Details
Stereochemistry | ACHIRAL |
Molecular Formula | 5O.2V |
Molecular Weight | 181.88 |
Optical Activity | NONE |
Defined Stereocenters | 0 / 0 |
E/Z Centers | 0 |
Charge | 0 |
SHOW SMILES / InChI
SMILES
[O--].[O--].[O--].[O--].[O--].[V+5].[V+5]
InChI
InChIKey=XHCLAFWTIXFWPH-UHFFFAOYSA-N
InChI=1S/5O.2V/q5*-2;2*+5
DescriptionSources: https://www.ncbi.nlm.nih.gov/pubmed/22749912
Sources: https://www.ncbi.nlm.nih.gov/pubmed/22749912
There is no information about pharmacological and biological application of vanadium pentoxide (V2O5). However, inhalation of this substance is a toxic for mammalian and repeated exposures to V2O5 containing particles may augment lung carcinogenesis in susceptible individuals through oxidative stress mediated pathways.
CNS Activity
Sources: https://www.ncbi.nlm.nih.gov/pubmed/15882783
Curator's Comment: Known to be CNS penetrant in mouse. Human data not available
blood-brain barrier disruption
Approval Year
Targets
Primary Target | Pharmacology | Condition | Potency |
---|---|---|---|
Target ID: CHEMBL335 Sources: https://www.ncbi.nlm.nih.gov/pubmed/11128645 |
30.8 µM [IC50] | ||
Target ID: CHEMBL4804 Sources: https://www.ncbi.nlm.nih.gov/pubmed/22524450 |
|||
Target ID: CHEMBL205 Sources: https://www.ncbi.nlm.nih.gov/pubmed/15664814 |
11.6 mM [IC50] | ||
Target ID: CHEMBL3729 Sources: https://www.ncbi.nlm.nih.gov/pubmed/15664814 |
44.8 mM [IC50] | ||
Target ID: CHEMBL3594 Sources: https://www.ncbi.nlm.nih.gov/pubmed/15664814 |
42.6 mM [IC50] |
Conditions
Condition | Modality | Targets | Highest Phase | Product |
---|---|---|---|---|
PubMed
Title | Date | PubMed |
---|---|---|
Toxic metals stimulate inflammatory cytokines in hepatocytes through oxidative stress mechanisms. | 1998 Aug |
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Vanadium stimulates human bronchial epithelial cells to produce heparin-binding epidermal growth factor-like growth factor: a mitogen for lung fibroblasts. | 2001 Feb |
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Map kinase activation correlates with K-ras mutation and loss of heterozygosity on chromosome 6 in alveolar bronchiolar carcinomas from B6C3F1 mice exposed to vanadium pentoxide for 2 years. | 2002 Oct |
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Vanadium-induced HB-EGF expression in human lung fibroblasts is oxidant dependent and requires MAP kinases. | 2003 May |
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Single-walled carbon nanotube (SWCNT)-induced interstitial fibrosis in the lungs of rats is associated with increased levels of PDGF mRNA and the formation of unique intercellular carbon structures that bridge alveolar macrophages in situ. | 2006 Nov 29 |
|
Genomic analysis of human lung fibroblasts exposed to vanadium pentoxide to identify candidate genes for occupational bronchitis. | 2007 Apr 25 |
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STAT-1 signaling in human lung fibroblasts is induced by vanadium pentoxide through an IFN-beta autocrine loop. | 2008 Mar 15 |
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Use of short-term transcriptional profiles to assess the long-term cancer-related safety of environmental and industrial chemicals. | 2009 Dec |
|
Vanadium induces dopaminergic neurotoxicity via protein kinase Cdelta dependent oxidative signaling mechanisms: relevance to etiopathogenesis of Parkinson's disease. | 2009 Oct 15 |
Sample Use Guides
In Vivo Use Guide
Sources: https://www.ncbi.nlm.nih.gov/pubmed/14600283
toxicity study:
Female F344 rats and B6C3F1 mice were exposed to vanadium pentoxide (V2O5) at concentrations of 0, 0.5, 1, or 2 mg/m3 (rats) and 0, 1, 2, or 4 mg/m3 (mice) for 6 h/day, 5 days/week (for up to 18 months), by whole-body inhalation.
Route of Administration:
Respiratory
In Vitro Use Guide
Sources: https://www.ncbi.nlm.nih.gov/pubmed/21721017
It was study to evaluate the effect of vanadium pentoxide (V2O5) on endothelial cells since they are key participants in the pathogenesis of several cardiovascular and inflammatory diseases. Cell adhesion, the expression of adhesion molecules and oxidative stress, as well as proliferation, morphology and cell death of human umbilical vein endothelial cells (HUVECs) exposed to V2O5, were evaluated. Vanadium pentoxide at a 3.12 µg cm(-2) concentration induced an enhanced adhesion of the U937 macrophage cell line to HUVECs, owing to an increased expression of late adhesion molecules. HUVECs exposed to V2O5 showed an increase in ROS and nitric oxide production, and a diminished proliferation. These changes in vanadium-treated HUVECs were accompanied by severe morphological changes and apoptotic cell death. Vanadium pentoxide induced serious endothelial cell damage, probably related to the increased cardiovascular morbidity and mortality observed in individuals living in highly air-polluted areas.
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BVG363OH7A
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Vanadium pentoxide
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215-239-8
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m11377
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1024
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1314-62-1
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C066075
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SUBSTANCE RECORD