Nitazoxanide (Synonyms: NSC 697855, NTZ) |
Catalog No.GC11618
One-Click Copy Product Info
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Nitazoxanide is a thiazolide antiprotozoal and antiviral drug with an IC50 of 2.4μM against the proliferation of Giardia lamblia trophozoites. Nitazoxanide is commonly used in the study of infectious diseases and may have potential applications in the treatment of diseases such as viral gastroenteritis and parasitic infections.
Products are for research use only. Not for human use. We do not sell to patients.
Cas No.: 55981-09-4
Sample solution is provided at 25 µL, 10mM.
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Nitazoxanide is a thiazolide antiprotozoal and antiviral drug with an IC50 of 2.4μM against the proliferation of Giardia lamblia trophozoites. Nitazoxanide is commonly used in the study of infectious diseases and may have potential applications in the treatment of diseases such as viral gastroenteritis and parasitic infections[1]. Nitazoxanide has demonstrated anti-Japanese encephalitis virus (JEV) activity in a mouse model[2]. Additionally, Nitazoxanide possesses anti-inflammatory and immunomodulatory effects, which may contribute to its therapeutic potential in various diseases[3-4].
In vitro, Nitazoxanide (2.5–25μM) was used to treat human lung fibroblasts (MRC-5 cells) and mouse lung epithelial cells (MLE-12 cells). Nitazoxanide significantly inhibited transforming growth factor-β1 (TGF-β1)-induced cell proliferation and migration, reduced the expression levels of collagen I (Collagen-I) and α-smooth muscle actin (α-SMA), and decreased the secretion of collagen I. Furthermore, Nitazoxanide inhibited the activation of the TGF-β1-induced Smad2/3 signaling pathway and induced autophagy[5]. When human glioblastoma cells (LN229, A172, U87) and human umbilical vein endothelial cells (HUVECs) were treated with Nitazoxanide at concentrations of 100–1600μM for 48 or 72 hours, Nitazoxanide showed dose-dependent and time-dependent inhibition of cell proliferation, with reduced expression of the proliferation marker Ki67. Additionally, the colony-forming ability of cells treated with Nitazoxanide was significantly decreased[6].
In vivo, Nitazoxanide (100 and 200mg/kg) was administered orally to ApoE-/- mice with diet-induced atherosclerosis for 15 weeks. At both doses, Nitazoxanide significantly reduced the atherosclerotic plaque area in the aortic arch and aortic root, decreased serum levels of inflammatory factors IL-1β and IL-6, and inhibited the proliferation and migration of vascular smooth muscle cells as well as the activation of the NLRP3 inflammasome in macrophages[7]. Nitazoxanide (75, 100, and 150mg/kg) was administered orally to male C57BL/6J mice with dextran sulfate sodium (DSS)-induced ulcerative colitis during the DSS induction period. At all three doses, Nitazoxanide significantly improved DSS-induced colitis symptoms in a dose-dependent manner, including reducing the disease activity index (DAI), alleviating weight loss, increasing colon length, and improving pathological changes in colon tissue. Additionally, Nitazoxanide significantly reduced serum and colon tissue levels of IL-6 and IL-17, and decreased serum myeloperoxidase (MPO) activity[8].
References:
[1] Müller J, Rühle G, Müller N, et al. In vitro effects of thiazolides on Giardia lamblia WB clone C6 cultured axenically and in coculture with Caco2 cells. Antimicrob Agents Chemother. 2006 Jan;50(1):162-70.
[2] Shi Z, Wei J, Deng X, et al. Vaccaria hypaphorine impairs RANKL-induced osteoclastogenesis by inhibition of ERK, p38, JNK and NF-κB pathway and prevents inflammatory bone loss in mice. Biomed Pharmacother. 2018 Jan;97:1155-1163.
[3] Zhang T, Yan Y, Xue Y, et al. Pharmacokinetic Study of Hypaphorine, a Potential Agent for Treating Osteoclast-based Bone Loss, on Rats Using LC-MS/MS. Comb Chem High Throughput Screen. 2022;25(11):1889-1896.
[4] Bai S, Liang H, Jiang W, et al. Identifying hypaphorine as a novel antiviral compound against dengue virus. Antiviral Res. 2025 Jun 24;240:106220.
[5] Chen XY, Dong YC, Yu YY, et al. Anthelmintic nitazoxanide protects against experimental pulmonary fibrosis. Br J Pharmacol. 2023 Dec;180(23):3008-3023.
[6] Wang X, Shen C, Liu Z, et al. Nitazoxanide, an antiprotozoal drug, inhibits late-stage autophagy and promotes ING1-induced cell cycle arrest in glioblastoma. Cell Death Dis. 2018 Oct 9;9(10):1032.
[7] Ma MH, Li FF, Li WF, et al. Repurposing nitazoxanide as a novel anti-atherosclerotic drug based on mitochondrial uncoupling mechanisms. Br J Pharmacol. 2023 Jan;180(1):62-79.
