Sodium metavanadate, 99%
Based on 1 publication(s) in Google Scholar
Sodium metavanadate, 99% (Sodium vanadate (V), 99%) is an orally active phosphate structural analog and protein tyrosine phosphatase (PTPases) inhibitor. Sodium metavanadate, 99% mimics phosphate to interfere with phosphoprotein reactions, inhibits GAPDH, Na+/K+-ATPase and microbial membrane ATPase, and acts as a terminal electron acceptor for anaerobic respiration. Sodium metavanadate, 99% induces ROS production, G2/M phase arrest, mitochondrial membrane potential loss and apoptosis in breast cancer cells, and reduces tumor volume in tumor-bearing mice. Sodium metavanadate, 99% also exhibits oral insulin-sensitizing and metabolic regulatory activities, and reduces plasmodium parasitemia levels. Sodium metavanadate, 99% can be used in studies related to cadmium exposure-induced metabolic syndrome, plasmodium infection, breast cancer and type 1 diabetes.
For research use only. We do not sell to patients.
- Purity: 99.34%
- CAS No.: 13718-26-8
- Formula: NaVO3
- Molecular Weight:121.93
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Storage:
Store at room temperature, keep dry and cool.
In solvent -80°C, 1 year , -20°C, 6 months
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Biological Activity
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Chemical Information
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Solvent & Solubility
- Purity & Documentation
- References
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Help & FAQs
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Publications Citing Use of MedChemExpress (MCE) Sodium metavanadate, 99%
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Biological Activity
Description
Cellular Effect
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Cell Line
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Type | Value | Description | References |
|---|---|---|---|---|
| 4T1 | IC50 |
8.19 μM
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Cytotoxicity against murine breast cancer 4T1 cells assessed as reduction in cell viability incubated for 24 hrs by MTT assay.
Cytotoxicity against murine breast cancer 4T1 cells assessed as reduction in cell viability incubated for 24 hrs by MTT assay.
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33689084 |
| 4T1 | IC50 |
1.92 μM
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Cytotoxicity against murine breast cancer 4T1 cells assessed as reduction in cell viability incubated for 48 hrs by MTT assay.
Cytotoxicity against murine breast cancer 4T1 cells assessed as reduction in cell viability incubated for 48 hrs by MTT assay.
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33689084 |
In Vitro
Sodium metavanadate, 99% (0.1-20 mM; 24 h) exhibits medium-dependent inhibitory effects. In Sabouraud's complex medium, the MIC of SC-1 is 16 mM, while the MICs of DBVPG 6173, 6174/6176 and 6037/6220 are 4 mM, 6 mM and 8 mM, respectively. In YNB basal medium, SC-1 tolerates concentrations up to 10 mM, whereas DBVPG 6173 and 6037 are significantly inhibited when the concentration exceeds 4 mM[1].
Sodium metavanadate, 99% (2-10 mM; 18-24 h) exhibits strain-dependent uptake, reduction and resistance characteristics in Saccharomyces cerevisiae: SC-1 does not accumulate vanadate at high concentrations, but accumulates moderate levels of total vanadium and reduces it to vanadyl ions at lower concentrations; DBVPG 6173 and 6037 show significant differences in accumulation levels and cannot reduce this compound; the drug resistance of SC-1 is constitutive, and pre-exposure does not alter its growth lag phase[1].
Sodium metavanadate, 99% (0.01-1000 μM; 24-48 h) potently inhibits the proliferation of 4T1 mouse breast cancer cells, with an IC50 value of 8.19 μM at 24 h and 1.92 μM at 48 h, and autophagy enhances this inhibitory effect[4].
Sodium metavanadate, 99% (1-100 μM; 24 h) increases the intracellular ROS level in 4T1 mouse breast cancer cells in a concentration-dependent manner[4].
Sodium metavanadate, 99% (10-100 μM; 24 h) induces G2/M phase arrest in 4T1 mouse breast cancer cells[4].
Sodium metavanadate, 99% (1-100 μM; 24 h) induces concentration-dependent apoptosis in 4T1 mouse breast cancer cells, and necroptosis is not involved in this cell death pathway[4].
