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Abstract From PubMed US National Library of Medicine National Institutes of Health

Recent large clinical trials failed to confirm the supposed beneficial effects of N-acetylcysteine (NAC) in preventing oxidative stress-related diseases. This may be due to its low bioavailability. We thought that esterification of the carboxyl group of NAC to produce N-acetylcysteine ethyl ester (NACET) would drastically increase the lipophilicity of NAC, thus greatly improving its pharmacokinetics. In the present work, we report on representative chemical, pharmacological and anti-oxidant properties of NACET, especially in direct comparison with its congener NAC.

We found that NACET is rapidly absorbed in rats after oral administration but reaches very low concentrations in plasma. This is due to a unique feature of NACET: it rapidly enters the cells where it is trapped being transformed into NAC and cysteine. After oral treatment, NACET (but not NAC) was able to increase significantly the glutathione content of most tissues examined, brain included, and to protect from paracetamol intoxication in the rat.

NACET has also the unique feature to accumulate in human erythrocytes where it behaves as a potent protector against hydroperoxide-induced oxidative damage. Our study shows that being able to enter cells and to produce NAC and cysteine, NACET increases circulating hydrogen sulfide (H(2)S), thus representing a good candidate for the oral use as an H(2)S producer, with clear advantages over NAC. NACET has the potential to substitute NAC as a mucolytic agent, as a paracetamol antidote and as a GSH-related antioxidant.

PMID: 23000913  DOI: 10.1016/j.bcp.2012.09.010

About NACET

Note that NACET will have major advantages over NAC so theraputic use will likely include other things that NAC has not been shown effective against. Note also how some research indicates NAC crosses the blood brain barrier (BBB), but it only does so in slight amounts, and is only absorbed approximately 3-6% orally. NACET is more like 70% + absorbed, and goes intracellular instead of outside the cells, as well as penetrating the brain more.

NAC was also proven beneficial in patients with the autoimmune disorder Systematic lupus erythematosus (SLE). NAC has a diversity of applications in both an experimental setting, as a tool for studies of oxidative stress induced by various agents including HNE, and in a clinical setting, as a therapeutic agent against several neurodegenerative diseases sharing primary or secondary mitochondrial defects that result in ROS overproduction and/or mitochondria-associated apoptosis. As a drug, NAC represents perhaps the ideal Xenobiotic, that is, it is capable of directly entering endogenous biochemical processes as a result of its own metabolism.

Since NAC may cross the BBB, it is hoped that the experience gained with this unique agent will help in future efforts to design antioxidants and chemoprotective principles that are able to more accurately utilize endogenous biochemical processes for therapy of neurodegenerative diseases. Abnormalities in the glutamatergic pathways may cause a number of complications. An imbalance in the excitatory/ inhibitory systems with abnormalities in the glutamatergic pathways has been implicated in the pathophysiology of autism. Furthermore, chronic redox imbalance was also recently linked to autism. It has been shown that using oral N-acetylcysteine (NAC), a glutamatergic modulator and an antioxidant, in the treatment of behavioral disturbance in children with ADHD and autism.

NAC Derivatives

Derivatives of NAC also have many biological properties and aid in maintaining proper biological functions. Some of these derivatives include: N- acetyl-L-cysteine amide, N-acetyl-L-cysteine methyl ester, N-acetyl-L-cysteine ethyl ester, N-acetyl-L-cysteine propyl ester, and N-acetyl-L-cys teine isopropyl ester.

The esterification of the carboxyl group to produce N-acetyl cysteine ethyl ester increases the lipophilicity of NAC and greatly improves its pharmacokinetics. NACET has much higher bioavailability (around 60%) than NAC. NACET rap idly enters the cells, then is trapped, and transforms into NAC and Cysteine. NACET is found in the cells of different tissues, including brain as it is able to cross the blood-brain barrier. NACET also provides a variety of protective antioxidant effects. NACET may be taken orally and helps increase glu tathione. It can accumulate in human erythrocytes. NACET may also behave as a potent protector against hydroperoxide induced oxidative damage.

N acetylcysteine amide (NACA) is a derivative of NAC and has been synthesized to improve the lipophilicity, membrane permeability, and antioxidant property. Studies have demonstrated the blood-brain barrier permeability and therapeutic potentials of NACA in neurological disorders including Parkinson’s disease, Alzheimer’s disease, Multiple sclerosis, Tardive dyskinesia, and HIV- associated neurological disorders. Additionally, NACA displays protective effect against pulmonary inflammation and antibiotic-induced apo ptosis.

NAC Ester (NACET) is the simplest cysteine derivative.

Ongoing research continues on the possible therapeutic tic properties of NACA and its generics in the management of pathologies associated with extracellular matrix degradation and oxidative stress-related inflammation. NACA has superior bio- availability than NAC as well as a molecule to improve the endurance and resident time of bio scaffolds and biomaterials. More than 800 reviews on NAC have been published. However, no comprehensive review is available on the therapeutic applications of NACA. US 9,062,086 B2 5 NACA

Supplementation may be used to reduce, prevent, or counteract oxidative stress and free radical oxidant formation and overproduction in cells and tissues, as well as to provide a new Source of glutathione. Some studies show that NACA ameliorates cellular damage and Subsequent loss of vision. Treatment of human retinal pigment epithelial cells with NACA was shown to protect against Oxidative stress-induced cellular injury and death. NACA acted mechanistically by Scavenging existing reactive oxygen species while halting production of reactive oxygen species by reversing lipid peroxidation.

Furthermore, NACA functioned by increasing the levels of reduced glutathione and the phase II detoxification enzyme glutathione peroxi dase. NACA protects against oxidative stress-induced retinal pigment epithelial and photoreceptor cell death. Providing NACA may treat and in rescue retinal function and prevent vision loss secondary to retinal degenerative diseases, includ ing age-related macular degeneration.

The esterification of the carboxyl group to produce N-acetylcysteine ethyl ester increases the lipophilicity of NAC and greatly improves its pharmacokinetics. NACET has much higher bioavailability (around 60%) than NAC. NACET rapidly enters the cells, then is trapped, and transforms into NAC and Cysteine. NACET is found in the cells of different tissues, including brain as it is able to cross the blood-brain barrier.

NACET also provides a variety of protective antioxidant effects. NACET may be taken orally and helps increase glutathione. It can accumulate in human erythrocytes. NACET may also behave as a potent protector against hydroperoxide-induced oxidative damage.

N-acetylcysteine amide (NACA) is a derivative of NAC and has been synthesized to improve the lipophilicity, membrane permeability, and antioxidant property. Studies have demonstrated the blood-brain barrier permeability and therapeutic potentials of NACA in neurological disorders including Parkinson’s disease, Alzheimer’s disease, Multiple sclerosis, Tardive dyskinesia, and HIV-associated neurological disorders.

Additionally, NACA displays protective effect against pulmonary inflammation and antibiotic-induced apoptosis. Ongoing research continues on the possible therapeutic properties of NACA and its generics in the management of pathologies associated with extracellular matrix degradation and oxidative stress-related inflammation.

NACA has superior bioavailability than NAC as well as a molecule to improve the endurance and resident time of bioscaffolds and biomaterials. More than 800 reviews on NAC have been published. However, no comprehensive review is available on the therapeutic applications of NACA.

NACA supplementation may be used to reduce, prevent, or counteract oxidative stress and free radical oxidant formation and overproduction in cells and tissues, as well as to provide a new source of glutathione