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Bis(maltolato)oxovanadium(IV) Sale

(Synonyms: 双(麦芽醇)氧钒(IV),BMOV) 目录号 : GC60647

BMOV (Bis maltolato oxovanadium, Bis(maltolato)oxovanadium (IV)) is a potent oral vanadium complex with anti-diabetic properties and insulin-mimicking effects.BMOV is shown to improve cardiac dysfunctions in diabetic models.

Bis(maltolato)oxovanadium(IV) Chemical Structure

Cas No.:38213-69-3

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10mg
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产品描述

BMOV (Bis maltolato oxovanadium, Bis(maltolato)oxovanadium (IV)) is a potent oral vanadium complex with anti-diabetic properties and insulin-mimicking effects.BMOV is shown to improve cardiac dysfunctions in diabetic models.

[1] Cong XQ, et al. Biol Trace Elem Res. 2016 Oct;173(2):390-8.

Chemical Properties

Cas No. 38213-69-3 SDF
别名 双(麦芽醇)氧钒(IV),BMOV
Canonical SMILES O=[V+2]([O-]C1=C2C)([O]=C1C=CO2)([O]=C3C=CO4)[O-]C3=C4C
分子式 C12H10O7V 分子量 317.15
溶解度 DMSO : 25 mg/mL (78.83 mM; ultrasonic and warming and heat to 60°C) 储存条件 Store at -20°C
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1 mM 3.1531 mL 15.7654 mL 31.5308 mL
5 mM 0.6306 mL 3.1531 mL 6.3062 mL
10 mM 0.3153 mL 1.5765 mL 3.1531 mL
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Research Update

Bis(maltolato)oxovanadium(IV) Induces Angiogenesis via Phosphorylation of VEGFR2

Int J Mol Sci 2020 Jun 30;21(13):4643.PMID:32629855DOI:10.3390/ijms21134643.

VEGFR2 and VEGF-A play a pivotal role in the process of angiogenesis. VEGFR2 activation is regulated by protein tyrosine phosphatases (PTPs), enzymes that dephosphorylate the receptor and reduce angiogenesis. We aim to study the effect of PTPs blockade using Bis(maltolato)oxovanadium(IV) (BMOV) on in vivo wound healing and in vitro angiogenesis. BMOV significantly improves in vivo wound closure by 45% in C57BL/6JRj mice. We found that upon VEGFR2 phosphorylation induced by endogenously produced VEGF-A, the addition of BMOV results in increased cell migration (45%), proliferation (40%) and tube formation (27%) in HUVECs compared to control. In a mouse ex vivo, aortic ring assay BMOV increased the number of sprouts by 3 folds when compared to control. However, BMOV coadministered with exogenous VEGF-A increased ECs migration, proliferation and tube formation by only 41%, 18% and 12% respectively and aortic ring sprouting by only 1-fold. We also found that BMOV enhances VEGFR2 Y951 and p38MAPK phosphorylation, but not ERK1/2. The level of phosphorylation of these residues was the same in the groups treated with BMOV supplemented with exogenous VEGF-A and exogenous VEGF-A only. Our study demonstrates that BMOV is able to enhance wound closure in vivo. Moreover, in the presence of endogenous VEGF-A, BMOV is able to stimulate in vitro angiogenesis by increasing the phosphorylation of VEGFR2 and its downstream proangiogenic enzymes. Importantly, BMOV had a stronger proangiogenic effect compared to its effect in coadministration with exogenous VEGF-A.

Bis(maltolato)-oxovanadium (IV)-induced phosphorylation of PKB, GSK-3 and FOXO1 contributes to its glucoregulatory responses (review)

Int J Mol Med 2009 Sep;24(3):303-9.PMID:19639221DOI:10.3892/ijmm_00000233.

Over the last several decades, a large body of evidence has accumulated to suggest that organo-vanadium compounds (OVC) are more potent than inorganic vanadium salts in regulating hyperglycemia and insulin-resistance in rodent models of both type I and type II diabetes. Among these OVC, vanadium (IV) oxo bis(maltolato) (BMOV) was the first to be investigated for its higher potency over inorganic vanadium salts in eliciting insulin-like properties in both in vitro and in vivo systems. While the precise molecular mechanism by which BMOV exerts its insulin-mimetic effects remains poorly defined, studies have shown that BMOV is a potent activator of several key components of the insulin signaling pathways, such as phosphatidyl-inositol 3-kinase (PI3-K), and its downstream effector, protein kinase B (PKB). In addition, BMOV-induced phosphorylation of PKB has also been associated with the enhanced phosphorylation of glycogen synthase kinase-3 (GSK-3) and forkhead box protein 1 (FOXO1). Since PKB is instrumental in mediating the effects of insulin on glucose transport, glycogen synthesis and gluconeogenesis, it is reasonable to suggest that activation of this pathway by BMOV serves as a mechanism for its insulin-like effects.

