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Chemical Structure| 616-91-1 Chemical Structure| 616-91-1

Structure of Ac-Cys-OH
CAS No.: 616-91-1

Chemical Structure| 616-91-1

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Acetylcysteine is an inhibitor of ROS and the production of TNF. It is a pharmaceutical drug and nutritional supplement used as mucolytic agent.

Synonyms: NAC; N-Acetylcysteine; N-Acetyl-L-cysteine

4.5 *For Research Use Only! Not for Human Use. We Do Not Sell to Patients.

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Wang, Shengmei ; Ma, Ding ; Yang, Minghua ; Zhang, Ye ; Wang, Shengfeng ; Zhou, Wenhu

Abstract: Chemotherapy remains a primary treatment option for hepatocellular carcinoma (HCC), yet its clinical benefits are often unsatisfactory. Utilizing arsenic trioxide (ATO) as a model, this study elucidates the role of autophagy inhibition in modulating the cellular response to chemotherapy, shifting cell death from apoptosis to pyroptosis via the caspase-3–GSDME pathway, thereby augmenting the anti-tumor efficacy. Building upon these findings, an ATO nanomedicine delivery system capable of autophagy inhibition to promote pyroptosis for enhanced tumor treatment was developed. Folic acid-modified albumin served as the stabilizer for nano selfassemblies formed through ion pairing between Mn2+ and ATO, encapsulating DNAzyme (Dz) targeting Beclin 1, a key autophagy regulator. Characterization studies confirmed efficient encapsulation of ATO and Dz within nanoparticles, designed to disintegrate in the intracellular microenvironment, releasing the all-active components, i.e., ATO, Mn2+, and Dz. Mn2+ acted as a metal cofactor to activate Dz for Beclin 1 mRNA cleavage, inhibiting autophagy and augmenting ATO-induced cell pyroptosis. Elevated cell pyroptosis levels not only enhance ATO’s direct tumor cell killing capacity but also trigger anti-tumor immune responses, synergistically enhancing efficacy. Upon intravenous injection, the nanomedicine accumulated in tumor tissue and targeted liver cancer cells. Compared to free ATO, the nanomedicine exhibited significantly improved in vivo anti-tumor effects, achieving a 100% 45-day survival rate in mice with favorable biosafety profiles. This study offers novel insights into tumor chemotherapy sensitization and presents a promising strategy for ATO nanoformulation development.

Keywords: Nanoparticles ; Cell death ; Chemotherapy ; Targeting ; Tumor immunity ; Drug delivery ; Arsenic trioxide ; Hepatocellular carcinoma

Purchased from AmBeed:

Li, Chengyu ; Liu, Zhaojun ; Zhu, Linjie ; Wu, Gang ; Fu, Chen ; Li, Hongmin , et al.

Abstract: HMGB1, one of the most abundant nuclear non-histone proteins, also performs extracellular functions, and its nuclear export mechanisms have been extensively studied. Here, a novel mechanism of nuclear export for HMGB1 driven by lactylation is proposed. In addition, it is revealed that hypoxia-induced lactylation of HMGB1 facilitates its nuclear export in a complex with TIAR, promoting stress granule (SG) formation in the cytosol. Mass spectrometry revealed 12 lysine residues in HMGB1 undergoing lactylation, with K172 and K177 being the most susceptible. Functional studies using lysine-to-arginine mutants (K→R) demonstrated that lactylation at K177 is crucial for HMGB1-TIAR complex export, as K177R mutation completely blocked this export and subsequent SG formation. Notably, this lactylation-mediated mechanism is specific to hypoxic stress, while other stressors, such as sodium arsenite exposure and heat shock, triggered TIAR nuclear export and SG assembly independently of HMGB1. These findings reveal a previously unrecognized role of HMGB1 lactylation in mediating nuclear export and SG formation under hypoxia.

Keywords: HMGB1 ; hypoxic stress granules ; lactylation ; nuclear export ; TIAR

Purchased from AmBeed:

Ge, Xiao ; Yang, Guang-ming ; Zhang, Xiao-long ; Cao, Jing ; Qing, Ying-jie ; Shen, San-bing , et al.

