Use of N-Acetylcysteine (NAC) in the Treatment of Repetitive Behaviors (RB) and Self-Injurious Behaviors (SIB) in Cornelia de Lange Syndrome: A Randomized Double-Blind Placebo-Controlled Pilot Study

This research project is a randomized cross-over pilot trial which aims to test the efficacy of N-acetylcysteine (NAC) for the treatment of Repetitive Behaviors (RB) and self-injurious behavior (SIB) in patients with Cornelia de Lange Syndrome (CdLs).
NAC is a known anti-oxidative stress and neuroprotective agent, which has been shown to decrease the occurrence of SIB such as skin picking. NAC has also shown partial response in trials for compulsive behaviors in Obsessive Compulsive Disorder (OCD) and related disorders in autism.
Cornelia de Lange syndrome (CdLS) is a genetic disorder with autistic features, including RBs and SIB. In this randomized clinical trial, participants with CdLS will be blindly assigned one of two possible treatment arms: 1) placebo (8 weeks) and NAC (8 weeks); or 2) NAC (8 weeks) and placebo (8 weeks), with an intermediate 2-week washout period.

Start Date01 Mar 2026

Sponsor / Collaborator

The Johns Hopkins University

CTRI/2025/12/099949

/ Not yet recruitingPhase 2/3IIT

Investigation of the effect of add on N-acetylcysteine (NAC) and its correlation with oxidative stress and quality of life in patients with obstructive sleep apnea: A randomized, double blind, placebo-controlled, two-arm, proof of concept study - NIL

Start Date26 Feb 2026

Sponsor / Collaborator-

NCT06956482

/ Not yet recruitingPhase 3IIT

PROlonged Corticosteroid Treatment or N-ACetylcysteine for Severe Alcoholic Hepatitis

Only patients suffering from a severe form of alcoholic hepatitis (Maddrey's discriminant function greater than 32) require medical treatment. Oral prednisolone for 28 days is the only treatment which has been proven to improve short-term survival over placebo in patients with severe alcoholic hepatitis. However, prednisolone alone cannot be regarded as an ideal treatment because some patients still have a bad outcome despite being treated with corticosteroids. Response to treatment can be predicted by the Lille score, a simple tool that is calculated after 7 days of prednisolone course. The ideal binary cut-off of the Lille is 0.45, responders having a Lille score < 0.45 and non-responders having a Lille score ≥0.45. In terms of treatment management, approximately 30% of patients with severe alcoholic hepatitis do not take benefit from prednisolone and are classified as null responders by a Lille score greater than 0.56. In them, there is a consensus for stopping prednisolone after a 7-day course of treatment (Lille score is calculated after 7 days) while patients with a Lille score <0.56 continue treatment for a total of 30 days.
Numerous trials have attempted to test the impact of other strategies in association with prednisolone, but none of them has shown an improvement in survival (primary endpoint) as compared to prednisolone alone. These strategies include for instance pentoxifylline, amoxicillin-clavulanic acid and enteral nutrition.
Because oxidative stress is a major driver of liver injury during alcohol-related liver disease, antioxidants, especially N-acetylcysteine, have been tested for many years to treat alcoholic hepatitis. N-acetylcysteine alone does not seem to bring a survival benefit over placebo while it may improve outcome when combined to prednisolone.
Historically in severe alcoholic hepatitis, treatment is only given for one month. However, a significant proportion of patients still disclose impaired hepatic function after treatment has been stopped (e.g. 50% of patients still have a MELD score ≥17 after 60 days in). It is thus tempting to hypothesize that a proportion of patients will recover slowly and may take benefit from a prolonged treatment. Such strategy has been proposed in some old studies with relatively limited sample size but never tested with a rigorous approach.
In the present study, for the first time in alcoholic hepatitis, we will take into account the recent recommendations of international experts by choosing an innovative primary endpoint that does not only include mortality and evaluate this endpoint at the preferred timepoint of 90 days.
After more than 30 years of negative trials in severe alcoholic hepatitis, the present study is aimed to evaluate two important new strategies to decrease both mortality and liver impairment.

