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acetylcysteine

✓ Approved

Cumberland Pharmaceuticals Inc · 小分子 · 小分子

什么是 acetylcysteine？

acetylcysteine 是一种小分子，由Cumberland Pharmaceuticals Inc研发。该药已获批，用于治疗相关适应症，给药途径：Injectable (Others)、Intravenous (IV)。

药物档案

公司Cumberland Pharmaceuticals Inc
药物类别小分子
给药途径Injectable (Others), Intravenous (IV)
状态Approved
来源： ClinicalTrials.gov, Cumberland Pharmaceuticals Inc

治疗适应症

acetylcysteine 针对 2 个适应症，涉及 2 个治疗领域。

治疗领域疾病/病症分期
Hepatobiliary disordersHepatic function abnormal✓ Approved
Injury, poisoning and procedural complicationsToxicity to various agents✓ Approved

相关研究文献

PubMedFree radical research2026-07-27

Beyond Antioxidant Activity, Towards Redox Modulation: N-Acetylcysteine (NAC) in Endometriosis and Uterine Leiomyomas.

Mohebbi Lili L, Sanz Maset Angela A, Macri Valeria V, Jospeh Emily E et al.

Endometriosis and uterine leiomyomas are common chronic gynecologic diseases associated with immune dysregulation, inflammation and aberrant cellular proliferation, processes that contribute to increased oxidative stress. Current management relies largely on surgical and hormonal interventions, highlighting the need for effective long-term nonhormonal therapeutic strategies. N-acetylcysteine (NAC), a glutathione precursor, exhibits antioxidant and anti-inflammatory properties that may target key mechanisms underlying both conditions. NAC functions as both a direct reactive oxygen species scavenger and regulator of intracellular redox homeostasis through replenishment of glutathione stores. These findings suggest that NAC may represent a potential adjunctive therapy warranting further investigation and may influence disease-associated biological pathways. Future clinical and translational studies are needed to define its efficacy, optimal dosing, and role in redox-based management of endometriosis and uterine leiomyomas.

PMID 42506968
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PubMedMetabolites2026-07-27

The Effects of Short-Term N-Acetylcysteine Supplementation on Biochemical Parameters in Endurance-Trained Adults: A Randomized Clinical Trial.

Sadowski Marcin M, Zawieja Emilia E, Muzsik-Kazimierska Agata A, Bulczak Ewa E et al.

Background: The main aim of this study was to assess the effects of short-term N-acetylcysteine (NAC) supplementation on concentrations of homocysteine (Hcy) and reduced glutathione (rGSH), blood lipid profile and liver enzyme activities in endurance-trained adults, and to determine whether these effects are modified by methylenetetrahydrofolate reductase (MTHFR) C677T and glutathione S-transferase Pi 1 (GSTP1) A313G. Methods: A total of 56 males and 21 females completed a randomized, double-blind, placebo-controlled crossover trial. Participants received 1200 mg of NAC or a placebo for seven days in a crossover design. Serum Hcy and plasma rGSH concentrations were assessed using dedicated biochemical assays, while blood lipid profile and liver enzyme activities were measured using the biochemical analyzer Konelab 20i. Genotyping was conducted using TaqMan probes. A series of within-subject/between-subject repeated-measures analysis of variance (ANOVA) within a general linear model framework were performed to compare Hcy, rGSH, blood lipid profile and liver enzymes activities before and after the intervention. Results: Hcy concentrations significantly decreased following NAC supplementation (18.58 ± 5.45 µmol/L vs. 16.51 ± 4.97 µmol/L; p = 0.009), although subgroup analysis indicated that the decrease was significant only among females (15.40 ± 4.96 µmol/L vs. 13.60 ± 3.68 µmol/L; p = 0.002) without any significant effect among males. We did not observe any significant changes in rGSH, lipid profile, or liver enzyme activities. There was no interaction between NAC supplementation, MTHFR and GSTP1 genotypes and the changes noted in the parameters we analyzed. Conclusions: In conclusion, short-term NAC supplementation may reduce circulating Hcy concentrations in endurance-trained adults, particularly in females. No consistent effects were observed for rGSH, lipid profile, or liver enzyme activities.

PMID 42506456
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PubMedGels (Basel, Switzerland)2026-07-27

Formulation Feasibility of a Mechanically Compliant Stearate Organogel-Methylcellulose/Gelatin Bigel for Localized Neurotherapeutic Delivery.

Moswatsi Botle Matha BM, Mahumane Gillian Dumsile GD, Kumar Pradeep P, Choonara Yahya Essop YE

Traumatic brain injury (TBI) presents a mechanically sensitive and pharmacologically complex environment in which therapeutic delivery remains challenging. Bigels may offer a formulation strategy for incorporating therapeutics with differing physicochemical properties while providing soft, viscoelastic matrices with properties that may be relevant to neural delivery applications. This study evaluated the in vitro formulation feasibility of a biphasic stearate organogel-methylcellulose/gelatin bigel as a mechanically compliant biphasic vehicle for localized delivery of neurotherapeutic agents. Bigels were fabricated by hot emulsification and genipin crosslinking to generate hydrogel-dominant dual-phase systems. Hydrogel:organogel formulations of 95:5 (BG1) and 85:15 (BG2) showed storage moduli of approximately 250 Pa and 200 Pa, respectively, and compressive Young's moduli of 0.39 and 0.70 kPa, within reported ranges for soft brain tissue. Stress relaxation confirmed viscoelastic behaviour, while minimal oil leakage (<0.2%) indicated phase stability. BG1 showed 52% porosity, pore sizes of 1.8-22 µm, and approximately 14% weight gain. Drug release followed Weibull kinetics (R2 = 0.99-0.999), with nicotinamide showing faster release and N-acetylcysteine and TPGS showing more sustained release. Both unloaded and drug-loaded bigels maintained >70% PC12 cell viability. These findings support the formulation feasibility of biphasic bigels as mechanically compliant vehicles capable of accommodating therapeutics with differing physicochemical properties and exhibiting differential release behaviour. Further studies are required to evaluate degradation, tissue interactions, retention, and therapeutic performance in advanced in vitro and in vivo models.

PMID 42505258
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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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