N-Acetyl-L-Cysteine

2 TO 2.75 (1 IN 100 ML)

log Kow = -0.66 /Estimated/

SLIGHT ACETIC ODOR

CHARACTERISTIC SOUR TASTE

Crystals from water

WHITE, CRYSTALLINE POWDER

1 G IN 5 ML WATER, 4 ML ALC; PRACTICALLY INSOL IN CHLOROFORM & ETHER

Soluble in water, alcohol, hot isopropyl alcohol, methyl acetate, and ethyl acetate

>24.5 [ug/mL] (The mean of the results at pH 7.4)

109-110

109.5 °C

109.5 °C

1.1X10-5 mm Hg at 25 °C /Estimated/

Specific optical rotation: +5 deg at 20 °C (concn = 3 g/100 mL water)

Henry's Law constant = 1.7X10-13 atm-cu m/mole at 25 °C /Estimated/

Solid

Stable in ordinary light; stable at temp up to 120 °C; nonhygroscopic (oxidizes in moist air)

This chemical does not meet GHS hazard criteria for 12.3% (28 of 228) of reports.

Warning

H319 (87.3%): Causes serious eye irritation [Warning Serious eye damage/eye irritation]

P264+P265, P280, P305+P351+P338, and P337+P317 (click each P-code to see the statement)

Aggregated GHS information provided per 228 reports by companies from 10 notifications to the ECHA C&L Inventory.；Reported as not meeting GHS hazard criteria per 28 of 228 reports by companies.；There are 9 notifications provided by 200 of 228 reports by companies with hazard statement code(s).；Information may vary between notifications depending on impurities, additives, and other factors. The percentage value in parenthesis indicates the notified classification ratio from companies that provide hazard codes. Only hazard codes with percentage values above 10% are shown. For more detailed information, please visit ECHA C&L website.

Regulation (EC) No 178/2002 (amended)

Status: Active Update: 15-01-2019 https://echa.europa.eu/registration-dossier/-/registered-dossier/24043；Status: Active Update: 21-03-2017 https://echa.europa.eu/registration-dossier/-/registered-dossier/19220

L-Cysteine, N-acetyl-: Does not have an individual approval but may be used under an appropriate group standard

IMAP assessments - L-Cysteine, N-acetyl-: Environment tier I assessment；IMAP assessments - L-Cysteine, N-acetyl-: Human health tier I assessment

The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies currently marketed prescription drug products, incl acetylcysteine, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act.

A REVIEW WITH 55 REFERENCES ON THE BIOCHEMISTRY & PHARMACOLOGY OF ACETYLCYSTEINE.[MCKINNEY GR, SISSON GM; ACETYLCYSTEINE; PHARMACOL BIOCHEM PROP DRUG SUBST 2: 479 (1979)]

A REVIEW WITH 28 REFERENCES OF THE EFFECT OF N-ACETYLCYSTEINE ON THE ANTITUMOR ACTIVITY OF DOXORUBICIN & THE LATTER'S CARDIOTOXICITY.[OLSON RD ET AL; INFLUENCE OF N-ACETYLCYSTEINE ON THE ANTITUMOR ACTIVITY OF DOXORUBICIN; SEMIN ONCOL 10(1) 29 (1983)]

Haddad LM, Winchester JF; Clinical Management of Poisoning and Drug Over Dose 2nd ed (1990). Acetaminophen and the use of N-acetylcysteine in treatment of overdose (review). pp 893-908.

Eye Irrit. 2A (87.3%)

Acetylcysteine is a reducing agent and is incompatible with oxidizing agents. Solutions of acetylcysteine become discolored and liberate hydrogen sulfide upon contact with rubber, some metals, particularly iron and copper, and/or when subjected to autoclaving. ... Solutions containing amphotericin B, tetracyclines, erythromycin lactobionate, or ampicillin sodium. ... Acetylcysteine solutions are also physically imcompatible with iodized oil, trypsin, hydrogen peroxide.

Unopened vials of acetylcysteine sodium solution should be stored at 15-30 °C. Following exposure to air, solutions should be stored at 2-8 °C to retard oxidation and should be used within 96 hr.

Unopened vials of acetylcysteine sodium solution should be stored at 15-30 °C. Following exposure to air, oral and oral inhalation solutions should be stored at 2-8 °C to retard oxidation and should be used within 96 hours.

Acetylcysteine solution does not contain an antimicrobial agent; therefore, care must be taken to minimize contamination of the sterile solution. After opening, the vial should be stored in the refrigerator; the opened vial should be discarded after 96 hours.