Sodium metavanadate, 99% (1-100 μM; 24 h) reduces the mitochondrial membrane potential of 4T1 mouse breast cancer cells in a concentration-dependent manner[4].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Cell Line:murine breast cancer 4T1 cells
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Concentration:0.01, 0.1, 1, 10, 100 and 1000 μM (24 h, 48 h); 10 μM (24 h, combined with 3-M (AHY-19312))
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Incubation Time:24 h; 48 h
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Result:Exhibited time- and concentration-dependent cytotoxicity toward 4T1 cells.
Reached IC50 values of 8.19 μM at 24 h and 1.92 μM at 48 h.
Enhanced cytotoxicity was observed when co-treated with autophagy inducer rapamycin.
Slightly increased cell viability was observed when co-treated with autophagy inhibitor 3-MA.
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Cell Line:murine breast cancer 4T1 cells
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Concentration:10, 50 and 100 μM
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Incubation Time:24 h
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Result:Induced G2/M phase arrest in 4T1 cells.
Increased the proportion of cells in G2/M phase to 13.7% at 10 μM, 14.8% at 50 μM, and 42.1% at 100 μM, compared to 9.8% in control.
Decreased the proportion of cells in G0/G1 phase to 34.4% at 10 μM, 32.8% at 50 μM, and 16.7% at 100 μM, compared to 51.0% in control.
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Cell Line:murine breast cancer 4T1 cells
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Concentration:1, 10, 50 and 100 μM (apoptosis assays); 10 μM (24 h, combined with 20-80 μM Nec-1 (HY-15760))
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Incubation Time:24 h
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Result:Induced apoptosis in 4T1 cells in a concentration-dependent manner.
Reached total apoptosis rates of 11.3% at 1 μM, 14.6% at 10 μM, and 39.3% at 100 μM, compared to 6.5% in control.
Reached early apoptosis rates of 10.1% at 1 μM, 13.5% at 10 μM, and 15.8% at 100 μM.
Reached late apoptosis rates of 1.2% at 1 μM, 1.1% at 10 μM, and 23.5% at 100 μM.
Did not show significant reduction in apoptosis when co-treated with Nec-1.
In Vivo
Sodium metavanadate, 99% (10 mg/kg/day; oral administration; once daily for 4 consecutive days) reduces the level of parasitemia in CD-1 mice infected with Plasmodium yoelii yoelii, and causes extensive ultrastructural damage to the cell membrane, mitochondria and nucleus of all blood-stage malaria parasites[3].
Sodium metavanadate, 99% (10 mg/kg/day; p.o.; daily administration; for 4 consecutive days) does not alter the red blood cell morphology of healthy CD-1 mice[3].
Sodium metavanadate, 99% (10-20 mg/kg; i.p.; once daily; for 21 consecutive days) exhibits dose-dependent anticancer activity in a mouse breast cancer xenograft model. Doses higher than 15 mg/kg inhibit tumor growth but cause significant body weight loss[4].
Sodium metavanadate, 99% (0.1-0.3 mg/mL; p.o.; ad libitum access to drug-containing drinking water; 7 days) delays the onset of spontaneous type 1 diabetes in BB-DP rats in a concentration-dependent manner, reduces the severity of diabetes in affected rats, but cannot prevent disease onset[5].
MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.
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Animal Model:Wistar (male, starting weight 80-100 g, conditioned to 120 g prior to study initiation, cadmium-induced metabolic syndrome model)[2]
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Dosage:5 μM/kg
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Administration:p.o.; twice a week; 2 months
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Result:Reduced fasting glycemia by 27% after 1 month.
Improved oral glucose tolerance significantly at 30, 60, and 90 minutes after 1 month.
Increased glycogen levels above control levels by 65.6% in liver, 190% in muscle, 91.5% in heart, 46.3% in renal cortex, and 115% in renal medulla after 1 month.
Lowered BMI and body fat percentage significantly from the first week of monitoring.
Reduced cadmium concentrations in liver, kidney, heart, muscle, and adipose tissue after 1 month.
Increased adipose tissue triglyceride content by 18.5% compared to untreated cadmium group after 1 month.
Reduced fasting glycemia slightly significantly after 2 months.
Improved oral glucose tolerance with glucose levels reduced by 28.6% at 30 minutes and 21.8% at 60 minutes after 2 months.
