| Vanadyl acetylacetonate | |
|---|---|
|
oxobis(2,4-pentanedionato)vanadium(IV) |
|
|
Other names
VO(acac)2, VO(pd)2 |
|
| Identifiers | |
| CAS number | 3153-26-2 |
| PubChem | 16217092 |
| Properties | |
| Molecular formula | C10H14O5V |
| Molar mass | 265.157 |
| Appearance | blue-green |
| Density | 1.50 g/cm3 |
| Melting point |
258 °C |
| Boiling point |
174 °C (at 0.2 torr) |
| Solubility in water | CHCl3, CH2Cl2, Benzene, CH3OH, CH3CH2OH |
| (verify) (what is: /?) Except where noted otherwise, data are given for materials in their standard state (at 25 °C, 100 kPa) |
|
| Infobox references | |
Vanadyl acetylacetonate is the chemical compound with the formula VO(C5H7O2)2. This blue-green coordination complex consists of the vanadyl group, VO2+, bound to two acetylacetonate anions, acac−. Like other charge-neutral acetylacetonates, this complex is soluble in organic solvents.
Contents |
The complex is prepared from vanadium(IV), e.g. vanadyl sulfate, or vanadium(V) precursors, such as vanadium pentoxide.[1] The equation for the redox reaction starting from the pentoxide can be described by this approximate equation:
The compound is recrystallized from chloroform.
The complex has a square pyramidal structure with a short V=O bond. This d1 compound is paramagnetic. Its optical spectrum exhibits two transitions. It is a weak Lewis acid, forming adducts with pyridine and methylamine.[1]
It is used in organic chemistry as a reagent in the epoxidation of allylic alcohols in combination with tert-butyl hydroperoxide (TBHP). The VO(acac)2-TBHP system exclusively epoxidizes geraniol at the allylic alcohol position. For comparison, another epoxidizing agent m-CPBA, reacts with both groups, creating the products in a two to one ratio, favoring the allylic position away from the alcohol. TBHP oxidizes VO(acac)2 to a vanadium(V) species which coordinates the alcohol of the substrate and the hydroperoxide.[2][3]
Vanadyl(acac) exhibits insulin mimetic properties, in that in can stimulate the phosphorylation of protein kinase B (PKB/Akt) and glycogen synthase kinase-3 (GSK3).[4] It has also been shown inhibit tyrosine phosphatase(PTPase), PTPases such as PTP1B, which dephosphorylates insulin receptor beta subunit, thus increasing its phosphorylation, allowing for a prolonged activation of IRS-1, PKB, and GSK3, allowing them to exert their anti-diabetic properties.[4]