Nitrovin
Nitrovin (Difurazon) is a thioredoxin reductase 1 (TrxR1) inhibitor with both antibacterial and anticancer activities. Nitrovin interacts with TrxR1 to generate reactive oxygen species (ROS), which in turn induces cytoplasmic vacuolization, activates MAPK and inhibits Alix. Nitrovin induces paraptosis-like non-apoptotic cell death, thereby exerting significant cytotoxicity against cancer cells. Nitrovin can be used in the research of heart disease and glioblastoma multiforme.
For research use only. We do not sell to patients.
- CAS No.: 804-36-4
- Formula: C14H12N6O6
- Molecular Weight:360.28
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Storage:
Please store the product under the recommended conditions in the Certificate of Analysis.
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Biological Activity
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Chemical Information
- Purity & Documentation
- References
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Help & FAQs
Biological Activity
Nitrovin (0.625-10 μM; 24 h) potently reduces viability across 16 cancer cell lines (IC50=1.31-5.00 μM) and is less cytotoxic to normal LO2 and HK2 cells (IC50=5.34-6.60 μM) after 24 h treatment in vitro[1].
Nitrovin (1.25-10 μM; 24 h) concentration-dependently reduces viability and intracellular ATP levels in human glioblastoma U251 and U87 cells after 24 h treatment in vitro[1].
Nitrovin (0.625-5 μM; 24 h) induces non-apoptotic cell death in human glioblastoma U251 cells, as it does not activate caspase-3/7, cause nuclear fragmentation, or trigger Annexin V positivity after 24 h treatment in vitro[1].
Nitrovin (1.25-5 μM; 4 h) concentration-dependently increases intracellular ROS and mitochondrial superoxide levels in human glioblastoma U251 and U87 cells after 4 h treatment, and thiol-containing antioxidants NAC and GSH reverse this ROS generation in vitro[1].
Nitrovin (0.625-5 μM; 24 h) induces paraptosis-like cell death in human glioblastoma U251 and U87 cells, as Cycloheximide (HY-12320) reverses cell death and vacuolation, and nitrovin downregulates Alix expression without Alix overexpression rescuing cell death in vitro[1].
Nitrovin (5 μM; 0-24 h) induces ER stress and MAPK activation in human glioblastoma U251 cells, but these pathways do not mediate nitrovin-induced cell death in vitro[1].
Nitrovin (1.25-10 μM; 30 min-24 h) directly targets TrxR1 to inhibit its activity, and TrxR1 overexpression reverses Nitrovin-induced ROS generation and paraptosis-like cell death in human glioblastoma U251 cells in vitro[1].
Nitrovin (1-5 μM; days 6-14 of 14-day culture) promotes differentiation of CMK 6.4 cynomolgus monkey ES cells into cardiac muscle cells, as shown by increased GFP fluorescence intensity[2].
Nitrovin (5 μM; administered during days 6-14 of 18-day culture) more effectively promotes differentiation of CMK 6.4 cynomolgus monkey ES cells into cardiac muscle cells than a cytokine mixture, and exhibits a synergistic effect when combined with cytokines[2].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:16 human/murine cancer cell lines (HCT-116, HT-29, A549, H460, H596, MDA-MB-231, MCF-7, A375, HepG2, Hep3B, Bel-7402, K562, 4T1, T24, U251, U87), 2 normal human cell lines (LO2, HK2)
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Concentration:0.625-10 μM
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Incubation Time:24 h
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Result:Reduced cell viability in a concentration-dependent manner across all tested cancer cell lines, with IC50 values ranging from 1.31 μM (A375) to 5.00 μM (HT-29).
Exhibited relatively low cytotoxicity to normal cell lines LO2 and HK2, with IC50 values of 5.34 μM and 6.60 μM, respectively.
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Cell Line:human glioblastoma U251 and U87 cells
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Concentration:1.25-10 μM
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Incubation Time:24 h
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Result:Reduced U251 and U87 cell viability in a concentration-dependent manner, with significant decreases at all tested concentrations.
Significantly decreased intracellular ATP levels in both cell lines in a concentration-dependent manner.
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Cell Line:human glioblastoma U251 cells
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Concentration:0.625-5 μM
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Incubation Time:24 h
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Result:Had no significant effect on caspase-3 activity or cleavage of caspase-3/7.
Showed no condensed chromatin or fragmented nuclei via Hoechst staining.
Detected only a very small proportion of apoptotic cells via Annexin V/7AAD staining.
Pretreatment with pan-caspase inhibitor Z-VAD-FMK (20 μM for 1 h) did not reverse nitrovin-induced cell death or morphological changes.
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Cell Line:CMK 6.4 cynomolgus monkey ES cells (expressing GFP under control of the α-MHC promoter)
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Concentration:1-5 μM
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Incubation Time:days 6-14 of 14-day culture
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Result:Resulted in high GFP fluorescence intensity, indicating promoted differentiation into cardiac muscle cells.
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Cell Line:CMK 6.4 cynomolgus monkey ES cells (expressing GFP under control of the α-MHC promoter)
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Concentration:1-20 μM
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Incubation Time:added at day 6 of 18-day culture
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Result:Increased GFP fluorescence intensity up to ~5-fold relative to control.
Increased the number of beating colonies up to ~10-fold relative to control.
Exhibited the most effective activity at 5 μM concentration.
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Cell Line:Kh-1 human ES cells (expressing GFP under control of the α-MHC promoter)
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Concentration:1-20 μM
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Incubation Time:added at day 6 of 18-day culture
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Result:Increased GFP fluorescence intensity relative to control, indicating promoted differentiation into cardiac muscle cells.
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Cell Line:CMK 6.4 cynomolgus monkey ES cells (expressing GFP under control of the α-MHC promoter)
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Concentration:5 μM
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Incubation Time:administered during days 6-14 of 18-day culture
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Result:Increased GFP fluorescence intensity, number of beating colonies, and Troponin T expression more effectively than a cytokine mixture.
Exhibited a synergistic effect on GFP fluorescence intensity and beating colony number when combined with the cytokine mixture.
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:wild-type larvae Zebrafish with Glioblastoma multiforme[1]
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Dosage:2.5 μM; 5 μM; 10 μM
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Administration:continuous exposure; 2-3 days
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Result:Reduced tumor fluorescence area to ~100% of control at 2.5 μM.
Reduced tumor fluorescence area to ~60% of control at 5 μM.
Reduced tumor fluorescence area to ~45% of control at 10 μM.
Showed inhibitory effect at 5 μM comparable to that of 100 μM TMZ.
Restored tumor fluorescence area to ~70% of control when co-treated with 5 mM NAC (10 μM nitrovin).
Failed to reverse anticancer effect when co-treated with 100 μM vitamin C (10 μM nitrovin).
Chemical Information
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CAS No. 804-36-4
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Molecular Weight 360.28
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Formula C14H12N6O6
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SMILES
O=[N+](C1=CC=C(/C=C/C(/C=C/C2=CC=C([N+]([O-])=O)O2)=N\NC(N)=N)O1)[O-]
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Synonyms
Difurazon
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Please store the product under the recommended conditions in the Certificate of Analysis.
Purity & Documentation
References
Calculators
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
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