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

PubMedBasic & clinical pharmacology & toxicology2026-10-15

Evidence on Glutathione and Boosters for Prevention of Chemotherapy-Induced Neuropathy: A Systematic Review and Network Meta-Analysis.

Geum Min Jung MJ, Jeon Jinyoung J, Moon JinYoung J, Lee Hyun Woo HW et al.

Chemotherapy-induced peripheral neuropathy (CIPN) adversely affects treatment efficacy and quality of life. Despite studies on glutathione (GSH) or GSH boosters' antioxidative effects for prevention, optimal management remains uncertain. We conducted a systematic review and network meta-analysis of randomized controlled trials to consolidate and critically appraise the current evidence and to compare the efficacy of GSH and GSH boosters for the prevention of CIPN. The MEDLINE, Embase and CENTRAL databases were searched through March 2025. Twenty-five RCTs involving 1625 patients were included. No intervention significantly reduced all-grade CIPN compared with placebo. N-acetylcysteine (odds ratio [OR] 0.19, 95% credible intervals [CrI] 0.05-0.63), GSH (OR 0.34, 95% CrI 0.13-0.79) and vitamin E (OR 0.33, 95% CrI 0.11-0.91) were associated with a reduced incidence of grade 3/4 CIPN compared with placebo. N-acetylcysteine ranked highest for both all-grade and grade 3/4 CIPN prevention. These findings remained consistent in sensitivity analyses excluding patients with pre-existing neuropathy but were not retained in analyses restricted to double-blind studies. Overall, N-acetylcysteine, GSH, and vitamin E were associated with potential reductions in severe CIPN, with N-acetylcysteine consistently ranking highest, although these associations should be regarded as preliminary. Further rigorously conducted and adequately powered trials are warranted to confirm these findings and evaluate agents demonstrating potential benefits.

PMID 42876024
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PubMedFrontiers in veterinary science2026-10-15

Polystyrene nanoplastics potentiate cadmium-induced pyroptosis and apoptosis in primary duck hepatocytes: differential responses to N-acetylcysteine.

Chen Zhixuan Z, Chen Yan Y, Yu Zhili Z, Xu Qingqing Q et al.

Nanoplastics (NPs) can act as carriers for heavy metals, and co-exposure to NPs and co-pollutants may produce greater toxicity than single exposure. However, the combined toxicity of nanoplastics and heavy metals in poultry liver cells remains poorly understood. Primary duck embryonic hepatocytes (PDEH) were used as an in vitro model. Cells were exposed to polystyrene nanoplastics (PS-NPs, 80 nm, 10 μg/mL) and/or cadmium chloride (CdCl2, 4 μg/mL) for 12 h. Pyroptosis- and apoptosis-associated endpoints were assessed by brightfield microscopy, PI staining, SEM, flow cytometry, qRT-PCR, and Western blotting. The antioxidant N-acetylcysteine (NAC, 5 μg/mL) was used to evaluate the responses of these pathways. Co-exposure to PS-NPs and Cd potentiated cadmium-induced pyroptosis-associated morphological changes, including cell swelling, rounding, membrane blebbing, and surface pore formation. Mechanistically, co-exposure activated the NLRP3/Caspase-1/GSDMD signaling axis, as indicated by increased NLRP3, cleaved Caspase-1 (P20/P10), GSDMD-NT, and intracellular IL-1β maturation. Co-exposure also exacerbated apoptosis-associated changes, including an increased Bax/Bcl-2 ratio and a higher Annexin V-positive cell population. NAC effectively reversed the apoptosis-associated endpoints but did not significantly alter the selected pyroptosis-associated markers under the present in vitro exposure conditions. These findings suggest that PS-NPs potentiate Cd-induced hepatotoxicity in primary duck hepatocytes, with concurrent activation of pyroptosis- and apoptosis-associated signaling. The differential responses to NAC indicate that antioxidant intervention may preferentially attenuate apoptosis-associated injury under the present in vitro exposure conditions, while pyroptosis-associated signaling may require alternative targeted interventions. These results provide new insights into the combined toxicity of nanoplastics and heavy metals in avian hepatocytes.

