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

PubMedIUBMB life2026-08-29

N-Acetyl Cysteine Mitigates d-Ribose-Induced Protein Glycation and Aggregation Through Multiple Protective Mechanisms.

Nabi Rabia R, Faruqui Tabrez T, Khan Mohd Shahnawaz MS, Alafaleq Nouf Omar NO et al.

Advanced glycation end-products (AGEs) arise from non-enzymatic reactions between reducing sugars and proteins, contributing to oxidative stress and metabolic dysfunction. Excessive AGE accumulation is implicated in chronic diabetic complications and may also be relevant to acute metabolic disturbances encountered in emergency medicine. N-acetylcysteine (NAC), a naturally occurring antioxidant found in Allium species, has demonstrated potential to attenuate oxidative and glycation-mediated damage. The effect of NAC on d-ribose-induced glycation of bovine serum albumin (BSA) was investigated using multiple physicochemical and spectroscopic techniques. AGE formation was assessed by measuring hyperchromicity, early glycation products (ketoamines), carbonyl content, hydroxymethylfurfural (HMF) levels, and fluorescent AGEs. The protective effect of NAC was further evaluated by determining free lysine and arginine contents. Protein aggregation and conformational changes were analyzed using Congo Red binding and fluorescence assays including thioflavin-T and 1-anilinonaphthalene-8-sulfonic acid. NAC significantly inhibited d-ribose-mediated glycation of BSA in a concentration-dependent manner. Treatment with NAC resulted in reduced hyperchromicity, decreased ketoamine formation, and lower carbonyl, HMF, and fluorescent AGE levels. NAC preserved protein integrity by maintaining higher free lysine and arginine contents. In addition, NAC markedly attenuated glycation-induced protein aggregation, as evidenced by reduced Congo Red binding and diminished thioflavin-T and ANS fluorescence, with maximal protection observed at 300 μM. NAC exhibits pronounced anti-glycation and anti-aggregation effects by limiting oxidative stress and glycation-mediated protein modification. These findings demonstrate that NAC effectively attenuates d-ribose-induced glycation and protein aggregation in vitro and provide mechanistic insights into its anti-glycation properties through multiple complementary biochemical mechanisms. Further studies are warranted to evaluate its biological relevance in more complex experimental models.

PMID 42666005
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PubMedClinical toxicology (Philadelphia, Pa.)2026-08-28

Clinical outcomes of "massive" acetaminophen overdose treated with standard vs. augmented dose acetylcysteine.

Testa Joseph W JW, Bompard Madison M, Oyekanmi Oyeyimika O, Wills Brandon K BK et al.

This was a single-center retrospective cohort study of acute acetaminophen overdoses reported to a regional poison center from January 2010 to March 2025. Cases were reviewed before and after the poison center adopted augmented acetycysteine dosing for massive acetaminophen overdoses in January 2020. The group who received standard acetylcysteine dosing served as the control. Cases were included if a single acute acetaminophen concentration plotted above the 300-, 450-, or 600 mcg/mL nomogram line. Standard univariate statistical analysis was conducted to describe the cohort, and a multivariate logistic model was utilized to calculate odds ratios for risk of hepatotoxicity. Of 174 included cases, 107 received standard acetylcysteine dosing and 67 received augmented acetylcysteine dosing. Among cases that received acetylcysteine less than eight hours post-ingestion, the incidence of hepatotoxicity was 8.7% (4/46) in the standard dose cohort compared to 8.6% (3/35) in the augmented dose cohort (unadjusted OR 0.98, 95% CI 0.21-4.71) Among those that received acetylcysteine greater than eight hours post-ingestion, the incidence of hepatotoxicity was 34.4% (21/61) in the standard dose cohort compared to 37.5% (12/32) in the augmented dose cohort (unadjusted OR 1.14, 95% CI 0.47-2.78).DiscussionAugmented acetylcysteine dosing did not reduce hepatoxicity compared with standard dosing in massive acetaminophen ingestions. Early initiation of acetylcysteine remains the most important factor associated with prevention of hepatotoxicity. Interpretation is limited based on small sample sizes, potentially inaccurate ingestion histories, and reliance on poison center data. In this cohort of massive acetaminophen overdose, there was no difference in incidence of hepatotoxicity between standard versus augmented acetylcysteine dosing when stratified by time-to-acetylcysteine post-ingestion.

