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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

PubMedAnnals of medicine and surgery (2012)2026-09-11

Favorable outcome in paraquat poisoning with acute kidney injury in a resource-limited setting: a case report.

Shah Ujjwal Kumar UK, Koirala Achyoot Sharan AS, Hathi Kanchan K, Pandey Parishrut Prasad PP et al.

Paraquat poisoning remains a major public health challenge in Asia, with a mortality rate of 60%-80%, and acute kidney injury being a common complication. An 18-year-old female presented 6 hours after ingestion of approximately 5 mL of 24% (1.2 g) paraquat. Gastric lavage was performed within 30 minutes. She developed oral mucosal ulcers, dysphagia, and progressive AKI with serum creatinine rising from 1.0 mg/dL on the day of admission to 7.3 mg/dL by day 6 (eGFR declining from 83.7 mL/min/1.73m2 to 7.7 mL/min/1.73 m2). Chest radiography on day 3 showed prominent bronchovascular markings, and liver enzymes were significantly elevated. Despite indications for hemodialysis, it was not performed due to financial constraints. The patient was managed with intensive supportive care, including corticosteroids, N-acetylcysteine, antibiotics, proton pump inhibitors, and fluid resuscitation. Three-month follow-up showed no respiratory, gastrointestinal, or renal manifestations. Favorable prognostic factors included young age, rapid gastric decontamination, a moderate ingested dose (26 mg/kg), relatively preserved initial renal function, and early, aggressive supportive therapy. This case demonstrates that survival is possible in cases of moderate-dose paraquat poisoning with AKI, even without hemodialysis, when early supportive care is promptly initiated. While this single case cannot be generalized, it highlights the critical importance of rapid decontamination and aggressive supportive management in resource-limited settings where paraquat remains readily accessible, and it underscores the need for further research to develop affordable, evidence-based treatment protocols for paraquat poisoning in developing countries.

PMID 42724759
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PubMedFrontiers in medicine2026-09-10

Clinical efficacy, safety evaluation, and mechanism of acetylcysteine in improving first-line anti-tuberculosis treatment of newly diagnosed pulmonary TB: an open-label, randomized, single-center trial.

Zhang Huan H, Liu Ming M, Shi Lu L, Wang Xianlei X et al.

To investigate the clinical efficacy, safety and mechanism of N-acetylcysteine combined with conventional antituberculosis drugs in the treatment of newly diagnosed pulmonary tuberculosis. A total of 90 newly diagnosed pulmonary tuberculosis patients were randomly assigned to a Control group (n = 30), Aerosol NAC group (n = 30), or Oral NAC group (n = 30). The Control group received standard HRZE therapy, whereas the Aerosol NAC and Oral NAC groups received additional nebulized N-acetylcysteine (300 mg twice daily) or oral N-acetylcysteine (600 mg once daily), respectively. Clinical efficacy, sputum conversion, St. George's Respiratory Questionnaire (SGRQ) scores, liver function indices, oxidative stress biomarkers, inflammatory markers, and adverse events were assessed over 3 months. Data were analyzed using one-way ANOVA, repeated-measures ANOVA, Chi-square tests, and Bonferroni-adjusted post hoc analyses. Treatment successful response rates were significantly higher in the Aerosol NAC group (96.67%) and Oral NAC group (93.33%) than in the Control group (70.00%) (p < 0.05). At 3 months, sputum conversion rates reached 93.33 and 96.67% in the Aerosol NAC and Oral NAC groups, respectively, compared with 73.33% in the Control group (p < 0.05). Both NAC groups demonstrated significantly lower SGRQ scores, improved liver function parameters (AST, ALT, TBIL, and GGT), higher antioxidant enzyme levels (SOD and GSH-Px), lower MDA concentrations, and reduced inflammatory markers (IFN-γ, PCT, and IL-4) compared with the Control group (all p < 0.05). The incidence of adverse reactions was lower in both NAC groups (10.0%) than in the Control group (40.0%) (p < 0.05). Adjunctive N-acetylcysteine, administered either by aerosol inhalation or orally, significantly improved treatment outcomes, accelerated sputum conversion, reduced oxidative stress and inflammation, protected liver function, and decreased adverse events in patients with newly diagnosed pulmonary tuberculosis.