Start Date01 Feb 2026

Sponsor / Collaborator-

100 Clinical Results associated with Acetylcysteine

100 Translational Medicine associated with Acetylcysteine

100 Patents (Medical) associated with Acetylcysteine

29,557

Literatures (Medical) associated with Acetylcysteine

31 Dec 2026·Adipocyte

Lack of receptor for advanced glycation end products attenuates obesity-induced adipose tissue senescence in mice

Article

Author: Chen, Ni ; Ma, Xiaoyu ; Xu, Jin ; Li, Ziyu ; Wu, Jianbo ; Wu, Jiaqi ; You, Jingcan ; Du, Zuoqin ; Zhang, Tao

The receptor for advanced glycation end products (RAGE) and its ligands are critical drivers of adipose tissue inflammation. While RAGE expression increases in ageing cells and pathological conditions, its specific role in high-fat diet (HFD)-induced adipose tissue senescence remains to be fully elucidated. In this study, we investigated the function of RAGE in the development of adipose tissue senescence associated with obesity. We observed that HFD-fed RAGE-deficient (RAGE^-/-) mice exhibited significantly reduced body weight and adipocyte hypertrophy compared to wild-type (WT) controls. At the molecular level, RAGE^-/- mice displayed lower mRNA expression of cell cycle regulators and markers of the senescence-associated secretory phenotype. This anti-senescent phenotype was accompanied by decreased reactive oxygen species (ROS) production and elevated expression of anti-oxidant genes. Mechanistically, the lack of RAGE resulted in the upregulation of silent information regulator type 1 (SIRT1) in adipose tissues. Notably, the inhibition of SIRT1 reversed these anti-senescent effects and attenuated anti-oxidant gene expression in RAGE-deficient mice. Furthermore, while antioxidant treatment with N-acetylcysteine (NAC) reduced p53 in WT mice, it failed to fully suppress p16 and p21, whereas NAC treatment in RAGE^-/- mice significantly downregulated all senescence markers, suggesting a synergistic protective effect. In conclusion, our results demonstrated that RAGE deficiency improved anti-oxidant properties and prevents adipocyte senescence via the SIRT1 signalling pathway, highlighting a potential therapeutic target for obesity-associated tissue dysfunction.

01 Dec 2026·MOLECULAR BIOLOGY REPORTS

Excavatolide E triggers oxidative stress-associated apoptosis and DNA damage to inhibit bladder cancer cell proliferation

Article

Author: Yang, Che-Wei ; Chang, Hsueh-Wei ; Chang, Fang-Rong ; Yen, Chia-Hung ; Sheu, Jyh-Horng ; Chien, Tsu-Ming ; Yu, Szu-Yin

BACKGROUND:

Excavatolide E (EXCE), a biocompound extracted from the gorgonian octocoral Briareum excavatum, has received limited attention for its anticancer properties, especially in the context of bladder cancer.

METHODS:

Cell viability, flow cytometry, and Western blotting were performed to assess the antiproliferative effects and mechanisms against bladder cancer cells.

RESULTS:

In the present study, the impacts and mechanisms of EXCE's antiproliferative effects on bladder cancer cells were assessed, along with its impacts on normal cells. EXCE selectively inhibited proliferation of bladder cancer cells, as compared to normal cells, i.e., selectivity index > 2, and induced greater oxidative stress in bladder cancer cells than normal cells, regarding the induction of cellular and mitochondrial ROS, as well as the depletion of mitochondrial membrane potential. Moreover, EXCE triggered higher levels of apoptosis, both extrinsic and intrinsic caspase activation, and DNA damage in bladder cancer cells than in normal cell; these EXCE-triggered antiproliferative mechanisms were alleviated by N-acetylcysteine (NAC), a ROS inhibitor.

CONCLUSION:

Therefore, EXCE's antiproliferative activity offers a promising therapeutic approach for targeting bladder cancer cells by modulating oxidative stress, while preserving the safety of normal cells.