PMID 42663261
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PubMedFrontiers in immunology2026-08-28

Mitochondrial DNA in systemic lupus erythematosus: pathogenic mechanisms, clinical biomarkers, and precision therapeutic strategies.

Huang Fugang F, Sun Ke K, Diao Lijia L, Lu Keda K et al.

Mitochondrial DNA (mtDNA) is increasingly recognized as an active driver of immune dysregulation in systemic lupus erythematosus (SLE), yet most existing reviews treat it as a single damage signal rather than a multifunctional pathological mediator. This review presents an integrated framework examining mtDNA as a central hub linking mitochondrial dysfunction to systemic autoimmunity. We conducted a comprehensive synthesis of published evidence on mtDNA biology, its dysregulation in SLE, organ-specific injury mechanisms, and the clinical landscape of mtDNA-targeted therapeutic strategies. In SLE, intracellular mtDNA depletion coexists paradoxically with markedly elevated circulating cell-free mtDNA, a pattern correlating with disease activity and organ involvement. Sequential cytoplasmic and extracellular release of mtDNA engages cyclic GMP-AMP synthase-stimulator of interferon genes (cGAS-STING), Toll-like receptor 9 (TLR9), and inflammasome platforms, establishing self-amplifying interferon and pro-inflammatory circuits that drive multi-organ pathology. We consolidate emerging evidence for mtDNA-related parameters as clinical biomarkers and propose a provisional patient stratification framework distinguishing two pathological subtypes with distinct therapeutic implications. Among current therapeutic strategies, N-acetylcysteine (NAC) and metformin carry the strongest clinical evidence, while cGAS-STING inhibitors and TLR9 antagonists represent compelling emerging candidates. mtDNA operates as an integrative pathological hub in SLE, and its dysregulation pattern carries both diagnostic and therapeutic significance. Incorporating mtDNA-based biomarkers into clinical monitoring and developing precision strategies targeting mtDNA-driven inflammatory circuits represent important steps toward individualized SLE management.

PMID 42662156
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PubMedComparative biochemistry and physiology. Toxicology & pharmacology : CBP2026-08-28

Acetaminophen-induced developmental neurobehavioral and sensory organ toxicity in zebrafish.

Wang Huan H, Chen Chaobao C, Onoo Shuta S, Yuge Mizuki M et al.

Acetaminophen (APAP) also known as paracetamol, is the only antipyretic and analgesic agent that can be administered to pregnant women. In addition to hepatotoxicity in cases of an overdose, the developmental neurotoxicity of APAP has been reported in model organisms. In this study, developing zebrafish were used to assess the neurotoxic effects of waterborne APAP exposure (0.039-2.5 mM). At 120 hpf, the spontaneous swimming distance was significantly reduced at all tested APAP concentrations under alternating light-dark conditions. Touch-evoked escape velocity, which assesses the motor function, was not significantly affected at any concentration and it increased at moderate APAP doses. The optokinetic response was only reduced at 2.5 mM APAP concentrations, suggesting that the decrease in spontaneous swimming at low APAP doses is unlikely to be due to motor or visual impairments. Vibration-evoked responses, indicative of the sensory function, were slightly but significantly diminished at 0.625 and 2.5 mM APAP concentrations. At 72 h post-fertilization (hpf), acridine orange and terminal deoxynucleotidyl transferase dUTP nick-end labeling (TUNEL) staining showed that exposure to 2.5 mM APAP resulted in regulated cell death in the cerebellum, retina, and dorsal trunk. Some APAP-induced cell death in the dorsal trunk was confirmed to be of neuronal origin using Tg(eno2:Cerulean) transgenic zebrafish. N-acetylcysteine, a well-known antioxidant and antidote for APAP toxicosis in humans, partially attenuated APAP-induced cell death. These results suggest that APAP induces developmental neurobehavioral and sensory organ toxicity in the absence of detectable regulated cell death under the present experimental conditions.

