitable for tubular resorption. ...
... Studies have shown that the in utero admin of alcohol alters the activity of gamma-glutamyl transpeptidase, the major enzyme involved with the break down of glutathione. The implication is that the in utero admin of alcohol interferes with gamma-glutamyl cycle and ultimately alters glutathione levels. ... The in utero admin of alcohol results in a decr in brain and liver glutathione levels in the developing fetus. ... N-Acetylcysteine ... was given to pregnant mothers throughout gestation in a liquid diet concomitantly with a dose of alcohol which produces a decr in body and brain weights. ... N-Acetylcysteine antagonized the effects of alcohol in the developing fetus.

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Non-Human Toxicity Values
LD50 Dog oral 1 g/kg
LD50 Rat oral 3 g/kg
LD50 Mouse oral > 3 g/kg
LD50 Rat oral > 6 g/kg
LD50 Dog ip 700 mg/kg

[1]. ROS inhibitor N-acetyl-L-cysteine antagonizes the activity of proteasome inhibitors. Biochem J. 2013 Sep 1;454(2):201-8.

[2]. N-acetylcysteine (D- and L-stereoisomers) prevents apoptotic death of neuronal cells. J Neurosci. 1995 Apr;15(4):2857-66.

[3]. Induction of apoptosis by pyrrolidinedithiocarbamate and N-acetylcysteine in vascular smooth muscle cells. J Biol Chem. 1996 Feb 16;271(7):3667-70.

[4]. Prevention of PC12 cell death by N-acetylcysteine requires activation of the Ras pathway. J Neurosci. 1998 Jun 1;18(11):4042-9.

[5]. The antioxidants alpha-lipoic acid and N-acetylcysteine reverse memory impairment and brain oxidative stress in aged SAMP8 mice. J Neurochem. 2003 Mar;84(5):1173-83.

[6]. N-acetylcysteine ameliorates liver injury in a rat model of intestinal ischemia reperfusion. J Surg Res. 2016 Dec;206(2):263-272.

[7]. N-acetylcysteine lacks universal inhibitory activity against influenza A viruses. J Negat Results Biomed. 2011 May 9;10:5.

Therapeutic Uses
Antiviral Agents; Expectorants; Free Radical Scavengers
... 113 patients entered into the study were reported to be pregnant at the time of /acetaminophen/ overdose. Follow up including appropriate laboratory and pregnancy data outcome data, was available in 60 cases. Of these, 19 overdosed during the first trimester, 22 during the second trimester and 19 during the third trimester of pregnancy. Of the 24 patients with acetaminophen levels above the acetaminophen overdose nomogram line, 10 were treated with N-acetylcysteine within 10 hr postingestion; eight delivered normal infants, two had elective abortions. Of ten patients treated with N-acetylcysteine 10-16 hr postingestion, five delivered viable infants, two had elective abortions, and three had spontaneous abortions. Of four women treated with N-acetylcysteine 16-24 hr postingestion, one mother died, and there was one spontaneous abortion, one stillbirth, one elective abortion, and one delivery. ...
Acetylcysteine is indicated in the treatment of acetaminophen overdose to protect against hepatotoxicity . /Included in US product labeling/
Acetylcysteine is used in current medical practice in conjunction with chest physiotherapy as mucolytic in patients who have viscid or thickened airway mucus. When administered via direct instillation, it is used to loosen impacted mucus plugs during bronchoscopy. Acetylcysteine can irritate the airways and induce bronchospasm when given by inhalation; therefore, it should be administered simultaneously with or following administration of an inhaled beta-adrenergic bronchodilator. /NOT included in US product labeling/
To evaluate the effectiveness and safety of N-acetylcysteine (NAC) in treating chronic hepatitis B patients, 144 patients with chronic hepatitis B (total bilirubin, TBil>170 mmol/L) from several centers were chosen for a randomized and double blind clinical trial. The patients were divided into a NAC group and a placebo group and all of them were treated with an injection containing the same standardized therapeutic drugs. A daily dose of 8 microgram NAC was added to the injection of the NAC group. The trial lasted 45 days. Hepatic function and other biochemistry parameters were checked at the experimental day 0 and days 15, 30, 45. Each group consisted of 72 patients of similar demology and disease characteristics. During the trial, 28 cases of the 144 patients dropped out. In the NAC group, at day 0 and day 30, the TBil were401.7 vs. 149.2 and 160.1+/-160.6. In the placebo group, the TBil on the corresponding days were 384.1+/-134.0 and 216.3+/-199.9. Its decrease in the NAC group was 62% and 42% in the placebo group. At day 0 and day 45 of treatment, the effective PTa increase rate was 72% in the NAC group and 54% in the placebo group. The total effective rate (TBil + PTa) was 90% in the NAC group and 69% in the placebo group. The parameters of the two groups showed a remarkable difference. The rate of side effects was 14% in the NAC and 5% in the placebo groups. NAC can decrease the level of serum TBil, increase the PTa and reduce the time of hospitalization. NAC showed no serious adverse effects during the period of our treatment. We find that NCA is effective and secure in treating chronic hepatitis B patients.