PMID 42876470
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PubMedEuropean journal of pharmacology2026-10-14

N-acetylcysteine inhibits gene and protein expression of MUC5AC in COPD-relevant human models: evidence from a meta-analysis.

Calzetta Luigino L, Gholamalishahi Shima S, Manzetti Gian Marco GM, Pistocchini Elena E et al.

Chronic mucus hypersecretion is highly prevalent in chronic obstructive pulmonary disease and is associated with worse outcomes. MUC5AC is a key inducible gel-forming mucin driving pathological mucus overproduction. N-acetylcysteine (NAC) is widely used as a mucolytic and exhibits antioxidant and anti-inflammatory properties. Its quantitative impact on MUC5AC regulation has not been formally synthesized. We performed a systematic review and meta-analysis (OSF registration ID: 2vym4) of original studies evaluating the effect of NAC on MUC5AC gene and protein expression in human respiratory cell models of mucus hypersecretion. Standardized mean differences with 95% CIs were pooled using DerSimonian-Laird random-effects models. Heterogeneity, publication bias, sensitivity analyses, and random-effects meta-regression on NAC dose were conducted. Fifteen articles were included. NAC significantly reduced MUC5AC mRNA (standardized mean difference -1.30, 95% CI: -1.61 to -0.98; I2=37.07%), without significant dose-response. NAC produced very large reductions in extracellular (-2.70, 95% CI: -3.29 to -2.11; I2=48.89%) and intracellular (-2.38, 95% CI: -3.27 to -1.48; I2=67.35%) MUC5AC protein, with significant dose-response relationships for both. After sensitivity analyses, the pooled protein effect remained very large (-2.00, 95% CI: -2.38 to -1.62; I2=25.63%). Funnel plots and Egger's tests suggested publication bias, which diminished after exclusion of influential comparisons. NAC robustly inhibits MUC5AC gene and protein expression in human pre-clinical models of mucus hypersecretion, supporting a strong mucoregulatory action that complements mucolytic and antioxidant effects. These data reinforce the rationale for NAC use in chronic obstructive pulmonary disease patients with a hypersecretory phenotype.

PMID 42874904
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PubMedFrontiers in immunology2026-10-14

SPHK1 drives pyroptosis via ROS-dependent activation of the NLRP3 inflammasome in non-infectious uveitis.

Hu Lili L, Pan Shaoxin S, Wang Jing J, Mei Suyin S et al.

Non-infectious uveitis associated with systemic diseases is a sight-threatening inflammatory disorder often associated with dysregulated immune responses and oxidative stress. Although redox imbalance is thought to contribute to its pathogenesis, the precise molecular mechanisms remain poorly defined. We performed transcriptomic analysis of human non-infectious uveitis datasets (GSE17114 and GSE18781) encompassing Behçet's uveitis (BU), sarcoidosis-associated uveitis, and spondyloarthropathy (SpA)-associated uveitis, combined with experimental validation to elucidate oxidative stress-associated mechanisms. We identified 1,821 differentially expressed genes (DEGs) enriched in immune cell migration, T and B cell signaling, and T cell activation pathways. Among the oxidative stress-associated DEGs, six genes were validated in patients with BU: SPHK1, MMP8, and ARG1 were upregulated, while CCR7, PDGFD, and DDIT4 were downregulated. Knockdown of SPHK1 reduced ROS production, lipid peroxidation, and NLRP3 inflammasome-mediated pyroptosis, decreasing IL-1β and IL-18 secretion; SPHK1 overexpression promoted pyroptosis, reversed by the ROS inhibitor N-acetylcysteine. Molecular docking revealed strong binding affinity between SPHK1 and dexamethasone. All six oxidative stress-related DEGs demonstrated strong diagnostic potential. Immune cell abundance profiling revealed a significant decrease in activated CD4+ T cells, memory B cells, and NK cells in peripheral blood. Collectively, our findings highlight SPHK1 as a key mediator of oxidative stress-induced pyroptosis in non-infectious uveitis and propose the SPHK1-ROS-pyroptosis axis as a potential therapeutic target.