SRP: The most favorable course of action is to use an alternative chemical product with less inherent propensity for occupational exposure or environmental contamination. Recycle any unused portion of the material for its approved use or return it to the manufacturer or supplier. Ultimate disposal of the chemical must consider: the material's impact on air quality; potential migration in soil or water; effects on animal, aquatic, and plant life; and conformance with environmental and public health regulations.

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.

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).

TERRESTRIAL FATE: Based on a classification scheme(1), an estimated Koc value of 10(SRC), determined from a structure estimation method(2), indicates that acetylcysteine is expected to have very high mobility in soil(SRC). The pKa of the thiol group is 9.52(3) and the pKa of carboxylic acid moiety of acetylcysteine is 3.24(4), indicating that this compound will primarily exist as an anion in the environment and will not volatilize from moist soil surfaces. Acetylcysteine is not expected to volatilize from dry soil surfaces(SRC) based upon an estimated vapor pressure of 1.1X10-5 mm Hg(SRC), determined from a fragment constant method(5). Growth of 10 different bacteria strains were inhibited by acetylcysteine(6), suggesting that biodegradation is not an important environmental fate process in soil(SRC).

AQUATIC FATE: Based on a classification scheme(1), an estimated Koc value of 10(SRC), determined from a structure estimation method(2), indicates that acetylcysteine is not expected to adsorb to suspended solids and sediment(SRC). The pKa of the thiol group is 9.52(3) and the pKa of carboxylic acid moiety of acetylcysteine is 3.24(4), indicating that this compound will primarily exist as an anion in the environment and anions will not volatilize from water surfaces. According to a classification scheme(6), an estimated BCF of 3.2(SRC), from an estimated log Kow of -0.66(7) and a regression derived equation(8), suggests the potential for bioconcentration in aquatic organisms is low(SRC). Growth of 10 different bacteria strains were inhibited by acetylcysteine(9), suggesting that biodegradation is not an important environmental fate process in water(SRC).

ATMOSPHERIC FATE: According to a model of gas/particle partitioning of semivolatile organic compounds in the atmosphere(1), acetylcysteine, which has an estimated vapor pressure of 1.1X10-5 mm Hg at 25 °C(SRC), determined from a fragment constant method(2), will exist in both the vapor and particulate phases in the ambient atmosphere. Vapor-phase acetylcysteine is degraded in the atmosphere by reaction with photochemically-produced hydroxyl radicals(SRC); the half-life for this reaction in air is estimated to be 7 hours(SRC), calculated from its rate constant of 5.5X10-11 cu cm/molec-sec at 25 °C(SRC) that was derived using a structure estimation method(3). Particulate-phase acetylcysteine may be removed from the air by wet and dry deposition(SRC). Acetycysteine does not absorb UV light at wavelengths >290 nm; therefore, acetylcysteine is not expected to be susceptible to photolysis(SRC).

Oral NAC may cause nausea, vomiting, diarrhea, flatus, and gastroesophageal reflux. IV NAC can cause rate-related anaphylactoid reactions in up to 18% of patients, which is not an issue with the oral route. Most anaphylactoid reactions are mild (6%) or moderate (10%), with severe reactions like bronchospasm and hypotension rare at 1%. Interestingly, anaphylactoid reactions occur more commonly with lower APAP levels than with higher APAP levels. One possible explanation is that APAP decreases the histamine release from mast cells and mononuclear cells proportionate to the dose ingested. Bronchospasm more commonly occurs in patients with pre-existing reactive airway diseases, like asthma. Bronchodilating agents are effective in treating these patients.；When an anaphylactoid reaction occurs, NAC should be stopped immediately, and the patient should be treated with anti-histamine medication (eg, diphenhydramine) and IV fluid for hypotension. Vasopressors are not typically necessary. NAC therapy may restart at a slower rate after the resolution of the reaction. Oral NAC is the alternative approach if there is a persistent reaction. IV NAC can cause a spurious increase in INR, which normalizes when the infusion stops; it can also cause a false-positive result for urine ketones. Oral NAC may cause vomiting in up to 33% of cases. In patients with preexistent GI ulcers or varices, there may be concerns about inducing GI bleeding with oral NAC.；Drug-Drug Interaction: Nitroglycerin interacts moderately with NAC, as their coadministration may result in hypotension and nitroglycerin-induced headache. Carbamazepine, when co-administered with NAC, can result in a lower-than-desired blood concentration of carbamazepine.