01 Dec 2026·JOURNAL OF MOLECULAR MEDICINE-JMM

GATA1 controls metadherin transcription to promote oxidative stress-induced podocyte injury

Article

Author: Wu, Wenting ; Zheng, Xiaohong ; Peng, Fenfen ; Chen, Yihua ; Liang, Yunyi ; Zhao, Liyuan ; Tao, Danping ; Luo, Congwei ; Zheng, Zerong ; Shen, Lingyu ; Chen, Xiaowen ; Long, Haibo

Oxidative stress has been demonstrated to induce damage to podocytes, which play a pivotal role in the pathogenesis of chronic kidney disease (CKD). Metadherin (MTDH), an oncogene that has been extensively investigated in various malignancies, also contributes to podocyte injury in CKD. However, the relationship between oxidative stress and MTDH remains poorly elucidated. Here, we show that elevated oxidative stress in CKD serum induced MTDH expression and activated β-catenin signaling in podocytes, which were reversed by N-acetyl cysteine (NAC), a pharmacological antioxidant agent. Therefore, we established the oxidative stress model by administration of Advanced Oxidation Protein Products (AOPPs). As for the mechanism, oxidative stress enhanced MTDH expression both in mRNA and protein levels in podocytes. Furthermore, transcription factor prediction analysis and the Chip-qPCR assay identified that GATA1 was capable of directly binding to the MTDH promoter following AOPP stimulation. Silencing GATA1 repressed MTDH expression induced by AOPPs, while overexpressing GATA1 enhanced MTDH expression and subsequently activated β-catenin signaling. In conclusion, GATA1 induced by oxidative stress triggers MTDH transcription to activate β-catenin signaling, thereby promoting podocyte injury. Thus, targeting the GATA1/MTDH axis may present a promising therapeutic strategy for attenuating oxidative stress-induced damage in podocytes during CKD. KEY MESSAGES: Advanced Oxidative Protein Products (AOPPs) promote the accumulation of oxidative stress in circulation Metadherin is elevated in kidneys of AOPP-induced oxidative stress CKD model mice GATA1 controls transcription of MTDH in renal podocyte of CKD Silencing GATA1/MTDH axis interrupts β-catenin signaling and ameliorates podocyte injury and CKD pathology.