PMID 42718567
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PubMedJournal of medicinal chemistry2026-09-10

Potent Anticancer Tethered Organorhodium(III) Complexes Target the Mitochondria.

Villechenous Rojo Arturo A, Rodríguez-Fanjul Vanessa V, Pizarro Ana M AM

We report a family of tethered rhodium(III) complexes of formula [Rh(η5:κ1-C5Me4(CH2)npyN)(C,N)]+ (n = 1 or 2; C,N = 2-phenylpyridine or benzoquinoline), their nontethered analogues, and their iridium(III) counterparts. The tethered pyridine, κ1-coordinated to the metal, does not dissociate in water, yet the metal-Npy(tether) bond can be cleaved by strong nucleophiles, enabling metal activation. We corroborated that metal-Z bond reactivity correlated with cytotoxicity in breast cancer cells; complexes lacking reactive metal-Z bonds exhibited low anticancer potency, while excessive reactivity impaired efficacy likely through off-target reactions. For the highly potent tethered complexes, we determined the kinetics of pyridine cleavage using DMSO and confirmed that N-acetylcysteine can also promote pyridine dissociation. In tethered complexes, metal-mediated reactivity is crucial to potency, as metal-pyridine bonds with higher activation energy produce complexes less damaging to cells. We confirmed mitochondrial involvement in cell death, demonstrating that the most cytotoxic complexes inhibit OXPHOS more efficiently.

PMID 42720496
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PubMedPloS one2026-09-10

N-acetylcysteine attenuates oxidative-stress-associated apoptosis and collagen deposition after rat hindlimb ischemia-reperfusion injury.

Matsunaga Hideto H, Yonemitsu Ryuji R, Ideo Katsumasa K, Ide Junnosuke J et al.

Proper use of fingers and limbs is crucial for people to carry out normal activities of daily living. Therefore, when fingers or limbs are severed accidentally, replantation is attempted whenever possible. However, even when replantation is successful and fingers or limbs are preserved, functional limitations often arise due to contractures in reattached fingers or limbs, although mechanisms underlying contractures or countermeasures to ameliorate them are not well understood. Here, using a rat femoral artery ischemia-reperfusion (I/R) model, we show that oxidative stress caused by accumulation of oxidative DNA damage occurs in gastrocnemius and soleus muscles after I/R induces muscle cell apoptosis. Moreover, we demonstrate that administration of the antioxidant N-acetyl cysteine (NAC) significantly suppresses oxidative stress accumulation and apoptosis induction in both muscles. We observed that collagen fibers accumulate in the gastrocnemius and soleus muscles after I/R in our model, and that collagen fiber accumulation was significantly suppressed by NAC administration. We demonstrate that adding hydrogen peroxide (H2O2), a reactive oxygen species (ROS), to an in vitro C2C12 myoblast culture system significantly increased expression of the apoptosis-inducing factors Bcl-2-associated X protein (BAX) and Caspase 3, while co-treatment with NAC significantly counteracted this increase and increased expression of the anti-apoptotic factor B-cell lymphoma 2 (Bcl2). Also using the C2C12 myoblast culture system, we show that H2O2 significantly increased expression of Cellular Communication Network Factor 2 (CCN2), which induces fibrosis, while co-addition of NAC with H2O2 significantly suppressed CCN2 induction. Our findings shed light on mechanisms underlying I/R injury in limbs and suggest countermeasures.

PMID 42721182
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PubMedMedical oncology (Northwood, London, England)2026-09-10

p-Coumaric acid inhibits hepatocellular carcinoma through promoting ROS accumulation.