Increased glycogen levels above control levels by 45.2% in liver, 289.4% in muscle, 57.1% in heart, and 129.1% in renal medulla after 2 months.
Reduced cadmium concentrations in liver, kidney, heart, and muscle after 2 months.
Reduced adipose tissue triglyceride content by 12.8% compared to the 1-month monitoring time point after 2 months.
Exerted no effect on dyslipidemia or tissue triglyceride storage (except adipose tissue changes noted).
Altered no parameters in non-cadmium-exposed control rats.
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Animal Model:CD-1 (male, 30 g, infected i.p. with 25×103 erythrocytes parasitized with Plasmodium yoelii yoelii)[3]
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Dosage:10 mg/kg/day
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Administration:p.o.; daily; 4 days
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Result:Reduced parasitemia by approximately 50% compared to untreated infected mice.
Caused discontinuity of the parasitophorous vacuole, nuclear membranes, and digestive vacuole, plus edema in the cytoplasm and nucleoplasm in ring-stage parasites.
Induced cytoplasmic lipid droplets and vacuoles, plus lipid droplets and damage within mitochondrial matrices in mature trophozoites.
Caused cytoplasmic lipid droplets, mitochondrial membrane discontinuities and swelling, increased perinuclear cistern size, and cellular disorganization in immature schizont-stage merozoites.
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Animal Model:CD-1 (male, 30 g)[3]
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Dosage:10 mg/kg/day
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Administration:p.o.; daily; 4 days
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Result:Observed no morphological changes to erythrocytes; erythrocytes maintained their characteristic biconcave disc shape.
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Animal Model:BALB/C nude mice (4-6 weeks of age)[4]
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Dosage:10 mg/kg; 15 mg/kg; 20 mg/kg
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Administration:i.p.; daily; 21 days
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Result:Reduced tumor growth by approximately 50% compared to the saline group at 10 mg/kg.
Reduced tumor growth by approximately 64% compared to the saline group at 15 mg/kg and 20 mg/kg.
Did not cause obvious weight loss at 10 mg/kg.
Caused significant body weight decreases at 15 mg/kg and 20 mg/kg.
Reduced tumor cell proliferation (measured by Ki-67 density) in a dose-dependent manner.
Reduced tumor microvessel density (measured by CD31 staining) in a dose-dependent manner.
Increased tumor cell apoptosis (measured by TUNEL assay) in a dose-dependent manner.
Decreased pro-caspase-9 and PARP protein levels significantly across all doses.
Caused slight down-regulation of pro-caspase-3 across all doses.
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Animal Model:Bio-Breeding Diabetes Prone (BB-DP) (40-50 days old, 140-250 g, prediabetic, spontaneously developing autoimmune diabetes)[5]
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Dosage:0.1 mg/mL; 0.2 mg/mL; 0.3 mg/mL
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Administration:p.o.; ad libitum in drinking water; 7 days
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Result:Delayed age of diabetes onset to 84.8 days (0.1 mg/mL), 102.8 days (0.2 mg/mL), and 105.5 days (0.3 mg/mL).
Reduced diabetes incidence to 50% (0.1 mg/mL), 45.8% (0.2 mg/mL), and 45.8% (0.3 mg/mL).
Decreased blood glucose levels from 95.6 mg/dl to 63 mg/dl (0.1 mg/mL), 100.3 mg/dl to 73 mg/dl (0.2 mg/mL), and 98 mg/dl to 73 mg/dl (0.3 mg/mL) in week 1, with levels remaining lower than controls over 90 days.
Recorded blood glucose at diabetes onset as 276.8 mg/dl (0.1 mg/mL) and 286.1 mg/dl (0.2 mg/mL).
Increased body weight slightly from 309.4 g to 344 g across all treated groups in the two weeks before diabetes onset.
Reduced insulinemia to 0.43 µg/l (0.1 mg/mL), 0.38 µg/l (0.2 mg/mL), and 0.27 µg/l (0.3 mg/mL) at 7 days post-treatment start; levels rose to 1.15 µg/l (0.1 mg/mL), 2.89 µg/l (0.2 mg/mL), and 0.86 µg/l (0.3 mg/mL) by day 90.