109

News (Medical) associated with Acetylcysteine

18 Jan 2026

·www.sciencedaily.com

The real danger of Tylenol has nothing to do with autism

While social media continues to circulate claims linking acetaminophen to autism in children, medical experts say those fears distract from a far more serious and proven danger: overdose. Acetaminophen, found in Tylenol and many cold and flu remedies, is one of the leading causes of emergency room visits, hospitalizations, and acute liver failure in the United States.Social media and news feeds are filled with unverified claims about a possible connection between acetaminophen and autism in children. But medical experts say the far more serious and well-documented concern is something else entirely: overdose from the widely used pain and fever medication. Acetaminophen poisoning is one of the leading causes of hospitalization and death related to non-prescription drugs in the United States, according to Kennon Heard, MD, PhD, a professor in the CU Anschutz Department of Emergency Medicine and the department's section chief of medical toxicology. Each year, an estimated 56,000 people visit emergency departments because of acetaminophen poisoning, and about 2,600 are hospitalized. The drug is responsible for nearly half of all acute liver failure cases in the U.S. and roughly 20% of liver transplants nationwide. Heard has studied acetaminophen poisoning for more than 25 years. He is now helping to lead a long-term clinical trial that is testing a potential new way to reduce liver damage in severe overdose cases. The experimental approach uses a medication typically given to patients poisoned by antifreeze. Heard says CU and Denver Health, which is home to the Rocky Mountain Poison & Drug Safety center, have played a central role in this research for decades. "have been the center of the acetaminophen research universe for the past 40 years. There's been a long history of this type of work being done here, and it's great to be a part of it." Why Acetaminophen Overdoses Happen Acetaminophen is the main ingredient in Tylenol and many store-brand pain relievers used for mild to moderate pain and low-grade fever. It is also included in a wide range of over-the-counter products for colds, flu, sinus symptoms, and menstrual discomfort. The medication has been used safely for decades when taken according to instructions. Problems arise when people exceed recommended doses, either by taking too much at once or by repeatedly taking more than advised over time. "There are cases where people accidentally take too much acetaminophen," Heard says. "Or maybe they have a really bad toothache, and they think if two is good, four is better, eight is even better, and so on. Or it's someone who's taking multiple repeated overdoses. Those are the people who get into trouble." Overdoses are also frequently linked to suicide and self-harm, Heard notes. "The No. 1 rule at the Poison Center is that if it's available, people will take it, and a lot of people have Tylenol in their medicine chest." Limits of the Standard Antidote For decades, doctors have relied on a drug called acetylcysteine as an effective antidote for acetaminophen overdose. When given early, it can prevent serious liver damage. Its effectiveness drops sharply, however, if treatment begins more than eight hours after the overdose. "The problem is that many patients don't present with acetaminophen poisoning until after they have liver injury, at which point the acetylcysteine is less effective, and in some cases doesn't really work at all," Heard says. Testing an Antifreeze Antidote The current clinical trial led by Heard and his colleagues is focused on fomepizole, a drug approved to treat poisoning from ethylene glycol and methanol, substances commonly found in antifreeze. Exposure can occur accidentally, and in some cases people with alcohol use disorder have consumed antifreeze as a substitute for alcohol. Fomepizole works by blocking enzymes known as alcohol dehydrogenase, stopping the body from converting ethylene glycol and methanol into toxic byproducts. Heard says interest in using fomepizole for acetaminophen overdose dates back to the 1990s, when he was training in medical toxicology. Evidence came from individual patient case reports and animal studies, particularly in severe overdose cases. More recently, research has shown that doctors are increasingly using fomepizole off-label to treat serious acetaminophen poisoning. Richard Dart, MD, PhD, a professor of emergency medicine and Heard's longtime mentor, ultimately suggested formally testing the drug in a clinical trial. Dart has served as director of Rocky Mountain Poison & Drug Safety since 1992. A Proof of Concept Clinical Trial The ongoing phase II trial is designed to determine whether adding fomepizole to standard acetylcysteine treatment can reduce liver damage in patients at high risk after acetaminophen overdose. It is considered a "proof of concept" study to see whether the combination shows enough promise to justify larger trials. Participants are randomly assigned to receive either both medications or acetylcysteine alone. The study is double-blind, meaning neither the patients nor the researchers know which treatment each participant receives until the trial ends. "We'll compare the amount of liver damage, as measured by their liver enzymes, to see whether the fomepizole provides an added protective benefit beyond the standard treatment," Heard says. Patients are currently being enrolled at Denver Health, UCHealth University of Colorado Hospital, Children's Hospital Colorado, and several additional sites. Enrollment has been slow due to the challenge of finding patients who meet the study criteria, but researchers hope to enroll about 40 participants within 12 to 18 months. If the findings are positive, Heard expects the research to move into a larger trial that would examine longer-term outcomes, including survival and the need for liver transplants. A Caution for Medicine Cabinets Everywhere "The message that I would want to get out," Heard says, is that people should carefully read medication labels, avoid exceeding recommended doses, and recognize that acetaminophen may be present in multiple products at home. "We've started to recognize that the number of people who die from an accidental overdose is pretty close to the number of people who deliberately take an overdose," he says. Heard's collaborators on the study include Dart and Andrew Monte, MD, PhD, also a professor of emergency medicine.