Abstract: Mitochondrial DNA (mtDNA) damage and accumulation activate the cGAS-STING DNA-sensing pathway, which promotes immune clearance of tumor cells. Maintenance of the cytosolic level of mtDNA is key to sustain immune activation. T cell malignancies (T-CMs) are a general name of diseases with abnormal clonal proliferation of T lymphocytes at various stages. Immunotherapy of T-CMs is challenged by the lack of specific antigens to discriminate T-CMs from normal T cells. As intrinsic STING activation can promote the clearance of T-CMs by immune cells, we herein explored whether isoliensinine (IsoL), a natural compound from Nelumbinis Plumula could enhance NK clearance by mtDNA-mediated immune responses in tumor cells. To investigate whether IsoL modulated immune recognition and clearance of T-CMs, we pre-treated three T-CM cell lines (Jurkat, Molt4 and Hut102) with IsoL then co-cultured with NK-92MI cells. We showed that IsoL pre-treatment promoted cytosolic mtDNA accumulation by inducing ROS-dependent mitochondrial damage and inhibiting mitophagy via peroxiredoxin 1 (PRDX1), an antioxidant enzyme. Loss of PRDX1 in T-CMs also induced ROS-dependent mitochondrial DNA damage, and blocked mitophagy by preventing accumulation of mature PINK1, which was required to initiate mitophagy via recruiting Parkin to the damaged mitochondria. Remarkably, IsoL could induce expression of activating ligands in vitro, enhance NK cell infiltrations, and increase apoptosis of T-CMs. Moreover, we demonstrated that IsoL could sensitize T-CMs for NK clearance in vitro and in vivo. These results suggest that IsoL could be a potential therapeutic agent to enhance immune therapy of T-CMs.

Keywords: T cell malignancies ; immune clearance ; isoliensinine ; mitophagy ; NK cells ; peroxiredoxin 1

Purchased from AmBeed: 763113-22-0 ; ; ; ; ;

Gao, Yue ; Zhai, Xinyue ; Zhang, Caixia ; Zhao, Hongmei ; Ji, Bing ; Sun, Ruolan , et al.

Abstract: Repurposing existing drugs offers a promising approach to cancer therapy. , an (ACEI) approved for hypertension, has demonstrated antitumor effects in hepatocellular carcinoma. However, its activity in non-small cell lung cancer (NSCLC) remains poorly understood. Here, we explore the potential anti-NSCLC effects of in vitro and in vivo and its action mechanisms. The antiproliferative effects of on NSCLC cells were assessed through the A549 and H1299 cell lines. Network pharmacology and proteomics were utilized to predict fosinopril’s molecular mechanisms in NSCLC. A subcutaneous xenograft model in nude mice was established to evaluate the in vivo anticancer effects and mechanisms of . significantly inhibited the proliferation and colony formation of NSCLC cells. Additionally, induced in NSCLC cells, evidenced by GSDME cleavage and increased LDH release. Mechanistically, increased levels, which activated Bax and downregulated mitochondrial membrane potential (MMP), resulting in Caspase-9 and Caspase-3 cleavage. Moreover, suppressed tumor growth in a subcutaneous xenograft model and activated pyroptosis-related proteins. This study provides the first evidence that inhibits NSCLC via GSDME-dependent , triggered by ROS-induced mitochondrial dysfunction and activation. Further investigation into the detailed mechanisms of fosinopril’s anti-NSCLC activity is warranted.

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Yi, Chu ; Feng, Weifeng ; Zhang, Guijuan ; Luo, Jiali ; Chen, Yiliu ; Feng, Qing , et al.

Abstract: (CA), a natural bioactive compound derived from species, has demonstrated broad-spectrum antitumor activity. However, its therapeutic potential and precise mechanisms in ovarian cancer (OC) remain incompletely elucidated. In this study, we systematically investigated the inhibitory effects of CA on OC and the underlying molecular mechanisms through both in vitro and in vivo approaches. In vitro experiments demonstrated that CA significantly induces reactive oxygen species (ROS) accumulation in OC cells, activates mitochondria-mediated , and induces mitochondrial via the AMPK/ULK1/Beclin1 signaling axis. These synergistic effects collectively lead to significant suppression of OC cell proliferation. In a murine xenograft model of OC, CA administration substantially inhibited the growth of heterotransplanted tumors. Further in vivo analyses revealed a significant increase in the number of apoptotic cells and upregulation of the expression of the markers LC3B, PINK1, and Parkin in tumor tissues. Concurrently, the expression of the autophagic substrate p62 and the mitochondrial membrane protein TOMM20 decreased. These findings consistently corroborated the cellular mechanisms observed in vitro. This study provides the first evidence that CA suppresses OC progression via ROS-mediated dual mechanisms: induction and activation. Our results underscore the translational potential of CA as a promising therapeutic candidate and provide a robust experimental foundation for its further development against OC.