PMID 42665174
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PubMedAntioxidants (Basel, Switzerland)2026-08-27

A New Cosmeceutical Approach for Mature Skin: Antioxidant Activity, In Vitro Permeation, and Preliminary Clinical Efficacy of Melatonin-N-Acetylcysteine Creams.

Bîrsan Magdalena M, Ștefănescu Ruxandra R, Muntean Daniela-Lucia DL, Vlad Robert-Alexandru RA et al.

Skin ageing is associated with oxidative stress, mitochondrial dysfunction, extracellular matrix alterations, and impaired barrier function, supporting interest in antioxidant cosmeceuticals for mature skin. This study investigated the antioxidant activity of melatonin and N-acetylcysteine, the in vitro permeation of melatonin from different cream formulations, and their preliminary clinical performance in women aged 55-65 years. Antioxidant activity was assessed using 2,2-diphenyl-1-picrylhydrazyl (DPPH) and 2,2'-azino-bis(3-ethylbenzothiazoline-6-sulfonic acid)/Trolox equivalent antioxidant capacity (ABTS/TEAC) assays. Melatonin permeation across Strat-M® membranes was evaluated using Franz diffusion cells and quantified by a validated high-performance liquid chromatography method coupled with a photodiode-array detection (HPLC-PDA) method. Clinical changes were assessed over 28 days using the Glogau wrinkle scale and a lower facial ptosis scale. N-acetylcysteine exhibited greater antioxidant activity than melatonin in the DPPH assay, with half-maximal inhibitory concentration (IC50) values of 5.96 ± 1.02 and 530.11 ± 48.63 µg/mL, respectively. Melatonin permeation varied according to formulation composition, with cumulative amounts after 24 h ranging from 81.27 ± 17.47 to 1043.48 ± 33.43 µg/cm2. Reductions in periocular wrinkle and lower facial ptosis scores were observed after 28 days. These preliminary findings support further investigation of melatonin-N-acetylcysteine creams for mature skin. However, the present membrane model did not assess cutaneous retention, and the clinical observations require confirmation in larger, controlled studies.

PMID 42650255
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PubMedPharmaceutics2026-08-27

N-Acetylcysteine-Functionalized Mixed Micelles Overcome Multiple Intestinal Barriers to Improve Oral Bioavailability and Antioxidant Protection of Imperatorin.

Zhang Yu Y, Guo Jian J, Qiu Haonan H, Liu Jiale J et al.

Background: Imperatorin (IPT) is a natural furanocoumarin featuring robust anti-inflammatory, antifibrotic and antioxidant activities. However, poor aqueous solubility and insufficient oral bioavailability restrict its clinical application. Multiple gastrointestinal barriers, including the mucus barrier, limited epithelial penetration and P-glycoprotein-triggered drug efflux, are major obstacles hindering IPT oral absorption. Methods: N-acetylcysteine (NAC)-functionalized TPGS conjugates were synthesized first. Using Pluronic® F108 and Lipoid® S-100 as a matrix, imperatorin@N-acetylcysteine-TPGS/Pluronic® F108/Lipoid® S-100 (IPT@NAC-TFS) micelles were fabricated. We characterized their physicochemical features and in vitro release behavior. The Caco-2/HT29-MTX-E12 co-culture cell model was adopted to explore mucus permeation, cellular uptake and transepithelial transport mechanisms. In vivo intestinal distribution and pharmacokinetic tests in rats were carried out to confirm the oral absorption-enhancing effect of micelles. Results: Optimized micelles displayed a uniform shape and favorable encapsulation efficiency. Low CMC maintained structural stability upon gastrointestinal dilution. NAC modification conferred mucus-penetrating capacity on micelles. TPGS simultaneously improved epithelial barrier permeability and inhibited drug efflux, switching IPT transport mode. The micelles effectively cleared intracellular ROS, recovered SOD activity and lowered MDA levels in BLM-impaired MLg fibroblasts. In vivo results revealed enhanced intestinal drug accumulation, with the relative oral bioavailability of IPT increased by 6.07-fold. Conclusions: IPT@NAC-TFS micelles overcome multiple gastrointestinal barriers for oral IPT delivery. Combining mucus penetration, efflux suppression and antioxidative capacity, this system offers a promising strategy to develop oral formulations of poorly soluble antifibrotic natural products.

PMID 42654153
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