Phase 2

08 Jan 2026

·www.sciencedaily.com

Long COVID may be fueled by inflammation and tiny clots

Long COVID affects an estimated 65 million people worldwide and can damage the brain, heart, blood vessels, and immune system long after infection. Researchers now link symptoms to lingering virus, inflammation, micro-clots, and disrupted energy metabolism. While structured rehab and pacing can improve quality of life, a growing list of experimental treatments—from antivirals and metformin to microbiome therapies and biologics—shows early promise. Clear answers, however, are still limited by small studies and the lack of large, definitive trials.Long COVID is defined as symptoms that last at least two months after an initial SARS-CoV-2 infection, with no other clear medical explanation. An estimated 65 million people worldwide are now affected, yet there are still no approved, evidence-based treatments. Researchers are working to better understand what drives the condition and to test a wide range of possible therapies, from structured rehabilitation programs to antivirals, blood thinners, anti-inflammatory drugs, supplements, and new biologic treatments. Scientists believe long COVID is fueled by several overlapping biological problems. These include lingering virus in the body, ongoing low-level inflammation marked by elevated IL-1β, IL-6, and TNF-α, and the formation of tiny blood clots caused by interactions between the viral spike protein and fibrinogen. Other contributing factors include auto-immunity, disruptions in gut bacteria, and impaired mitochondrial function. Together, these processes can damage multiple organs, leading to blood vessel dysfunction, heart inflammation, neuro-inflammation, small-fiber neuropathy, ME/CFS-like fatigue, menstrual changes, problems with blood sugar regulation, and kidney or liver injury. Rehabilitation and Non-Drug Approaches For people with mild symptoms in the early stages, non-drug treatments remain the first option. Clinical trials show that online, group-based physical and mental rehabilitation programs can improve quality of life. Breathing exercises and inspiratory-muscle training have also been shown to boost heart and lung fitness. Additional strategies may include pacing daily activities, cognitive and speech therapy, smell retraining, and dietary counseling. However, exercise that is not carefully supervised can worsen inflammation. For this reason, activity programs need to be gradual and adjusted based on symptoms. Antivirals and Early Treatment Effects Antiviral drugs taken during the initial COVID-19 infection appear to slightly reduce the risk of developing long COVID. In Japan, ensitrelvir lowered long-COVID rates by 25% among out-patients. In high-risk individuals, nirmatrelvir/ritonavir and molnupiravir were linked to about a 25% reduction in risk, while favipiravir showed little benefit. Researchers are also studying monoclonal antibodies that target the spike protein for possible effects on neuro-toxicity, although phase-3 trial results are not yet available. Medications Targeting Specific Symptoms Some treatments focus on particular complications such as clotting, autonomic nervous system problems, and immune imbalance. Low-dose naltrexone has been shown to reduce fatigue and lower platelet aggregation. Apheresis can remove micro-clots and auto-antibodies from the blood, but it is expensive and its benefits tend to be short-lived. Other medications are being tested for symptom relief. β-blockers are used to treat postural-tachycardia syndrome. Famotidine, intravenous immunoglobulin, SGLT-2 inhibitors, and GLP-1 agonists are under investigation for neurological, immune-related, heart, and kidney symptoms. Targeting Inflammation at Its Source Reducing inflammation early appears to be one of the most active areas of research. When started within seven days of infection, metformin lowered the risk of long COVID by 41%, likely by reducing mTOR signaling. Plant-based supplements containing quercetin, curcumin, and piperine improved fatigue compared with placebo. Other approaches include sulphur-thermal-water inhalation and enzymatically liberated salmon oil, both of which lowered CRP levels and helped restore the lung's protective barrier. Baricitinib and rapamycin, which act on JAK and mTOR pathways, are now entering multi-centre trials aimed at interrupting widespread STAT3-driven inflammation. Gut Health, Supplements, and Energy Metabolism Adjusting the gut microbiome may also help. The synbiotic SIM01 eased overall symptoms after six months. Small randomized trials suggest that high doses of vitamins C and D, coenzyme Q10, magnesium, and creatine-glucose blends can improve cellular energy production and blood vessel function. Early-stage studies also report benefits from N-acetyl-cysteine and the amino-acid blend AXA1125, both of which improved mitochondrial respiration and reduced fatigue. Experimental Biologics and Emerging Therapies New biologic treatments are exploring the role of fibrin-driven neuro-inflammation. A humanized antibody that blocks the inflammatory region of fibrinogen is currently in phase-1 trials after animal studies showed protection against neuronal loss. Another experimental therapy, the DNA aptamer BC007, removes G-protein-coupled-receptor auto-antibodies and reversed fatigue and poor capillary blood flow in a single patient, though larger trials are still needed. Other non-drug approaches have shown potential. Hyperbaric oxygen therapy improved cognition, sleep, and pain in a six-month randomized trial. Case series of acupuncture reported reductions in brain-fog and joint pain. Vaccines and Long COVID Outcomes Vaccination provides limited protection against long COVID after breakthrough infections, lowering risk by about 15 to 41%. Among people who already had long COVID symptoms, outcomes after a booster were mixed. About 17% improved, 21% worsened, and 62% saw no change. Where the Science Stands Now Although many potential treatments are showing early promise, most evidence still comes from small or open-label studies that rely on indirect outcome measures. Large, adaptive randomized trials with consistent definitions and biomarker-based patient grouping are urgently needed. Until clearer answers emerge, experts support a flexible, team-based approach that includes early antiviral use, carefully graded exercise, targeted anti-thrombotic and anti-inflammatory treatments, gut microbiome support, and personalized rehabilitation. This strategy reflects the diverse, multi-system nature of long COVID while researchers continue searching for definitive, mechanism-based cures.