The panel concluded that the 115 amino acid alkyl amides listed below are safe in the present practices of use and concentration in cosmetics, when formulated to be non-irritating...Acetyl Cysteine

Safe for use in cosmetics, with qualifications

Given the drug's complicated regime, NAC has a high potential for iatrogenic errors, including overdose. The signs of overdose are documented to include hemolysis, thrombocytopenia, metabolic acidosis, acute renal failure, and elevated serum bilirubin. Though the mild signs improve within a few days, severe signs may lead to fatal consequences. Massive accidental NAC administration of 100 mg/kg/hr had resulted in cerebral edema, seizures, uncal herniation, and permanent brain injury in a patient with an APAP overdose.

The following link will take the user to the National Toxicology Program (NTP) Test Agent Search Results page, which tabulates all of the "Standard Toxicology & Carcinogenesis Studies", "Developmental Studies", and "Genetic Toxicity Studies" performed with this chemical. Clicking on the "Testing Status" link will take the user to the status (i.e., in review, in progress, in preparation, on test, completed, etc.) and results of all the studies that the NTP has done on this chemical. [http://ntp-apps.niehs.nih.gov/ntp_tox/index.cfm?fuseaction=ntpsearch.searchresults&searchterm=616-91-1]

Using a structure estimation method based on molecular connectivity indices(1), the Koc for acetylcysteine can be estimated to be 10(SRC). According to a classification scheme(2), this estimated Koc value suggests that acetylcysteine is expected to have very high mobility in soil. The pKa of acetylcysteine is 3.24(3), indicating that this compound will primarily exist as an anion in the environment anions generally do not adsorb more strongly to organic carbon and clay than their neutral counterparts(4).

/SIGNS AND SYMPTOMS/ The features of n-acetyl-l-cysteine overdose are similar to the anaphylactoid reactions but more severe. Cardiovascular collapse and death were temporally assocated with the administration of intravenous n-acetyl-l-cysteine in a 4 year old with subtoxic plasma acetaminophen levels. Several fatalities occurred following intravenous n-acetyl-l-cysteine administration, but the contribution of fulminant hepatic failure to mortality limits conclusions about n-acetyl-l-cysteine effects.

/CASE REPORTS/ A case of serum sickness like illness assoc with acetylcysteine therapy in a 29 yr old man who was admitted with an acetaminophen overdose is reported. Acetylcysteine was started at 5 g orally every 6 hr. Three days after admission, the patient developed fever, diffuse abdominal tenderness, and bilateral, symmetric swelling of the knee and elbow joints. Had a discrete erythematous maculopapular eruption on the chest, abdomen, back and extremities with a few erythematous macules on the palms and face. The platelet count was 233 x 109/l. Twelve hr after antibiotic admin for suspected intraabdominal abscess, his temperature was 40 °C and he had tender, palpable cervical, axillary and inguinal lymph nodes. a hypersensitivity reaction to acetylcysteine was suspected and the drug was discontinued. ...

/CASE REPORTS/ A healthy 30-month-old girl allegedly ingested acetaminophen at 418 mg/kg. Because the emergency physician feared the time of ingestion might not be accurate, he decided to start the 20.5-hour intravenous N-acetylcysteine protocol 8 hours after ingestion. He mistakenly prescribed the maximum milliliter-per-kilogram volume of the dextrose 5% diluent for the milliliter-per-kilogram volume of N-acetylcysteine 20% to be administered. Five hours after the error was detected (19.5 hours postingestion), the patient started developing myoclonus on the left side of her body, with left eye deviation. This condition persisted intermittently for 3 hours despite treatment with diazepam, lorazepam, and phenytoin. A first computed tomographic scan result was normal. A few hours later, she sustained shorter recurrences of the myoclonus. At 30 hours after ingestion, she started to have irregular breathing and became unresponsive to pain. A repeated computed tomographic scan showed diffuse cerebral edema. A postmortem examination showed the presence of acute anoxic encephalopathy with marked cerebral edema and the beginning of uncal herniation that confirmed the clinical diagnosis of intracranial hypertension and brain death. A cumulative intravenous dose of 2,450 mg/kg of N -acetylcysteine was associated with status epilepticus, intracranial hypertension, and death in a child.

