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-gram dose of acetylcysteine dissolved in solution as an effervescent tablet showed a mean peak plasma concentration (Cmax) of 26.5 µg/mL, a time to peak concentration (Tmax) of 2 hours, and an area under the curve (AUC) of 186 µgh/mL. Following oral administration of radiolabeled acetylcysteine, 13-38% was excreted in the urine and 3% in the feces within 24 hours. The volume of distribution of acetylcysteine was 0.47 L/kg. The mean clearance of acetylcysteine was 0.11 L/hr/kg. After oral administration (e.g., as an antidote for acetaminophen overdose), acetylcysteine is absorbed via the gastrointestinal tract. Oral absorption of acetylcysteine is rapid, but its bioavailability is low. Due to significant first-pass metabolism, its metabolites account for 10-30% of the total metabolites. The volume of distribution of intact acetylcysteine is relatively small (0.5 L/kg). Following an initial intravenous loading dose of 150 mg/kg administered over 15 minutes, serum concentrations are approximately 500 mg/L. A steady-state plasma concentration of 35 mg/L (10–90 mg/L) is achieved approximately 12 hours after the loading dose, followed by a continuous infusion of 50 mg/kg for 4 hours, and then 100 mg/kg for 16 hours. Metabolism/Metabolites Acetylcysteine is deacetylated by aminoacylase 1 or other undefined deacetylases before undergoing normal cysteine metabolism. After oral inhalation or intratracheal infusion, most of the administered dose appears to participate in the thiol-disulfide reaction; the remainder is absorbed by the lung epithelium, deacetylated in the liver to cysteine, and subsequently metabolized. Acetylcysteine is rapidly deacetylated in vivo to cysteine or oxidized to diacetylcysteine.

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Biological Half-Life
The mean terminal half-life of acetylcysteine in adults is 5.6 hours, and in premature newborns it is 11 hours.
It has been reported that the mean elimination half-life after intravenous administration of acetylcysteine in adults and newborns is 5.6 hours and 11 hours, respectively. The mean elimination half-life is prolonged by 80% in patients with severe liver injury (e.g., alcoholic cirrhosis (Child-Pugh score 7–13) or primary and/or secondary biliary cirrhosis (Child-Pugh score 5–11)).

Hepatotoxicity
Acetylcysteine is a simple modified amino acid that appears to have hepatoprotective effects. In multiple studies on acetylcysteine for the treatment of acetaminophen overdose and other conditions (such as contrast-induced nephropathy, pulmonary fibrosis, cystic fibrosis, and ulcerative colitis), no association was found with elevated serum enzymes or clinically significant liver injury during treatment. Since the approval of oral and intravenous acetylcysteine, no published reports on its hepatotoxicity have been received, and liver injury is not listed as an adverse reaction on product labels. In fact, acetylcysteine may be beneficial for the treatment of general liver diseases, although its current indications are limited to acetaminophen overdose or acetaminophen-related acute liver injury. Probability Score: E (Unlikely to be a cause of clinically significant liver injury). Pregnancy and Lactation Effects ◉ Overview of Use During Lactation There is currently no information regarding the use of acetylcysteine during lactation. To avoid infant exposure, breastfeeding women may consider expressing and discarding breast milk within 30 hours of taking acetylcysteine. Acetylcysteine is absorbed very little after inhalation, therefore breastfeeding can continue without special precautions.
◉ Effects on breastfed infants
No published information found as of the revision date.
◉ Effects on lactation and breast milk
No published information found as of the revision date.

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Protein binding
Acetylcysteine has a protein binding rate of 66-97% in serum and is usually bound to albumin.

