Drug Database
AC

acetylcysteine

✓ Approved

Cumberland Pharmaceuticals Inc · Small Molecule · Small Molecule

What is acetylcysteine?

acetylcysteine is a small molecule developed by Cumberland Pharmaceuticals Inc. It is approved for therapeutic indications via injectable (others) or intravenous (iv).

Drug Profile

CompanyCumberland Pharmaceuticals Inc
Drug ClassSmall Molecule
RouteInjectable (Others), Intravenous (IV)
StatusApproved
Sources: ClinicalTrials.gov, Cumberland Pharmaceuticals Inc

Therapeutic Indications

acetylcysteine is developed for 2 unique indications across 2 therapeutic areas.

Therapeutic AreaConditionPhase
Hepatobiliary disordersHepatic function abnormal✓ Approved
Injury, poisoning and procedural complicationsToxicity to various agents✓ Approved

Related Research Articles

PubMedUrologia2026-07-25

Testicular damage from electromagnetic radiation in rats and evaluation of protective agents.

Gözüküçük Ali A, Çakıroğlu Basri B, Uyanik Bekir Sami BS, Kılıç Hasan Hüseyin HH et al.

Male infertility has been associated with various environmental, physiological, and genetic factors. In recent years, the widespread use of mobile phones has raised concerns regarding exposure to electromagnetic radiation (EMR). EMR emitted from mobile devices may adversely affect male reproductive function by inducing oxidative stress and impairing spermatogenesis. This study aimed to evaluate the potential protective effects of vitamin E and N-acetylcysteine (NAC) against EMR-induced testicular damage in rats. A total of 35 adult male Wistar rats were randomly divided into five groups (n = 7 per group): control, EMR exposure, EMR + NAC, EMR + vitamin E, and EMR + NAC + vitamin E. Rats were exposed to EMR generated by a mobile phone operating in the GSM frequency band (900/1800 MHz) in active call mode, positioned at a fixed distance of 15 cm from the cages, for 3 h daily over 28 days. The specific absorption rate (SAR) was based on manufacturer-reported values. Biochemical analyses were performed to assess total antioxidant capacity (TAC), glutathione peroxidase (GPX), superoxide dismutase (SOD), and malondialdehyde (MDA) levels. Data distribution was evaluated using the Shapiro-Wilk test, and group comparisons were conducted using the Kruskal-Wallis test with appropriate post-hoc analyses. Significant differences were observed among groups in terms of total antioxidant capacity (TAC) (p < 0.001). TAC levels were reduced in the EMR-only group compared to controls, whereas antioxidant supplementation (NAC and/or vitamin E) resulted in increased TAC levels. Post-hoc analyses demonstrated significant improvements in TAC in treatment groups compared to both control and EMR-only groups. However, no statistically significant differences were observed among groups for GPX, SOD, and MDA levels (p > 0.05). N-acetylcysteine (NAC) and vitamin E may exert partial protective effects against EMR-induced oxidative alterations in rat testes, particularly as reflected by improvements in total antioxidant capacity. However, given that other oxidative stress markers did not demonstrate statistically significant differences, these findings should be interpreted with caution. Further experimental and clinical studies with larger sample sizes and detailed histopathological evaluation are required to better elucidate the potential therapeutic role and clinical relevance of these antioxidant agents.

PMID 42499284
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PubMedToxicology2026-07-24

Exposure to polystyrene nanoplastics provokes vascular endothelial senescence through eliciting nucleolar stress.

Wang Linjuan L, Wan Yiqi Y, Wu Lihai L, Cao Huaming H et al.

Polystyrene nanoplastics (PS-NPs) are emerging environmental contaminants with unclear cardiovascular impacts. This study evaluated PS-NPs-induced endothelial senescence using murine models and HUVECs. PS-NPs caused aortic wall thickening and structural disruption in mice, and induced DNA damage, apoptosis, cell cycle arrest, and impaired migration/vasculogenesis in vitro. Both models showed excessive ROS production and nucleolar stress (NPM1 relocalization), leading to premature senescence via p53/p21 upregulation. These effects were reversed by NPM1 inhibitor NSC348884 or ROS scavenger N-acetylcysteine. Collectively, PS-NPs promote vascular endothelial senescence through ROS-dependent nucleolar stress, highlighting their vasotoxic potential and cardiovascular risks.

PMID 42492616
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PubMedActa neuropathologica2026-07-24

Targeting chordoma via an isocitrate dehydrogenase-1-dependent susceptibility to redox metabolism.

Pun Matthew M, Deogharkar Akash A, Natarajan Siva Kumar SK, Nuechterlein Nicholas N et al.

Chordomas are rare cancers that arise along the axial skeleton. Alterations in metabolism are a hallmark of cancer, and we sought to identify metabolic vulnerabilities in chordoma. We discovered that the tricarboxylic acid (TCA)-related enzyme isocitrate dehydrogenase-1 (IDH1) was expressed highly in bulk and single-cell patient-derived chordomas and was associated with worse survival outcomes. IDH1 catalyzes the conversion of isocitrate and nicotinamide adenine dinucleotide phosphate (NADP+) to alpha-ketoglutarate (⍺-KG) and NADPH. This critical reaction influences TCA cycle metabolism, regulates epigenetic pathways, and affects redox balance. Both IDH1 knockdown and treatment with an inhibitor targeting IDH1 were toxic to chordoma cells. An integrated analysis of the transcriptomic, chromatin, and metabolomic responses on IDH1 inhibition converged on deregulated glutathione metabolism. IDH1 inhibition was associated with increased expression and enrichment of activating H3K27ac at NRF2 (nuclear factor erythroid 2-related factor 2) signature genes including those in the glutathione biosynthetic pathway. This was accompanied by reduction of both NADPH/NADP+ and reduced/oxidized glutathione (GSH/GSSG) ratios. Importantly, IDH1 inhibitor-driven toxicity was rescued via media supplementation with the antioxidant N-acetylcysteine, suggesting that IDH1 inhibition in chordomas creates a redox-dependent metabolic vulnerability. Finally, IDH1 inhibitor treatment reduced tumor growth in two independent chordoma mouse xenograft models. Our findings suggest a potential therapeutic avenue for further exploration in chordoma.