Clinical ResultPhase 1Phase 3AHA

15 Dec 2025

·www.businesswire.com

Ophidion, Inc. and Neuronasal, Inc. Announce Strategic Collaborations to Tackle Parkinson’s Disease, Obesity, and Diabetes via Novel CNS Delivery Platform

PASADENA, Calif.--(BUSINESS WIRE)--Ophidion, Inc., a biotechnology company pioneering non-invasive delivery of gene-silencing and large-molecule therapeutics to the brain, and Neuronasal, Inc., a clinical-stage company advancing patented nose-to-brain delivery of therapeutics, today announced a strategic partnership to co-develop multiple therapeutic candidates targeting key pathways in Parkinson’s disease as well as the treatment of obesity and diabetes. Under the agreement, Ophidion will deploy its proprietary intravenous “Trojan-horse” carrier technology to deliver oligonucleotide payloads and peptide therapeutics across the blood-brain barrier aiming to improve brain exposures and clinical outcomes for multiple candidates involved in Parkinson’s disease pathology, as well as another candidate to treat obesity and diabetes. The collaboration spans the full lifecycle -- from proof-of-biology through IND (Investigational New Drug) enabling studies. The deal structure includes upfront and development milestone payments as well as the formation of a joint venture to advance the programs through clinical development once each product reaches the IND stage. Key highlights of the collaboration: Several Parkinson’s-related molecular targets will be advanced in parallel, combining Ophidion’s oligonucleotide/gene-silencing, protein and peptide delivery approach. A single target to treat obesity and diabetes will also be advanced, combining Ophidion’s oligonucleotide/gene-silencing, protein and peptide delivery approach. The programs are advancing de-risked cargos from pre-clinical proof-of-concept into proof-of-biology studies in relevant pre-clinical models prior to IND-enabling work. With the selected cargos and delivery platforms de-risked, the companies anticipate accelerated timelines and improved translational potential for Parkinson’s disease and obesity/diabetes therapies. “We are excited to partner with Neuronasal and advance these therapeutics with our Central Nervous System (CNS)-delivery platform,” said Yacoub Habib, CEO of Ophidion. “Parkinson’s disease remains a major unmet need, and by tackling multiple targets simultaneously, we believe we can increase the probability of success and speed translation into patients. Additionally, improving the delivery of therapeutics to the brain for obesity and diabetes has the potential to produce better efficacy in this commercially attractive market.” Thomas I. Bradshaw, CEO of Neuronasal, added: “Neuronasal is excited to add Ophidion’s brain delivery capability to our Parkinson’s disease developments; combining our expertise with Ophidion’s CNS delivery platform will enhance our clinical program for disease-modifying therapies.” About Ophidion, Inc. Ophidion is an early-stage CNS biopharmaceutical company developing non-invasive therapeutics for neurodegenerative disorders. Its proprietary carrier technology is designed to deliver large molecules and oligonucleotides into the brain via intravenous administration. The company is advancing programs in Huntington’s disease, Alzheimer’s disease, and Parkinson’s disease. (Ophidion) About Neuronasal, Inc. Neuronasal is a clinical-stage biotechnology company focused on nose-to-brain delivery of therapeutics for central nervous system disorders, including Parkinson’s disease and other related CNS diseases. Its intranasal technology is patent-protected and has achieved human pilot proof-of-concept for brain delivery of N-acetylcysteine. It is currently being assessed in Phase 1 clinical trials. (neuronasal.com) Forward-Looking Statements This press release contains forward-looking statements, including statements about the schedule, benefits, and commercial potential of the collaboration and therapeutic programs. Actual results may differ due to risks inherent in biopharmaceutical development, regulatory uncertainties, and the ability to execute on the collaboration.