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Drug interactions
Guinea pigs were administered the following drugs daily: Group 1 received a subcutaneous injection of 200 mg/kg kanamycin, Group 1 received an intraperitoneal injection of 300 mg/kg N-acetylcysteine, and Group 3 received N-acetylcysteine first, followed by kanamycin one hour later. The detection threshold for compound action potentials was measured after a 7-day recovery period. N-acetylcysteine alone had no detectable effect on hearing thresholds. Kanamycin alone caused moderate hearing loss (10-20 dB) below 10 kHz and more severe hearing loss above 10 kHz. Animals treated with both N-acetylcysteine and kanamycin showed severe hearing loss (40-60 dB) across all frequencies from 3 to 30 kHz. These data suggest a strong synergistic effect between N-acetylcysteine and kanamycin, leading to severe hearing loss and cochlear damage. The main side effect of photodynamic therapy (PDT) injection of the photosensitizer Photofrin is increased skin sensitivity to sunlight, which can persist for 3-8 weeks post-injection. The formation of singlet oxygen and free radicals is believed to be involved in the fundamental mechanisms inducing skin damage. Reducing this side effect would make PDT more widely acceptable, especially in palliative care. The effects of different light doses were assessed by intraperitoneal injection of 10 mg/kg Photofrin 24 hours before light exposure on hairless skin on the backs of mice. The light source was a halogen lamp, with light transmitted via optical fiber, illuminating an area of 2.5 cm². After establishing the dose-response relationship of single or fractionated light exposure to the skin, the protective effects of drugs known to scavenge free radicals, quench singlet oxygen, or interfere with histamine release were tested. Intraperitoneal injection of N-acetylcysteine (1000 and 2000 mg/kg) one hour before light exposure significantly reduced skin damage at light doses >50 J/cm² (protection coefficients 1.3–1.8). However, no protective effect was observed at a dose of 500 mg/kg. Fractionated light exposure combined with multiple injections of N-acetylcysteine (1000 mg/kg) also failed to show any protective effect. Pre-treatment administration of the histamine blocker ranitidine (25–100 mg/kg) provided only limited protection at high light doses. These results suggest that N-acetylcysteine may help improve photosensitivity in patients undergoing photodynamic therapy (PDT). This study also investigated the effect of acetylcysteine on cisplatin nephrotoxicity in female Wistar rats. Administration of 0.6 mg/100 g body weight of cisplatin resulted in oliguria, proteinuria, and a significant increase in blood urea nitrogen (BUN). Intraperitoneal injection of 0.6 mg/100 g body weight of cisplatin, followed by subcutaneous injection of 100 mg/100 g body weight of acetylcysteine, completely eliminated the nephrotoxic effects of cisplatin. However, subsequent acetylcysteine treatment significantly reduced renal platinum concentrations due to increased urinary platinum excretion. The same effect on cisplatin nephrotoxicity was also observed when cisplatin and acetylcysteine were dissolved in the same solution prior to injection. The study showed that in this solution, cisplatin and acetylcysteine immediately undergo a ligand exchange reaction, leading to increased renal excretion and decreased renal platinum concentrations. …These results indicate that the protective effect of acetylcysteine against cisplatin nephrotoxicity is based on the formation of a complex unsuitable for renal tubular reabsorption. Studies have shown that intrauterine alcohol intake alters the activity of gamma-glutamyl transferase, the main enzyme responsible for glutathione breakdown. This means that intrauterine alcohol intake interferes with the gamma-glutamyl cycle, ultimately altering glutathione levels. Intrauterine alcohol intake leads to decreased glutathione levels in the developing fetus's brain and liver. Throughout pregnancy, pregnant women ingesting N-acetylcysteine via a liquid diet, along with a certain dose of alcohol, resulted in decreased body weight and brain weight. N-acetylcysteine antagonizes the effects of alcohol on the developing fetus.