PMID 42870831
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PubMedTranslational oncology2026-10-14

NR3C2 suppresses triple-negative breast cancer progression by regulating mitochondrial ROS homeostasis via NDUFB3.

Shi Haihong H, Zeng Xian X, Guo Qiaonan Q, Lin Jianqing J

Triple-negative breast cancer (TNBC) is an aggressive subtype of breast cancer characterized by high molecular heterogeneity and a lack of effective targeted therapies. Increasing evidence indicates that metabolic reprogramming and redox homeostasis are critical determinants of TNBC progression; however, the transcriptional mechanisms linking these processes to mitochondrial function remain incompletely understood. In this study, integrative bioinformatics analyses identified nuclear receptor subfamily 3 group C member 2 (NR3C2) as a potential regulatory factor in TNBC. NR3C2 expression was significantly decreased in TNBC and was associated with patient prognosis. Functional assays demonstrated that NR3C2 overexpression markedly inhibited cell proliferation and migration in vitro and suppressed tumor growth and dissemination in zebrafish xenograft models. Mechanistically, RNA sequencing identified NDUFB3, an accessory subunit of mitochondrial complex I, as a downstream target of NR3C2. Dual-luciferase reporter assays further confirmed that NR3C2 directly regulates NDUFB3 transcription. Functional analyses revealed that NR3C2 modulates mitochondrial activity, as evidenced by increased mitochondrial membrane potential and complex I activity, accompanied by reduced ATP production and elevated reactive oxygen species (ROS) levels. Notably, NR3C2-induced ROS accumulation promoted apoptosis, whereas these effects were partially reversed by NDUFB3 knockdown or treatment with the ROS scavenger N-acetylcysteine (NAC). Consistently, in vivo experiments demonstrated that NR3C2 suppresses tumor growth and metastasis in a ROS-dependent manner. Collectively, these findings indicate that NR3C2 inhibits TNBC progression by regulating mitochondrial function and ROS homeostasis, at least in part through NDUFB3. This study provides new insights into the interplay between transcriptional regulation and mitochondrial redox balance and highlights NR3C2 as a potential therapeutic target for TNBC.

PMID 42874536
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PubMedCNS & neurological disorders drug targets2026-10-13

Aging-driven Mechanisms Underlying Parkinson's Disease Pathogenesis: Molecular, Cellular, and Systemic Perspectives.

Lee Amanda Yee Jing AYJ, Khoo Leanne L, Ng Khuen Yen KY, Chye Cien Leong CL et al.

Aging is a major risk factor for Parkinson's Disease (PD) and is linked to various biological processes at the molecular, cellular, and systemic levels. At the molecular level, aging-related oxidative stress, mitochondrial dysfunction, genetic factors, and impaired proteostasis contribute to dopaminergic neuronal death. Cellular alterations include persistent glial cell activation, autophagylysosomal dysfunction, and impaired cellular repair mechanisms. At the systemic level, aging is associated with metabolic imbalance, gut microbiota dysbiosis, and immune system dysfunction, which may contribute to PD pathogenesis through the gut-brain axis. Antioxidant therapy, stem cell therapy, anti-aging agents, and modulation of gut-brain communication have shown promise in the management of PD. Lifestyle modifications, including dietary changes and regular exercise, may exert anti-aging effects that could help delay or prevent the onset of PD. Emerging anti-aging interventions, including N-acetylcysteine and plant-derived compounds that support mitochondrial function, have also demonstrated therapeutic potential for PD.

PMID 42864799
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