Chemical Information
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CAS No. 13718-26-8
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Appearance Solid
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Molecular Weight 121.93
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Formula NaVO3
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Color Off-white to light yellow
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SMILES
O=[V](=O)([Na])=O
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Synonyms
Sodium vanadate(V), 99%
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Shipping
Room temperature in continental US; may vary elsewhere.
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Storage
Store at room temperature, keep dry and cool
In solvent -80°C 1 year -20°C 6 months
Publications (1)
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Journal Impact Factor
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Most Recent
Solvent & Solubility
In Vitro:
H2O : 10 mg/mL (82.01 mM; Need ultrasonic)
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 1 year; -20°C, 6 months. When stored at -80°C, please use it within 1 year. When stored at -20°C, please use it within 6 months.
* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 1 year; -20°C, 6 months. When stored at -80°C, please use it within 1 year. When stored at -20°C, please use it within 6 months.
* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.
Concentration (start) × Volume (start) = Concentration (final) × Volume (final)
Purity & Documentation
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Data Sheet (307 KB)
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SDS (789 KB)
- English - EN (789 KB)
- Français - FR (789 KB)
- Deutsch - DE (789 KB)
- Norwegian - NO (789 KB)
- Español - ES (789 KB)
- Swedish - SV (789 KB)
- Italian - IT (789 KB)
- Korean - KR (789 KB)
- Portuguese - PT (789 KB)
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Handling Instructions (2659 KB)
References
[1]. Bisconti L, et al. Reduction of vanadate to vanadyl by a strain of Saccharomyces cerevisiae. Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine. 1997 Oct;10(4):239-46. [Content Brief]
[5]. Cheta D, et al. The influence of sodium metavanadate on the process of diabetogenesis in BB rats. Journal of cellular and molecular medicine. 2003;7(4):447-54. [Content Brief]
Complete Stock Solution Preparation Table
Please refer to the solubility information to select the appropriate solvent. Once prepared, please aliquot and store the solution to prevent product inactivation from repeated freeze-thaw cycles.
Storage method and period of stock solution: -80°C, 1 year; -20°C, 6 months. When stored at -80°C, please use it within 1 year. When stored at -20°C, please use it within 6 months.
| Optional Solvent | Concentration Solvent Mass | 1 mg | 5 mg | 10 mg | 25 mg |
|---|---|---|---|---|---|
| H2O | 1 mM | 8.2014 mL | 41.0071 mL | 82.0143 mL | 205.0357 mL |
| 5 mM | 1.6403 mL | 8.2014 mL | 16.4029 mL | 41.0071 mL | |
| 10 mM | 0.8201 mL | 4.1007 mL | 8.2014 mL | 20.5036 mL | |
| 15 mM | 0.5468 mL | 2.7338 mL | 5.4676 mL | 13.6690 mL | |
| 20 mM | 0.4101 mL | 2.0504 mL | 4.1007 mL | 10.2518 mL | |
| 25 mM | 0.3281 mL | 1.6403 mL | 3.2806 mL | 8.2014 mL | |
| 30 mM | 0.2734 mL | 1.3669 mL | 2.7338 mL | 6.8345 mL | |
| 40 mM | 0.2050 mL | 1.0252 mL | 2.0504 mL | 5.1259 mL | |
| 50 mM | 0.1640 mL | 0.8201 mL | 1.6403 mL | 4.1007 mL | |
| 60 mM | 0.1367 mL | 0.6835 mL | 1.3669 mL | 3.4173 mL | |
| 80 mM | 0.1025 mL | 0.5126 mL | 1.0252 mL | 2.5629 mL |
* Note: If you choose water as the stock solution, please dilute it to the working solution, then filter and sterilize it with a 0.22 μm filter before use.
Sodium metavanadate, 99% Related Classifications
HY-D0852A Related Classifications
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Keywords
- Sodium metavanadate, 99%
- 13718-26-8
- Sodium vanadate(V), 99%
- Phosphatase
- Parasite
- Reactive Oxygen Species (ROS)
- Apoptosis
- Plasmodium yoelii yoelii
- 4T1 murine breast cancer cells
- Saccharomyces cerevisiae
- Na+/K+ pumps
- breast cancer cells
- BB-DP rats
- Pseudomonas
- Neurospora crassa
- Wistar rats
- glyceraldehyde-3-phosphate dehydrogenase
- Inhibitor
- inhibitor
- inhibit