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Non-human toxicity values
Dog oral LD50: 1 g/kg
Rat oral LD50: 3 g/kg
Mouse oral LD50: > 3 g/kg
Rat oral LD50: > 6 g/kg
Dog intraperitoneal LD50: 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 drugs; expectorants; free radical scavengers… This study included 113 pregnant patients who overdosed on acetaminophen. Follow-up information, including appropriate laboratory tests and pregnancy outcome data, was obtained for 60 of these patients. Of these 60 patients, 19 overdosed in early pregnancy, 22 in mid-pregnancy, and 19 in late pregnancy. Among the 24 patients whose acetaminophen levels were above the risk threshold for acetaminophen overdose, 10 received N-acetylcysteine treatment within 10 hours of administration; 8 of these resulted in successful delivery, and 2 underwent selective termination of pregnancy. Among the 10 patients who received N-acetylcysteine treatment 10–16 hours after administration, 5 resulted in successful delivery, 2 underwent selective termination of pregnancy, and 3 experienced spontaneous abortion. Of the four women who received N-acetylcysteine treatment within 16–24 hours after an acetaminophen overdose, one mother died, one had a spontaneous abortion, one stillbirth, one selective abortion, and one delivery. …
Acetylcysteine is indicated for the treatment of acetaminophen overdose to prevent hepatotoxicity. (This information is included on the US product label.)
Currently, acetylcysteine is used in clinical practice in conjunction with chest physical therapy as a mucolytic to treat thickened or viscous mucus in the airways. When administered via direct infusion, it can be used to loosen trapped mucus plugs during bronchoscopy. Inhaled acetylcysteine can irritate the airways and induce bronchospasm; therefore, it should be used concurrently with or following an inhaled β-adrenergic bronchodilator. /Not included in US product label/
To evaluate the efficacy and safety of N-acetylcysteine (NAC) in treating patients with chronic hepatitis B, we enrolled 144 patients with chronic hepatitis B (total bilirubin, TBil > 170 mmol/L) from multiple centers in a randomized, double-blind clinical trial. Patients were randomized to either the NAC group or the placebo group, and all patients received an injection containing the same standardized therapeutic agent. Patients in the NAC group received an additional 8 micrograms of NAC daily in the injection solution. The trial lasted 45 days. Liver function and other biochemical parameters were measured on days 0 and 15, 30, and 45 of the trial. Each group contained 72 patients, and the two groups had similar demographic and disease characteristics. During the trial, 28 of the 144 patients withdrew. In the NAC group, total bilirubin (TBil) levels on days 0 and 30 were 401.7 mmol/L and 149.2 mmol/L, respectively, compared to 160.1 ± 160.6 mmol/L and 216.3 ± 199.9 mmol/L in the placebo group. TBil decreased by 62% in the NAC group and by 42% in the placebo group. The effective prothrombin time (PTa) elevation rate was 72% in the NAC group and 54% in the placebo group at days 0 and 45 of treatment. The overall response rate (TBil + PTa) was 90% in the NAC group and 69% in the placebo group. Significant differences were observed between the two groups in all parameters. The incidence of adverse events was 14% in the NAC group and 5% in the placebo group. NAC can reduce serum TBil levels, increase PTa, and shorten hospital stay. No serious adverse events were observed with NAC during our treatment period. We found NAC to be effective and safe in treating patients with chronic hepatitis B.

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Drug Warning
…Acetylcysteine should only be used by pregnant women when clearly needed. …Because it is unclear whether acetylcysteine is excreted into human breast milk, breastfeeding women should use this drug with caution.
Anaphylactic reactions (i.e., acute hypersensitivity reactions such as rash, hypotension, wheezing, and/or dyspnea) have been reported in patients receiving intravenous acetylcysteine to treat acetaminophen overdose; in some cases, anaphylactic reactions have been severe, including the death of one asthmatic patient. Rash, urticaria, and pruritus are the most common adverse reactions in patients receiving intravenous acetylcysteine. Acute flushing and erythema have also occurred; these reactions usually occur 30–60 minutes after the start of infusion and subside with continued infusion. Other manifestations of acetylcysteine reactions besides flushing and erythema should be considered anaphylactic reactions and treated accordingly.
There have been reports of acetylcysteine causing chest tightness and bronchoconstriction. Clinically significant bronchospasm induced by acetylcysteine is rare and unpredictable, even in patients with asthmatic bronchitis or bronchitis complicated by bronchial asthma. Occasionally, patients receiving oral or inhaled acetylcysteine may experience varying degrees of unpredictable exacerbation of airway obstruction. Patients who have previously experienced adverse reactions to acetylcysteine may not respond to subsequent treatment with this drug; while patients who have previously received inhaled acetylcysteine without adverse reactions may respond to subsequent treatment. Nausea, vomiting, and other gastrointestinal symptoms may occur after oral acetylcysteine treatment for acetaminophen overdose. This drug may also exacerbate vomiting caused by acetaminophen overdose. Using a diluted acetylcysteine solution may help reduce the tendency of this drug to exacerbate vomiting. For more complete data on drug warnings for N-acetylcysteine (15 in total), please visit the HSDB record page.

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Pharmacodynamics
Acetylcysteine is indicated for expectorant therapy and treatment of acetaminophen overdose. This medication has a short duration of action and needs to be taken every 1-8 hours depending on the route of administration, but it has a wide therapeutic window. Patients should be informed that the oral solution can be diluted in cola to mask the taste, and they should be aware of the risks of allergies and upper gastrointestinal bleeding.

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.)