/CASE REPORTS/ Paracetamol overdose is a common reason for presentation to the emergency department and N-acetylcysteine is frequently used in the treatment of toxic paracetamol ingestions. Adverse reactions to N-acetylcysteine are common though usually mild and easily treated. Serious reactions to N-acetylcysteine however, are rare and there have been no previous reported fatalities with its therapeutic use. This report describes the case of a 40 year old brittle asthmatic patient who died after treatment with intravenous N-acetylcysteine. Asthma is a risk factor for adverse reactions to N-acetylcysteine and special caution should be exercised in its use in brittle asthmatic patients.

/CASE REPORTS/ Marked elevations in liver function test results (eg, AST (SGOT) and ALT (SGPT), occurred on 2 occasions following administration of high doses (total doses: 106 and 250 g over 3-4 days) of acetylcysteine rectally and via nasogastric tube in a 3 year old by with cystic fibrosis; these abnormalities were noted within a few days of initiation of acetylcysteine therapy and resolved gradually following discontinuance of the drug.

Acetylcysteine's production and use as a mucolytic, in the treatment of chronic bronchitis(1), cancer(1), paracetamol intoxication(1), acetaminophen overdose(2), corneal damage(2), and in veterinary application as an expectorant(2) may result in its release to the environment through various waste streams(SRC).

Growth of 10 different bacteria strains isolated from Swedish paper mills were inhibited by acetylcysteine at concentrations of 0.5 mg/mL(1). Also application of acetylcysteine decreased the production of extracellular polysaccarides in all of the bacteria at concentration of 0.25 mg/mL(1). This suggests that biodegradation is not an important environmental fate process.

Drug Induced Liver Injury Rank (DILIrank 2.0)

Acetylcysteine

vNo-DILI-concern

0

No match

DOI:10.1016/j.drudis.2016.02.015

An estimated BCF of 3.2 was calculated for acetylcysteine(SRC), using an estimated log Kow of -0.66(1) and a regression-derived equation(2). According to a classification scheme(3), this BCF suggests the potential for bioconcentration in aquatic organisms is low(SRC).

Regulation (EC) No 178/2002 (amended)

Status: Active Update: 15-01-2019 https://echa.europa.eu/registration-dossier/-/registered-dossier/24043；Status: Active Update: 21-03-2017 https://echa.europa.eu/registration-dossier/-/registered-dossier/19220

L-Cysteine, N-acetyl-: Does not have an individual approval but may be used under an appropriate group standard

The Approved Drug Products with Therapeutic Equivalence Evaluations List identifies currently marketed prescription drug products, incl acetylcysteine, approved on the basis of safety and effectiveness by FDA under sections 505 of the Federal Food, Drug, and Cosmetic Act.

R05CB01

V - Various；V03 - All other therapeutic products；V03A - All other therapeutic products；V03AB - Antidotes；V03AB23 - Acetylcysteine

S - Sensory organs；S01 - Ophthalmologicals；S01X - Other ophthalmologicals；S01XA - Other ophthalmologicals；S01XA08 - Acetylcysteine

R - Respiratory system；R05 - Cough and cold preparations；R05C - Expectorants, excl. combinations with cough suppressants；R05CB - Mucolytics；R05CB01 - Acetylcysteine

QS - Sensory organs；QS01 - Ophthalmologicals；QS01X - Other ophthalmologicals；QS01XA - Other ophthalmologicals；QS01XA08 - Acetylcysteine

QV - Various；QV03 - All other therapeutic products；QV03A - All other therapeutic products；QV03AB - Antidotes；QV03AB23 - Acetylcysteine

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

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.

A number of possible mechanisms for the mucolytic activity of acetylcysteine have been proposed. Acetylcysteine's sulfhydryl groups may hydrolize disulfide bonds within mucin, breaking down the oligomers, and making the mucin less viscous. Acetylcysteine has also been shown to reduce mucin secretion in rat models. It is an antioxidant in its own right but is also deacetylated to cysteine, which participates in the synthesis of the antioxidant glutathione. The antioxidant activity may also alter intracellular redox reactions, decreasing phosphorylation of EGFR and MAPK, which decrease transcription of the gene MUC5AC which produces mucin. In the case of acetaminophen overdoses, a portion of the drug is metabolized by CYP2E1 to form the potentially toxic metabolite N-acetyl-p-benzoquinone imine (NAPQI). The amount of NAPQI produced in an overdose saturates and depletes glutathione stores. The free NAPQI promiscuously binds to proteins in hepatocytes, leading to cellular necrosis. Acetylcysteine can directly conjugate NAPQI or provide cysteine for glutathione production and NAPQI conjugation.

