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

PubMedBMC plant biology2026-07-17

Cysteine derivatives coordinate photosynthetic performance and osmotic adjustment to enhance drought tolerance in vegetable soybean.

Khoza Bongiwe M BM, Bowden Ned B NB, Moloi Makoena J MJ

Drought stress severely constrains photosynthetic efficiency in vegetable soybean. However, the role of cysteine-based biostimulants in coordinating photosynthetic regulation and osmotic adjustment remains poorly understood. This study evaluated how N-acetylcysteine (NAC) and N-acetylcysteine trisulfide (NAC-TS) modulate photosynthetic function, photoprotection, and osmotic adjustment to enhance growth and reproductive performance under drought in two vegetable soybean (Glycine max L. Merr.) cultivars with different yielding capabilities and drought sensitivities (UVE17 and AGS429). Both cysteine derivatives slightly increased stomatal conductance under drought. N-acetylcysteine enhanced photosystem II (PSII) functionality in UVE17, as evidenced by increased performance index (PIabs), increased energy absorption and trapping per reaction centre, reduced energy dissipation, and improved pigment stability. In contrast, NAC-TS elicited stronger photochemical and energy flux responses in AGS429, while promoting higher chlorophyll and carotenoid accumulation in UVE17. These responses were closely associated with cultivar-dependent osmotic adjustment, where NAC increased relative water content and soluble sugars in UVE17, whereas NAC-TS enhanced proline and soluble sugars in AGS429. The coordinated improvement in water status, pigment stability, and osmotic balance helped sustain photosynthetic activity and protect the photosynthetic apparatus under drought stress. Consequently, these physiological adjustments translated into improved growth and reproductive performance, which were also strongly cultivar and treatment-dependent. NAC enhanced shoot biomass, leaf area, and shoot length (notably in UVE17), while NAC-TS increased shoot length and leaf area in both cultivars. At the reproductive level, NAC-TS showed improved reproductive development in AGS429 by increasing pod number. NAC and NAC-TS enhance drought resilience in vegetable soybean through coordinated regulation of photosynthesis, photoprotection, osmotic adjustment, and water relations, ultimately improving growth and reproductive performance. Their effects are strongly cultivar- and trait-dependent, highlighting the importance of genotype-specific optimisation of cysteine derivative applications for effective drought mitigation.

PMID 42464118
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PubMedJournal of affective disorders2026-07-17

A randomized trial of omega-3 fatty acids plus inositol versus N-acetylcysteine for the treatment of depression and mania in emotionally dysregulated youth age 5-17 with and without autism traits.

Wozniak Janet J, Iorini Maria M, DiSalvo Maura M, O'Connor Hannah H et al.

The aim of this study was to assess the effectiveness of the nutraceutical treatments combined omega-3 fatty acid plus inositol (O3I) versus N-acetylcysteine (NAC) in children and adolescents with emotional dysregulation and the impact of the co-occurrence of autism traits (AT). Participants were male and female children (5-17) with emotional dysregulation and the presence/absence of AT, as defined by Child Behavior Checklist score, randomized to receive open-label O3I (1020 mg EPA and 1000-2000 mg Inositol) or NAC (1800-2700 mg) daily for 6 weeks. Clinicians measured severity and improvement of depression and mania with the NIMH Clinical Global Improvement Scale (CGI). Parents completed Parent-Youth Mania Rating Scale (P-YMRS) and Children's Depression Inventory (CDI). Both O3I and NAC resulted in modest improvements in mania and depression and did not differ significantly in between group comparison in their effectiveness. Participants taking O3I, but not NAC, demonstrated statistically significant within group improvement in depression per CDI. Participants taking NAC had a greater decrease in P-YMRS scores versus O3I, but the difference did not reach statistical significance. In the presence of AT, NAC was more effective than O3I for mania but not for depression. Further, participants taking NAC, but not O3I, demonstrated significant within group improvement in SRS and BRIEF scores. These results suggest that O3I and NAC may be beneficial for mania and depression in youth, with trends towards O3I more effective for depression and NAC more effective for mania. The presence of AT in youth with emotional dysregulation may moderate the impact of NAC.

PMID 42462928
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PubMedmedRxiv : the preprint server for health sciences2026-07-17

N-Acetylcysteine Reduces Tryptophan-induced Abnormalities in People with Schizophrenia.