Phase 1Oligonucleotide

100 Deals associated with Acetylcysteine

External Link

KEGG	Wiki	ATC	Drug Bank
D00221	Acetylcysteine	V03AB23 S01XA08 R05CB01	DB06151

R&D Status

Approved

10 top approved records.

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Indication	Country/Location	Organization	Date
Bronchitis	China	Parexel China Co.,Ltd.	13 May 2025
Nails, Ingrown	Japan	Maruho Co., Ltd.	27 Mar 2023
Acetaminophen overdose	Australia	Pfizer Australia Pty Ltd.	17 Jul 2006
Pulmonary Disease, Chronic Obstructive	China	Jiangsu Jibeier Pharmaceutical Co. Ltd.	01 Jan 1985
Asthma	Japan	Sannova KK	05 Jan 1965
Bronchiectasis	Japan	Sannova KK	05 Jan 1965
Bronchitis, Chronic	Japan	Sannova KK	05 Jan 1965
Cystic Fibrosis	Japan	Sannova KK	05 Jan 1965
Laryngitis	Japan	Sannova KK	05 Jan 1965
Pharyngitis	Japan	Sannova KK	05 Jan 1965
Pneumonia	Japan	Sannova KK	05 Jan 1965
Pulmonary Emphysema	Japan	Sannova KK	05 Jan 1965
Pulmonary Tuberculosis	Japan	Sannova KK	05 Jan 1965
Chemical and Drug Induced Liver Injury	United States	Apothecon LLC	14 Sep 1963
Liver Injury	United States	Apothecon LLC	14 Sep 1963

Developing

10 top R&D records.

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Indication	Highest Phase	Country/Location	Organization	Date
Acute Bronchitis	Phase 3	China	Zambon SpA	21 Jun 2019
Acute Bronchitis	Phase 3	China	Zambon Switzerland Ltd.	21 Jun 2019
Idiopathic Pulmonary Fibrosis	Phase 3	Belgium	Zambon SpA	01 Mar 2000
Idiopathic Pulmonary Fibrosis	Phase 3	France	Zambon SpA	01 Mar 2000
Idiopathic Pulmonary Fibrosis	Phase 3	Germany	Zambon SpA	01 Mar 2000
Idiopathic Pulmonary Fibrosis	Phase 3	Italy	Zambon SpA	01 Mar 2000
Idiopathic Pulmonary Fibrosis	Phase 3	Netherlands	Zambon SpA	01 Mar 2000
Idiopathic Pulmonary Fibrosis	Phase 3	Spain	Zambon SpA	01 Mar 2000
Idiopathic Pulmonary Fibrosis	Phase 3	United Kingdom	Zambon SpA	01 Mar 2000
Common Cold	Phase 2	Canada	Novartis AG	01 Jan 2015

Clinical Result

Indication

Phase

Evaluation

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Study	Phase	Population	Analyzed Enrollment	Group	Results	Evaluation	Publication Date