Keywords: ; ; ; ovarian cancer ; mitochondrial

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Chen, Lei ; Yan, Yang ; Kong, Fangen ; Wang, Jikai ; Zeng, Jia ; Fang, Zhen , et al.

Abstract: Background: To better understand the Ca2+ overload mechanism of SDT killing gliomas, we examined the hypothesis that the early application of the mechanosensitive Ca2+ channel Piezo1 antagonist (GsMTx4) could have a better anti-tumor effect. Methods: The in vitro effect of low-energy SDT combined with GsMTx4 or agonist Yoda 1 on both the ROS-induced distribution of Ca2+ as well as on the opening of Piezo1 and the dissociation and polymerization of the Ca2+ lipid complex were assessed. The same groups were also studied to determine their effects on both tumor-bearing BALB/c-nude and C57BL/6 intracranial tumors, and their effects on the tumor-infiltrating macrophages were studied as well. Results: It was determined that ultrasound-activated Piezo1 contributes to the course of intracellular Ca2+ overload, which mediates macrophages (M1 and M2) infiltrating under the oxidative stress caused by SDT. Moreover, we explored the effects of SDT based on the dissociation of the Ca2+ lipid complex by inhibiting the expression of fatty acid binding protein 4 (FABP4). The Piezo1 channel was blocked early and combined with SDT treatment, recruited macrophages in the orthotopic transplantation glioma model. Conclusions: SDT regulates intracellular Ca2+ signals by upregulating Piezo1 leading to the inhibition of the energy supply from lipid and recruitment of macrophages. Therefore, intervening with the function of the Ca2+ channel on the glioma cell membrane in advance is likely to be the key factor to obtain a better effect combined with SDT treatment.

Keywords: grade 4 glioma ; sonodynamic therapy ; oxidative stress ; calcium homeostasis imbalance ; macrophage infiltrating

Purchased from AmBeed:

Ievtukhov, Vladyslav ; Zadykowicz, Beata ; Blazheyevskiy, Mykola Ye. ; Krzyminski, Karol ;

Abstract: Biologically active compounds containing sulfhydryl groups (RSHs: N-acetyl-L-cysteine, D-penicillamine, glutathione and acetylthiocholine chloride) were used to develop a luminometric method for their quantification. The title substrate capable of chemiluminescence (CL) was isolated in a highly pure state as a chloride salt (99.9% using RP-HPLC) and identified using mass spectrometry (ESI Q-TOF) and 1H NMR spectroscopy. The cation included in the salt, 9-CMA+, underwent oxidation in an alk. environment containing RSHs by mol. oxygen, generating CL of various intensities, with no need for the use of hydrogen peroxide. The amount of produced light was linearly proportional to the content of investigated analytes in the system over the concentration range ∼0.2-2μM, with the detection limits in the range 0.19-1.73μM. The mechanism of chemiluminogenic oxidation of 9-CMA+ in the presence of RSHs and mol. oxygen is proposed, using computational methods at the d.-functional theory level. The presence of RSHs in an alk. medium seems to be crucial to produce hydroperoxide anions (-OOH), which initiate the 'light path' of 9-CMA+ transformations, ending with the excretion of electronically excited mols. of 10 methyl-acridan-9-one.

Keywords: 9-cyano-10-methylacridinium cation ; chemiluminescence analysis ; DFT methods ; MS and NMR spectroscopy ; thiol nucleophiles

Purchased from AmBeed: ;

Alternative Products

Product Details of Ac-Cys-OH

CAS No. :616-91-1
Formula : C5H9NO3S
M.W : 163.19
SMILES Code : SC[C@@H](C(O)=O)NC(C)=O
Synonyms :
NAC; N-Acetylcysteine; N-Acetyl-L-cysteine
English Name :(R)-2-Acetamido-3-mercaptopropanoic acid
MDL No. :MFCD00004880
InChI Key :PWKSKIMOESPYIA-BYPYZUCNSA-N
Pubchem ID :12035

Safety of Ac-Cys-OH

Related Pathways of Ac-Cys-OH

pyroptosis

Isoform Comparison

Biological Activity

Target
  • TNF-α

In Vitro:

Cell Line
Concentration Treated Time Description References
Neutrophils 1 mM 30 min To assess the effect of NAC on NET formation, results showed that NAC reduced PMA-induced NET formation. Blood Adv. 2020 Jan 28;4(2):312-321.
LS174T 2.5-40 mM 72 h Acetylcysteine significantly inhibited the proliferation of LS174T cells, particularly at higher concentrations. J Exp Clin Cancer Res. 2014 Nov 12;33(1):92.
HT29-5M21 1-75 mM 72 h Acetylcysteine significantly inhibited the proliferation of HT29-5M21 cells, particularly at higher concentrations. J Exp Clin Cancer Res. 2014 Nov 12;33(1):92.
HT29-5F12 1-75 mM 72 h Acetylcysteine significantly inhibited the proliferation of HT29-5F12 cells, particularly at higher concentrations. J Exp Clin Cancer Res. 2014 Nov 12;33(1):92.
KATO-III 1-100 mM 72 h Acetylcysteine significantly inhibited the proliferation of KATO-III cells, particularly at higher concentrations. J Exp Clin Cancer Res. 2014 Nov 12;33(1):92.
MKN45 1-100 mM 72 h Acetylcysteine significantly inhibited the proliferation of MKN45 cells, particularly at higher concentrations. J Exp Clin Cancer Res. 2014 Nov 12;33(1):92.
Panc-1 cells 1 mM 72 h To evaluate the effect of NAC/Cu(II) on Panc-1 cells, it was found that NAC/Cu(II) significantly reduced cell viability. Cancer Lett. 2010 Dec 8;298(2):186-94.
T47D cells 1 mM 72 h To evaluate the effect of NAC/Cu(II) on T47D cells, it was found that NAC/Cu(II) significantly reduced cell viability. Cancer Lett. 2010 Dec 8;298(2):186-94.
MDA-MB-231 cells 1 mM 72 h To evaluate the effect of NAC/Cu(II) on MDA-MB-231 cells, it was found that NAC/Cu(II) significantly reduced cell viability. Cancer Lett. 2010 Dec 8;298(2):186-94.
A2780 cells 1 mM 72 h To evaluate NAC as a potential metal ionophore/shuttle, it was found that NAC is cytotoxic only in the presence of copper and inhibits cell growth by inducing apoptosis. Cancer Lett. 2010 Dec 8;298(2):186-94.
CF sputum 2.5 mM 30 min To compare the mucolytic effects of MUC-031 and NAC, MUC-031 was more effective in reducing the elastic modulus (G′) of sputum and acted faster. MUC-031 induced mucolysis in 69% of sputum samples within 15 min, compared to 25% for NAC. Eur Respir J. 2023 May 25;61(5):2202022.

In Vivo:

Species
Animal Model
Administration Dosage Frequency Description References
Mice JAK2V617F knockin mouse model Oral 2 g/L Starting from 4 to 6 weeks of age, replenished weekly, continuous administration. To investigate the effect of NAC on thrombosis in MPN mice, results showed that NAC extended the lifespan of JAK2V617F mice and reduced thrombus formation. Blood Adv. 2020 Jan 28;4(2):312-321.
Mice ΒENaC-Tg mice Intratracheal instillation (adult mice) or intranasal instillation (neonatal mice) 131 mg/mL Three times in one day (acute experiment) or twice daily for two weeks (chronic experiment) To evaluate the mucolytic efficacy of MUC-031 in βENaC-Tg mice. Acute treatment significantly reduced airway mucus plugging and inflammation; chronic treatment sustained these reductions and improved survival. Eur Respir J. 2023 May 25;61(5):2202022.
BALB/c mice Hind leg muscle model Diet 5% Daily for 14 days To investigate the effect of dietary NAC on radical-induced structural changes in DNA, results showed that NAC significantly reduced the concentration of 8-OH-Gua and decreased the variance in the oxidative status of DNA. Proc Natl Acad Sci U S A. 2002 Apr 30;99(9):5937-41
Rats and mice Early-life stress (ELS) model and EAAC1 knockout mice Intraperitoneal injection 50 mg/kg and 150 mg/kg Once daily for 2 days NAC injection alleviated depressive-like behaviors in NMS model rats and reduced oxidative stress and neuroinflammation. In EAAC1-/- mice, NAC improved depressive-like behaviors but not impulsive behaviors. Int J Biol Sci. 2024 Oct 7;20(14):5450-5473

Clinical Trial:

NCT Number Conditions Phases Recruitment Completion Date Locations
NCT04278898 Autism Spectrum Disorder PHASE2 RECRUITING 2025-01-27 Stanford University School of ... More >>Medicine, Stanford, California, 94305, United States Less <<
NCT06546475 Psychosis PHASE4 NOT_YET_RECRUITING 2027-07-31 -
NCT01808521 Purpura, Thrombotic Thrombocyt... More >>openic|TTP Less << EARLY_PHASE1 COMPLETED 2025-07-17 Puget Sound Blood Center, Seat... More >>tle, Washington, 98104, United States Less <<
NCT06260566 Biliary Atresia PHASE1 NOT_YET_RECRUITING 2025-02-27 -
NCT02094625 Neuroectodermal Tumors, Primit... More >>ive|Liver Neoplasms|Osteosarcoma|Other Childhood Cancers Using Cisplatin-based Regimens Less << PHASE1 COMPLETED 2025-08-21 Childrens Hospital Los Angeles... More >>, Los Angeles, California, 90027, United States Less <<
NCT00211653 Kidney Failure PHASE1|PHASE2 COMPLETED 2025-11-06 Veterans Affairs Medical Cente... More >>r, Minneapolis, Minnesota, 55417, United States Less <<
NCT01896492 PCOS PHASE4 COMPLETED 2025-06-13 -
NCT00396396 Creatinine Clearance UNKNOWN - Eastern Virginia Medical Schoo... More >>l/Nephrology Associates, Norfolk, Virginia, 23507, United States Less <<
NCT02788292 Adipose Tissue Atrophy|Deformi... More >>ty of Reconstructed Breast|Graft Loss Less << PHASE4 WITHDRAWN 2020-11-16 -
NCT05123365 Myeloproliferative Neoplasm|MP... More >>N|Essential Thrombocythemia|Polycythemia Vera|Myelofibrosis Less << PHASE1|PHASE2 RECRUITING 2026-11-15 University of California, Irvi... More >>ne, Irvine, California, 92617, United States|Chao Family Comprehensive Cancer Center, University of California, Irvine, Orange, California, 92868, United States Less <<
NCT05241262 Mitochondrial Disease PHASE1 RECRUITING 2025-04-25 Columbia University Irving Med... More >>ical Center, New York, New York, 10032, United States Less <<
NCT01800526 Sickle Cell Disease|Sickle Cel... More >>l Anemia Less << PHASE1|PHASE2 COMPLETED 2020-06-30 University of Washington, Seat... More >>tle, Washington, 98106, United States Less <<
NCT00542750 Cannabis Dependence PHASE1|PHASE2 COMPLETED 2025-12-08 Medical University of South Ca... More >>rolina, Charleston, South Carolina, 29425, United States Less <<
NCT05081479 Lymphoma PHASE1 RECRUITING 2025-10-21 Memorial Sloan Kettering Baski... More >>ng Ridge (Limited Protocol Activities), Basking Ridge, New Jersey, 07920, United States|Memorial Sloan Kettering Monmouth (Limited Protocol Activities), Middletown, New Jersey, 07748, United States|Memorial Sloan Kettering Bergen (Limited Protocol Activities), Montvale, New Jersey, 07645, United States|Memorial Sloan Kettering Suffolk - Commack (Limited Protocol Activities), Commack, New York, 11725, United States|Memorial Sloan Kettering Westchester (Limited Protocol Activities), Harrison, New York, 10604, United States|Memorial Sloan Kettering Cancer Center, New York, New York, 10065, United States|Memorial Sloan Kettering Nassau (Limited Protocol Activities), Uniondale, New York, 11553, United States Less <<
NCT01424033 Interstitial Lung Disease|Conn... More >>ective Tissue Disease Less << PHASE2|PHASE3 TERMINATED - University of Michigan, Ann Ar... More >>bor, Michigan, 48109, United States Less <<

Protocol

Bio Calculators
Preparing Stock Solutions 1mg 5mg 10mg

1 mM

5 mM

10 mM

6.13mL

1.23mL

0.61mL

30.64mL

6.13mL

3.06mL

61.28mL

12.26mL

6.13mL

Dissolving Methods
The prepared working fluid is recommended to be prepared now and used up as soon as possible in a short period of time. The percentage shown in front of the following solvent refers to the volume ratio of the solvent in the final solution; If precipitation or precipitation occurs in the preparation process, it can be assisted by heating and/or ultrasound.
Protocol 1

References

 

Historical Records

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