Hare Stephanie M SM, Kelly Deanna L DL, Pan Yezhi Y, Chen Shuo S et al.

The current study assessed whether N-acetylcysteine (NAC), which inhibits the kynurenic acid (KYNA)-synthesizing enzyme kynurenine aminotransferase (KAT) II, affects tryptophan (TRYP)-induced peripheral formation of the kynurenine pathway metabolites kynurenine and KYNA and improves selected functional outcome measures in people with schizophrenia. Fifty-eight participants with DSM-5 schizophrenia or schizoaffective disorder entered a double-blind, placebo-controlled, randomized cross-over challenge study, in which they were pretreated with either NAC (up to a maximum of 15 g) or placebo, then received TRYP, 6 g. Prior to and after receiving the study medications, participants underwent laboratory (serum kynurenine and KYNA), symptom (BPRS, SANS, and CDS), cognitive (6 MCCB tests) and brain MRI (ASL, DTI, 1 H-MRS) assessments. In contrast to placebo pre-treatment, NAC significantly reduced the TRYP-induced increase in peripheral serum levels of kynurenine (t=-2.02; p<0.05) and KYNA (t=-3.21; p=0.002). NAC pre-treatment was associated with significantly smaller increases in total white matter (WM) cerebral blood flow (CBF) (t=-2.15; p=0.04) and a trend for smaller increases in total gray matter (GM) CBF (t=-1.81; p=0.08). NAC pre-treatment significantly reduced the TRYP-induced decrease in MCCB composite score (t=2.07; p=0.04). There was no differential treatment effect on DTI or 1 H-MRS or symptom measures. The observation that NAC attenuated the de novo formation of KYNA, reduced WM CBF elevations, tended to decrease GM CBF, and blocked the worsening of cognitive performance in participants following TRYP administration, supports the concept that KAT II inhibition is a promising novel strategy for the treatment of cognitive impairments in people with schizophrenia.

PMID 42465956
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PubMedJournal of the American Heart Association2026-07-17

Dapagliflozin Attenuates Pericardial Adipose Tissue-Derived Leptin-Mediated Myocardial Remodeling in Obese Rats.

Luo Chaodi C, Luo Wenjie W, Zheng Tingting T, Wang Ping P et al.

The favorable cardiovascular effects of sodium-glucose co-transporter 2 inhibitors in diabetes are well established, but their potential to ameliorate obesity-related cardiac dysfunction remains unclear. Pericardial adipose tissue (PAT)-derived adipocytokines, particularly leptin, contribute to obesity-associated cardiac remodeling. We investigated the detrimental effects of PAT-derived leptin on cardiac remodeling and whether dapagliflozin confers cardioprotection by reducing and counteracting PAT-derived leptin in obese rodents. Male Wistar rats, C57BL/6J mice, and ob/ob mice were fed a normal or high-fat diet for 20 weeks, with or without dapagliflozin (1 mg/kg per day) for the final 8 weeks. PAT adipocytes from 8-week-old rats were isolated and induced to insulin resistance. Primary cardiac fibroblasts and cardiomyocytes were exposed to PAT-conditioned medium, leptin antagonist, dapagliflozin (10 μM), reactive oxygen species scavenger N-acetylcysteine (50 mM), pNaKtide (10 μM), Src inhibitor PP2 (10 μM). Na+-K+-ATPase expression and activity, mitochondrial membrane potential, and mitochondrial permeability transition pore opening were assessed. The intervention of dapagliflozin to high-fat diet-fed Wistar rats could reduce body weight and improve metabolic disorders. Furthermore, dapagliflozin significantly alleviated the adipocyte hypertrophy of PAT, cardiac fibrosis and apoptosis, as well as the leptin production and secretion from PAT. In vitro, dapagliflozin inhibits the leptin production and secretion in insulin-resistant adipocytes of PAT by regulating the phosphoinositide 3-kinase/protein kinase B and extracellular signal-regulated kinase 1/2 signaling pathway. Meanwhile, dapagliflozin could counteract the profibrotic effect of PAT-derived leptin via inhibiting the signal transducer and activator of transcription 3-reactive oxygen species/Na+-K+-ATPase/Src oxidative stress loop signaling pathway. Meanwhile, dapagliflozin could also attenuate cardiomyocytes apoptosis induced by PAT-derived leptin via suppressing Janus kinase 2/signal transducer and activator of transcription 3-Bax and inhibiting reactive oxygen species/Na+-K+-ATPase/Src oxidative stress loop. Dapagliflozin reduced PAT-derived leptin via phosphoinositide 3-kinase/protein kinase B and extracellular signal-regulated kinase 1/2 signaling and mitigated PAT-derived leptin-induced myocardial fibrosis and apoptosis by inhibiting signal transducer and activator of transcription 3-mediated reactive oxygen species/Na+-K+-ATPase/Src oxidative stress signaling.