PMID 42493667
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PubMedEcotoxicology and environmental safety2026-07-24

Quercetin alleviates high fluoride-induced hepatocyte ferroptosis via regulating the ROS/PERK signaling pathway.

Song Chao C, Yu Rui R, Zhang Aiguo A, Yan Yibo Y et al.

Ferroptosis is closely associated with fluoride-induced liver injury. As a natural flavonoid with potent anti-ferroptotic activity, quercetin (Que) could mitigate fluoride-triggered hepatotoxicity. Therefore, the aim of this study was to investigate the protective effects of Que against sodium fluoride (NaF)-induced ferroptosis and to elucidate its molecular mechanisms. In vivo data demonstrated that Que restored liver function, ameliorated hepatic pathological lesions, and alleviated mitochondrial damage in NaF-exposed mice. Additionally, Que suppressed NaF-induced apoptosis and inflammation. Both in mouse liver tissues and AML-12 cells, Que exerted anti-ferroptotic actions via restraining reactive oxygen species (ROS) and lipid peroxidation, alleviating iron overload, increasing reduced to oxidized glutathione (GSH/GSSG) ratio and GSH content, altering the expression of ferroptosis-related proteins including glutathione peroxidase 4, Acyl-CoA synthetase long-chain family member 4, transferrin receptor, and ferritin heavy chain 1. Mechanistically, molecular docking combined with molecular dynamics simulations indicated the high reliability and stability of Que binding to Protein kinase R-like ER kinase (PERK). Que inhibited the activation of PERK signaling pathway. Pharmacological intervention assays verified that PERK inhibitor GSK2606414 mimicked Que's anti-ferroptotic effects, whereas PERK agonist CCT abolished Que-mediated protection against NaF-induced ferroptosis. Importantly, ROS elimination by N-acetylcysteine suppressed PERK activation and subsequent ferroptosis triggered by NaF. Overall, Que mitigates NaF-induced hepatic ferroptosis via inhibiting the ROS/PERK signaling pathway, highlighting its potential therapeutic application against high fluoride-induced hepatotoxicity.

PMID 42492176
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PubMedFrontiers in pediatrics2026-07-23

Uncertain timing of reported acetaminophen ingestion in an adolescent analgesic overdose: a case report.

Alghamdi Wael A WA

A 16-year-old male presented after reported ingestion of acetaminophen and multiple NSAIDs for dental pain. Although he reported taking acetaminophen 6,000 mg, his concentration was 22.3 mg/L approximately 19 h after the first reported ingestion, higher than expected from the reported dose and timing. Aminotransferases were normal, indicating no acetaminophen-induced liver injury at presentation. N-acetylcysteine was initiated because the concentration was clinically relevant in the setting of uncertain or staggered ingestion, and recovery was uneventful. This case highlights the importance of prioritizing measured acetaminophen concentrations and laboratory assessment over reported dose alone.

PMID 42488230
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PubMedPain reports2026-07-23

Efficacy of N-acetylcysteine in enhancing paracetamol's analgesic effect and inhibiting hepatotoxicity: a preclinical mouse model.

Chrétien Basile B, Goy Romain R, Guillaume Mickaël M, Bazin Guillaume G et al.

Paracetamol (PCM) is extensively administered in clinical settings to alleviate mild to moderate pain and/or decrease fever. However, noncompliance with prescribed dosages can lead to severe and irreversible liver damage from PCM overdose. Although N-acetylcysteine (NAC) serves as the standard antidote for PCM toxicity, no commercially available combination of PCM and NAC has been marketed to mitigate its toxic effects. Objectives: This study aims to evaluate both the antinociceptive and hepatoprotective effects of the PCM and NAC combination in a murine model. Male and female C57Bl6/J mice were assigned to 4 groups. Group A received oral PCM exclusively, administered every 6 hours (4 doses within 24 hours), whereas groups B-D were administered PCM alone, a combination of PCM/L-NAC (N-acetyl-l-cysteine), or PCM/D-NAC (N-acetyl-d-cysteine) every 4 hours (6 doses within 24 hours). Both PCM/L-NAC and PCM/D-NAC combinations yielded superior analgesia compared with the standard regimen. Furthermore, L-NAC administration mitigated the increase of glutamate pyruvate transaminase, a key hepatic marker associated with PCM hepatotoxicity. In addition, a protective effect from D-NAC in conjunction with PCM on glutathione levels was suggested. Our findings suggest that NAC enhances the analgesic properties of PCM while concurrently reducing its hepatotoxic potential in mice. Moreover, data indicate that L-NAC may represent a more effective candidate than D-NAC for this purpose, particularly regarding hepatoprotection. This study presents novel insights into the synergistic effects of the PCM/NAC combination on pain relief and hepatic safeguarding, warranting consideration for the development of novel therapeutic strategies targeting pain and fever management in patients.

PMID 42491779
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