Zheng Jiahao J, Zhang Quanming Q, Wang Leyi L, Yuan Mengcheng M et al.

Hepatocellular carcinoma (HCC) remains one of the most life-threatening diseases. The regulation of redox homeostasis plays a pivotal role in the progression of HCC. p-Coumaric acid (PCA), a naturally occurring compound, exhibits diverse pharmacological activities; however, its potential anti-HCC effects have not been previously reported. This study aimed to investigate the potential anti-HCC effects of PCA, with a focus on its role in modulating reactive oxygen species (ROS) accumulation in HCC cells. The anti-HCC effects of PCA were evaluated through in vitro and in vivo experiments. In vitro assays, including cell growth, proliferation, wound healing, and Transwell migration, assessed PCA's inhibitory effects, while flow cytometry analyzed apoptosis. Mitochondrial function and ROS levels were measured, with the nuclear factor erythroid 2-related factor 2 (Nrf2) pathway's role explored. In vivo, a subcutaneous xenograft mouse model, using NAC as a ROS scavenger, validated PCA's effects. PCA significantly inhibited the growth and proliferation ability of HCC cells. It also impeded cell migration and induced cell shrinkage and apoptosis. Moreover, PCA suppressed the levels of anti-apoptotic and pro-proliferative proteins. From a mechanistic perspective, PCA reduced mitochondrial membrane potential and ATP production, subsequently promoting ROS accumulation. The inhibition of the Nrf2 signaling pathway by PCA further enhanced ROS levels. Hemin, an agonist of the antioxidant enzyme HO-1, counteracts the inhibitory effect of PCA on the viability of HCC cells. And, in vivo experiments demonstrated that the anti-HCC effects of PCA were reversed by N-acetylcysteine, confirming the critical role of ROS in PCA-mediated inhibition of HCC progression. Our findings indicate that PCA suppresses HCC progression by promoting ROS accumulation, suggesting its therapeutic potential for HCC.

PMID 42720830
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PubMedClinical and translational gastroenterology2026-09-09

Topical Vitamin C and N-Acetylcysteine for Reducing Symptoms After Lugol Chromoendoscopy: A Multicenter Randomized Controlled Trial.

Fu Xuan X, Chang Jiali J, Peng Shiyu S, Li Chenlu C et al.

Lugol chromoendoscopy improves detection of esophageal squamous neoplasia but can cause short-term retrosternal and pharyngeal discomfort. We evaluated topical vitamin C solution (VCS) and N-acetylcysteine (NAC) after Lugol staining. In this multicenter, randomized, double-blind, saline-controlled trial, 748 participants were allocated 1:1:1 to 0.9% normal saline (NS), 2% VCS, or 10% NAC after Lugol chromoendoscopy. The co-primary outcomes were overall post-procedure symptoms at 15 and 30 minutes. The main efficacy analysis was complete-case and included 681 participants; extreme-case analyses evaluated the effect of missing outcomes. At 15 minutes, symptoms occurred in 44.34% of the NS group, 8.80% of the VCS group, and 9.43% of the NAC group. Relative risks versus NS were 0.198 (95% CI 0.126-0.312) for VCS and 0.213 (95% CI 0.140-0.322) for NAC. At 30 minutes, the corresponding incidences were 31.67%, 4.17%, and 4.10%, with relative risks of 0.132 (95% CI 0.067-0.257) and 0.129 (95% CI 0.068-0.245). Conclusions were unchanged in extreme-case sensitivity analyses. VAS category distributions favored both active-treatment groups. Median time to onset of decolorization was 11 seconds with NS and 2 seconds with each active solution; median time to complete decolorization was >180, 6, and 12 seconds, respectively. Topical VCS and NAC each reduced short-term symptoms after Lugol chromoendoscopy compared with NS and promoted rapid mucosal decolorization. The direct comparison between VCS and NAC was exploratory and does not establish equivalence or non-inferiority.

PMID 42715145
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