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Drug Warnings
... /Acetylcysteine/ should be used during pregnancy only when clearly needed. ... Since it is not known if acetylcysteine is distributed into human milk, the drug should be used with caution in nursing women.
Anaphylactoid reactions (i.e., acute hypersensitivity reactions such as rash, hypotension, wheezing, and/or dyspnea) have been reported in patients receiving IV acetylcysteine for the treatment of acetaminophen overdosage; in some cases, the anaphylactoid reactions were serious, including death in a patient with asthma. Rash, urticaria, and pruritus are the most frequently reported adverse reactions in patients receiving IV acetylcysteine. Acute flushing and erythema also have occurred; these reactions generally occur 30-60 minutes after initiating the infusion and resolve despite infusion of the drug. Reactions to acetylcysteine that involve manifestations other than flushing and erythema should be considered anaphylactoid reactions and treated as such.
Chest tightness and bronchoconstriction have been reported with acetylcysteine. Clinically overt acetylcysteine-induced bronchospasm occurs rarely and unpredictably, even in patients with asthmatic bronchitis or bronchitis complicating bronchial asthma. Occasionally, patients receiving oral inhalation of acetylcysteine develop increased airway obstruction of varying and unpredictable severity. Patients who have had such reactions to previous therapy with acetylcysteine may not react during subsequent therapy with the drug, and patients who have had inhalation treatments with acetylcysteine without incident may react to subsequent therapy.
Nausea, vomiting, and other GI symptoms may occur following oral administration of acetylcysteine in the treatment of acetaminophen overdosage. The drug may also aggravate vomiting associated with acetaminophen overdosage. Administration of dilute acetylcysteine solutions may minimize the tendency of the drug to aggravate vomiting.
For more Drug Warnings (Complete) data for N-ACETYLCYSTEINE (15 total), please visit the HSDB record page.

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Pharmacodynamics
Acetylcysteine is indicated for mucolytic therapy and in the management of acetaminophen overdose. It has a short duration of action as it is given every 1-8 hours depending on route of administration, and has a wide therapeutic window. Patients should be counselled regarding diluting oral solutions in cola for taste masking, the risk of hypersensitivity, and the risk of upper gastrointestinal hemorrhage.

C5H9NO3S

163.1949

163.03

C, 36.80; H, 5.56; N, 8.58; O, 29.41; S, 19.65

616-91-1

Acetylcysteine-d3;131685-11-5;Acetylcysteine-15N

12035

White to off-white solid powder

1.3±0.1 g/cm3

407.7±40.0 °C at 760 mmHg

106-108 °C(lit.)

200.4±27.3 °C

0.0±2.0 mmHg at 25°C

1.519

Micro-organism; Ketones, Aldehydes, Acids

-0.15

3

4

3

10

148

1

S([H])C([H])([H])[C@@]([H])(C(=O)O[H])N([H])C(C([H])([H])[H])=O

PWKSKIMOESPYIA-BYPYZUCNSA-N

InChI=1S/C5H9NO3S/c1-3(7)6-4(2-10)5(8)9/h4,10H,2H2,1H3,(H,6,7)(H,8,9)/t4-/m0/s1

Cysteine, N-acetyl-, L-

Acetylcysteine; N-Acetyl-L-cysteine; acetylcysteine; 616-91-1; N-Acetylcysteine; mercapturic acid; Acetadote; L-Acetylcysteine; Broncholysin; Parvolex; Mucosil

2934.99.9001

Powder      -20°C    3 years

                     4°C     2 years

In solvent   -80°C    6 months

                  -20°C    1 month

Note: This product requires protection from light (avoid light exposure) during transportation and storage.

Room temperature (This product is stable at ambient temperature for a few days during ordinary shipping and time spent in Customs)

H2O : ~100 mg/mL (~612.78 mM)
DMSO : ≥ 100 mg/mL (~612.78 mM)

Solubility in Formulation 1: 120 mg/mL (735.34 mM) in PBS (add these co-solvents sequentially from left to right, and one by one), clear solution; with sonication.

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Solubility in Formulation 2: ~120 mg/mL (735 mM) in PBS

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 (Please use freshly prepared in vivo formulations for optimal results.)