NCT04155632 (COCA, CTgov)	Phase 2	Cocaine-Related Disorders	32	cTBS (Active Theta Burst Stimulation)	cdizmfsvjy(beztssyjpl) = ngkzrisgpu vcjpyvcmzu (idqmceajrn, 0.0080) View more	-	24 Sep 2025
				cTBS (Sham Theta Burst Stimulation)	cdizmfsvjy(beztssyjpl) = gkdaiuegzy vcjpyvcmzu (idqmceajrn, 0.0105) View more
NCT03707951 (Pubmed \| J Am Acad Child Adolesc Psychiatry)	Phase 2	Alcohol Use Disorder	126	N-acetylcysteine 2400 mg/day	iuazsjwzos(mxbmwpfuhn) = N-acetylcysteine did not significantly reduce alcohol use compared to placebo. voxjzblbzc (kwxjvlabsj ) View more	Positive	01 Sep 2025
				Placebo
NCT06024031 (Pubmed \| Cancer Lett)	Phase 2	Acute Myeloid Leukemia reactive oxygen species (ROS)	30	N-acetyl-L-cysteine	mnnshvtoql(miblucnnpq) = nghbouimns zwivvhekle (gvtecwkykt ) View more	Positive	01 Aug 2025
				N-acetyl-L-cysteine (Control Group)	mnnshvtoql(miblucnnpq) = uunvzklvto zwivvhekle (gvtecwkykt ) View more
NCT03757585 (CTgov)	Phase 4	Learning Disabilities \| Autism Spectrum Disorder \| Autistic Disorder	54	Open-label Treatment with N-acetylcysteine (N-Acetylcysteine)	gjxtjxjuhs(taokpzevfx) = qyookhyuwp rqhcqotcnd (yrklprbmkx, 8.1) View more	-	05 Jun 2025
				Omega-3 Fatty Acids+Inositol (Omega-3 Fatty Acids + Inositol)	kahamrmxtz(eeseploiwg) = fppndwpnqr hshwpnefca (tznidamimh, 7.7) View more
NCT04732000 (CTgov)	Phase 2	stress oxidative \| Pain, Postoperative	30	N-acetyl cysteine (N-acetyl Cysteine)	stsbljtyby(avahwiqmkr) = fnhlubswff lttqtesygl (sabbyoyqsp, atucaozwvl - kgvizoyijl) View more	-	30 Apr 2025
				Normal Saline (Normal Saline)	stsbljtyby(avahwiqmkr) = viwrfiyqrd lttqtesygl (sabbyoyqsp, mokbrcuiyh - dvvgpewclp) View more
NCT00585559 (CTgov)	Phase 3	Aneurysm, Intracranial Berry, 1 \| Vasospasm, Intracranial	44	N-acetylcysteine (N-acetylcysteine IV Infusion at 0.5 gm Hourly)	vsywlclshs(ldtlldtkty) = ujpwnvqggk mwzmvcpusm (zpvcycqvxt, tzadiajjsr - marxbrbmyc) View more	-	18 Apr 2025
				Placebo+N-acetylcysteine (Placebo for N-acetylcysteine IV Infusion at 0.5 gm Hourly)	vsywlclshs(ldtlldtkty) = noqkxipolf mwzmvcpusm (zpvcycqvxt, hxwwihxstc - ekjzxkiwyw) View more
RIBRON (Pubmed \| NEWS) Manual	Not Applicable	Bronchiectasis	2,461	N-AC (1200mg/d)	dnicbmwwnw(lchpavqhjd) = gdzmnoofdk nscurdqyyc (wmnwsvnccs )	Positive	01 Apr 2025
				N-AC (600mg/d)	stlybrosym(fthnryxwmi) = zolmtfejrl qwqurfatzg (sbeuvphghd ) View more
NCT03306979 (CTgov)	Phase 2	Cognitive Dysfunction	60	N Acetylcysteine (N-acetylcysteine)	orapyxjagw(yrhbtyfefc) = nojrrnyebi bqgvttgexn (xfmpcbwxum, kxxosynmep - hkjoorsanm) View more	-	26 Mar 2025
				Placebo oral capsule (Placebo)	orapyxjagw(yrhbtyfefc) = idxmmqewei bqgvttgexn (xfmpcbwxum, eaxbsniiuj - lglsaimafk) View more
NCT04766450 (Pubmed \| Diabetol Metab Syndr)	Phase 4	Diabetic peripheral neuropathy Adjuvant Glutathione peroxidase \| NRF-2 \| TNF	-	N-acetyl cysteine 2400 mg/day	socthuqqkq(dyztbqvwxb) = zvlygseloq ftennzrkcj (cfnnybbjka ) View more	Positive	04 Mar 2025
NCT03707951 (CTgov)	Phase 2	Alcohol Use Disorder	126	N-Acetyl Cysteine (N-acetylcysteine)	qrtoxapnjr(gdkivxrhja) = ooqwgnlmvu slsuzzzczu (vultitfevb, 28.3) View more	-	08 Jan 2025
				Placebo oral capsule (Placebo)	qrtoxapnjr(gdkivxrhja) = ikzisnqikx slsuzzzczu (vultitfevb, 43.1) View more

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Bio

Bio Sequences Search & Analysis

Chemical

Chemical Structures Search & Analysis

Acetylcysteine

Overview

Basic Info

Structure/Sequence

Related

External Link

R&D Status

Clinical Result

Translational Medicine

Deal

Core Patent

Clinical Trial

Approval

Regulation