Acetylcysteine exerts its mucolytic action through its free sulfhydryl group, which opens the disulfide bonds and lower the viscosity of the mucus. This action increases with increasing pH and is most significant at pH 7 to 9. The mucolytic action of acetylcysteine is not affected by the presence of DNA.

Acetylcysteine may protect against acetaminophen overdose-induced hepatotoxicity by maintaining or restoring hepatic concentrations of glutathione. Glutathione is required to inactivate an intermediate metabolite of acetaminophen that is thought to be hepatotoxic. In acetaminophen overdose, excessive quantities of this metabolite are formed because the primary metabolic (glucuronide and sulfate conjugation) pathways become saturated. Acetylcysteine may act by reducing the metabolite to the parent compound and/or by providing sulfhydryl for conjugation of the metabolite. Experimental evidence also suggests that a sulfhydryl-containing compound such as acetylcysteine may directly inactivate the metabolite.

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)).

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.

WYQ7N0BPYC

ACETYLCYSTEINE

Established Pharmacologic Class [EPC] - Antidote

Established Pharmacologic Class [EPC] - Antidote for Acetaminophen Overdose

Physiologic Effects [PE] - Decreased Respiratory Secretion Viscosity

Physiologic Effects [PE] - Increased Glutathione Concentration

Agents used in the prophylaxis or therapy of VIRUS DISEASES. Some of the ways they may act include preventing viral replication by inhibiting viral DNA polymerase; binding to specific cell-surface receptors and inhibiting viral penetration or uncoating; inhibiting viral protein synthesis; or blocking late stages of virus assembly.

Agents that increase mucous excretion. Mucolytic agents, that is drugs that liquefy mucous secretions, are also included here.

Substances that eliminate free radicals. Among other effects, they protect PANCREATIC ISLETS against damage by CYTOKINES and prevent myocardial and pulmonary REPERFUSION INJURY.

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.

Fibroblasts；Intestine；Kidney；Liver；Neuron；Placenta

Cytoplasm

CIR ingredient: Acetyl Cysteine

MUCOLYTIC AGENT (ADJUVANT) FOR BRONCHOPULMONARY DISORDERS

Medicine, biochemical research

Mucolytic; corneal vulnerary; antidote to acetaminophen poisoning

Secretolytic agent

For more Uses (Complete) data for N-ACETYLCYSTEINE (6 total), please visit the HSDB record page.

(1976) PROBABLY GREATER THAN 4.54X10+5 GRAMS

(1979) NOT PRODUCED COMMERCIALLY IN US

ESSENTIALLY 100% AS A MUCOLYTIC AGENT

Direct acetylation of naturally occurring L-cysteine

... Made by acylating L-cysteine hydrochloride hydrate with acetic anhydride in the presence of sodium acetate.

Preparation and use in treatment of respiratory diseases: Martin, Waller, US 3184505 (1965 to Mead Johnson)

Parenteral: For injection concentrate, for IV infusion: 200 mg/mL Acetadote (Cumberland).

Oral inhalation, intratracheal instillation, and oral: Solution: 100 mg (of acetylcysteine) per mL (10%), Acetylcysteine Sodium Solution, (Abbott, American Regent, Bedford, Dey, Mayne, Roxane); Mucomyst (Sandoz); 200 mg (of acetylcysteine) per mL (20%) Acetylcysteine Sodium Solution (Abbott, American Regent, Bedford, Dey, Mayne, Roxane); Mucomyst (Sandoz). /Acetylcysteine sodium/

Cosmetics -> Antioxidant

L-Cysteine, N-acetyl-: ACTIVE

Information available in 2005 indicated that Acetylcysteine was used in the manufacture of pharmaceutical preparations in the following countries: Algeria, Argentina, Australia, Austria, Belgium, Brazil, Canada, Chile, Colombia, Croatia, Czech Republic, Denmark, Ecuador, Finland, France, Germany, Greece, Hong Kong, Hungary, India, Indonesia, Ireland, Israel, Italy, Japan, Luxembourg, Malaysia, Monaco, Netherlands, New Zealand, Norway, Poland, Portugal, Romania, Russian Federation, Singapore, Slovenia, South Africa, Spain, Sweden, Switzerland, Thailand, Turkey, United Kingdom, United States, Yugoslavia (1,2)

Information available in 2005 indicated that Acetylcysteine sodium was used in the manufacture of pharmaceutical preparations in the following countries: Australia, Germany, Netherlands, Norway, Poland, Romania, Russian Federation, Switzerland, United States (1,2) /Acetylcysteine Sodium/