PMID 42466494
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PubMedLangmuir : the ACS journal of surfaces and colloids2026-07-16

Application of Acetylcysteine for Selective Separation of Chalcopyrite and Molybdenite: Flotation Performance and Depression Mechanism.

Zhang Taozhong T, Yin Wanzhong W, Yao Jin J, Ban Xiaoqi X et al.

Given the comparable natural floatability of molybdenite and chalcopyrite, together with the environmental concerns associated with conventional inorganic depressants, achieving their flotation separation remains a major challenge. Herein, acetylcysteine (NAC), a low-toxicity organic reagent, was investigated as a selective depressant for the flotation separation of molybdenite and chalcopyrite. Flotation results showed that, at pH 8.0 and 40.0 mg/L NAC, efficient separation of molybdenite from chalcopyrite was achieved, with a molybdenite recovery of 97.69%, a chalcopyrite recovery of 10.02%, and a selectivity index of 19.50. Furthermore, NAC remained highly effective in depressing chalcopyrite flotation under xanthate-containing conditions. To elucidate the interfacial origin of NAC selectivity, zeta-potential, wettability, adsorption capacity, FTIR, XPS, and DFT analyses were integrated to reveal the adsorption behavior and interaction mechanism of NAC on chalcopyrite and molybdenite. The results suggest that the -SH and -C═O groups of NAC participate in interfacial interactions with surface Cu sites on chalcopyrite, thereby contributing to its preferential adsorption, whereas only weak interaction is observed on molybdenite. This preferential adsorption markedly increased the hydrophilicity of chalcopyrite, while molybdenite retained its hydrophobicity. These findings indicate that NAC is a promising organic depressant for the selective flotation separation of molybdenite from chalcopyrite.

PMID 42461130
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PubMedFood and chemical toxicology : an international journal published for the British Industrial Biological Research Association2026-07-16

Di(2-ethylhexyl) phthalate exposure aggravates amyloid-beta-induced toxicity in transgenic AD Caenorhabditis elegans via lysosomal dysfunction and oxidative stress.

Yang Fan F, Zhao Yan Y

Di(2-ethylhexyl) phthalate (DEHP) is a widely used plasticizer and environmental contaminant. DEHP exposure has been linked to neurotoxicity in Alzheimer's disease (AD), yet the underlying mechanisms remain unclear. Here we found that DEHP exacerbated amyloid-beta (Aβ)-induced toxicity in transgenic AD Caenorhabditis elegans (C. elegans) models. Meanwhile the accumulation of SQST-1 was increased, indicating that the autophagic flux was impaired. Consistently, Aβ deposition was elevated in DEHP-treated AD C. elegans. Further investigation revealed that DEHP treatment resulted in lysosomal dysfunction accompanied by a significant decrease in lysosome number. The expression of hlh-30, a key transcription factor involved in lysosomal biogenesis, as well as its downstream lysosome-related genes, including cup-5, vha-17, and lmp-1, was reduced by DEHP. Moreover, hlh-30 RNAi abolished the exacerbation of Aβ toxicity by DEHP, indicating that the modulation of hlh-30 was a critical mechanism underlying the effects of DEHP. Additionally, DEHP aggravated oxidative stress in AD C. elegans, while the antioxidant N-acetylcysteine alleviated lysosomal impairment and reduced Aβ deposition, suggesting that the elevated oxidative stress was a key contributor to DEHP-induced lysosomal dysfunction and autophagy impairment. These findings highlight lysosomal impairment as a key mechanism contributing to DEHP-exacerbated toxicity in AD models, and suggest the possibility of using antioxidants to prevent DEHP-induced toxicity.

PMID 42456960
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