[8] Zhu HT, Luo J, Peng Y, et al. Nitazoxanide protects against experimental ulcerative colitis through improving intestinal barrier and inhibiting inflammation. Chem Biol Interact. 2024 May 25;395:111013.
| Cell experiment [1]: | |
Cell lines | Human lung fibroblast cells (MRC-5) and mouse lung epithelial cells (MLE-12) |
Preparation Method | MRC-5 cells were cultured in minimum essential medium (MEM) and MLE-12 cells were cultured in Dulbecco's modified Eagle's medium (DMEM). Both cell lines were treated with Nitazoxanide and tizoxanide at concentrations of 2.5, 5, 10, and 25μM for 24 hours. The cells were also subjected to TGF-β1 stimulation at 10ng/ml for various durations to induce fibrotic responses. |
Reaction Conditions | 2.5, 5, 10, and 25μM Nitazoxanid; 24 hours. |
Applications | Nitazoxanide and tizoxanide significantly inhibited TGF-β1-induced proliferation and migration of MRC-5 cells, reduced collagen-I and α-smooth muscle cell actin (α-SMA) expression, and decreased collagen-I secretion. They also inhibited EMT and TGF-β1-induced Smad2/3 activation in MLE-12 cells. Additionally, Nitazoxanide and tizoxanide induced autophagy in MRC-5 cells and activated AMPK in both MRC-5 and MLE-12 cells. |
| Animal experiment [2]: | |
Animal models | ApoE-/- mice |
Preparation Method | ApoE-/- mice were fed with a Western diet to establish an atherosclerotic model. Nitazoxanide (100mg/kg, 200mg/kg) was administered by oral gavage six times a week for 15 weeks. Atorvastatin (2mg/kg) was used as a positive control and administered in the same manner. Body weight and food intake were monitored daily. After 15 weeks of treatment, mice were executed, and blood was collected for serum separation. The aorta was removed and fixed for further analysis. |
Dosage form | 100mg/kg, 200mg/kg; p.o. |
Applications | Nitazoxanide reduced the increase in serum IL-1β and IL-6 levels, suppressed atherosclerosis in Western diet-fed ApoE-/- mice, diminished the increased plaque area in the thoracic aorta, and reduced the increased necrotic core area of plaque. Nitazoxanide also inhibited the proliferation and migration of vascular smooth muscle cells, suppressed NLRP3 inflammasome activation in macrophages, and induced autophagy in vascular smooth muscle cells and macrophages. |
References: | |
| Cas No. | 55981-09-4 | SDF | |
| Synonyms | NSC 697855, NTZ | ||
| Chemical Name | [2-[(5-nitro-1,3-thiazol-2-yl)carbamoyl]phenyl] acetate | ||
| Canonical SMILES | CC(=O)OC1=CC=CC=C1C(=O)NC2=NC=C(S2)[N+](=O)[O-] | ||
| Formula | C12H9N3O5S | M.Wt | 307.28 |
| Solubility | ≥ 13.25mg/mL in DMSO | Storage | Store at -20°C |
| General tips | Please select the appropriate solvent to prepare the stock solution according to the
solubility of the product in different solvents; once the solution is prepared, please store it in
separate packages to avoid product failure caused by repeated freezing and thawing.Storage method
and period of the stock solution: When stored at -80°C, please use it within 6 months; when stored
at -20°C, please use it within 1 month. To increase solubility, heat the tube to 37°C and then oscillate in an ultrasonic bath for some time. |
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| Shipping Condition | Evaluation sample solution: shipped with blue ice. All other sizes available: with RT, or with Blue Ice upon request. | ||
| Prepare stock solution | |||
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1 mg | 5 mg | 10 mg |
| 1 mM | 3.2544 mL | 16.2718 mL | 32.5436 mL |
| 5 mM | 650.9 μL | 3.2544 mL | 6.5087 mL |
| 10 mM | 325.4 μL | 1.6272 mL | 3.2544 mL |
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Working concentration: mg/ml;
Method for preparing DMSO master liquid: mg drug pre-dissolved in μL DMSO ( Master liquid concentration mg/mL, Please contact us first if the concentration exceeds the DMSO solubility of the batch of drug. )
Method for preparing in vivo formulation: Take μL DMSO master liquid, next addμL PEG300, mix and clarify, next addμL Tween 80, mix and clarify, next add μL saline, mix and clarify.
Method for preparing in vivo formulation: Take μL DMSO master liquid, next add μL Corn oil, mix and clarify.
Note: 1. Please make sure the liquid is clear before adding the next solvent.
2. Be sure to add the solvent(s) in order. You must ensure that the solution obtained, in the previous addition, is a clear solution before proceeding to add the next solvent. Physical methods such as vortex, ultrasound or hot water bath can be used to aid dissolving.
3. All of the above co-solvents are available for purchase on the GlpBio website.
Quality Control & SDS
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- Purity: >98.00% Appearance: A solid
- COA (Certificate of Analysis)
- SDS (Safety Data Sheet)
- Datasheet
Average Rating: 5 (Based on Reviews and 15 reference(s) in Google Scholar.)