Effect of Bis(maltolato)oxovanadium(IV) on Zinc, Copper, and Manganese Homeostasis and DMT1 mRNA Expression in Streptozotocin-Induced Hyperglycemic Rats

Biology (Basel) 2022 May 25;11(6):814.PMID:35741335DOI:10.3390/biology11060814.

Our aim was to examine whether vanadium (IV) corrects alterations in zinc, copper and manganese homeostasis, observed in streptozotocin-induced hyperglycemic rats, and whether such changes are related to divalent metal transporter 1 (DMT1) mRNA expression, and antioxidant and proinflammatory parameters. Four groups of Wistar rats were examined: control; hyperglycemic (H); hyperglycemic treated with 1 mg V/day (HV); and hyperglycemic treated with 3 mg V/day (HVH). Vanadium was supplied in drinking water as Bis(maltolato)oxovanadium(IV) for five weeks. Zinc, copper and manganese were measured in food, excreta, serum and tissues. DMT1 mRNA expression was quantified in the liver. Hyperglycemic rats showed increased Zn and Cu absorption and content in the liver, serum, kidneys and femurs; DMT1 expression also increased (p < 0.05 in all cases). HV rats showed no changes compared to H rats other than decreased DMT1 expression (p < 0.05). In the HVH group, decreased absorption and tissular content of studied elements (p < 0.05 in all cases) and DMT1 expression compared to H (p < 0.05) were observed. Liver zinc, copper and manganese content correlated positively with glutathione peroxidase activity and negatively with catalase activity (p < 0.05 in both cases). In conclusion, treatment with 3 mg V/d reverted the alterations in zinc and copper homeostasis caused by hyperglycemia, possibly facilitated by decreased DMT1 expression.

Bis(maltolato)oxovanadium(IV) attenuates hyperinsulinemia and hypertension in spontaneously hypertensive rats

Diabetes 1994 Jul;43(7):857-61.PMID:8013747DOI:10.2337/diab.43.7.857.

We previously reported that Bis(maltolato)oxovanadium(IV) (BMOV), an organic vanadium complex, decreased plasma insulin concentrations in nondiabetic rats without affecting plasma glucose levels (McNeill JH, Yuen VG, Hoveyda HR, Orvig C: Bis(maltolato)oxovanadium(IV) is a potent insulin mimic. J Med Chem 35:1489-1491, 1992). In this study, chronic oral BMOV treatment was started in 6-week-old spontaneously hypertensive (SH) rats and their Wistar-Kyoto (WKY) controls, and the effects of the drug on insulin sensitivity, plasma insulin, and blood pressure (BP) were studied. BMOV (0.35-0.45 mmol.kg-1.day-1) caused a sustained reduction in plasma insulin (198 +/- 6 vs. untreated 366 +/- 13.2 pM, P < 0.0001) and systolic BP (149 +/- 3 vs. untreated 184 +/- 3 mmHg, P < 0.0001) in SH rats. No changes were seen in WKY rats (plasma insulin: treated 228 +/- 4.8 vs. untreated 222.6 +/- 3.6 pM, P > 0.05; BP: treated 134 +/- 3 vs. untreated 134 +/- 5 mmHg, P > 0.05). At 13 weeks of age, euglycemic clamps were performed in fasted, conscious, mobile rats. During low-dose insulin infusions (14 pmol.kg-1.min-1) with concomitant somatostatin administration, neither hepatic glucose output nor total body glucose uptake differed between the untreated SH and WKY rats. Insulin sensitivity, expressed as steady-state glucose clearance per unit of plasma insulin, was higher in the untreated SH compared with the untreated WKY rats (2.1 +/- 0.2 vs. 1.2 +/- 0.1 ml.kg-1.h-1.pM-1, P < 0.002). BMOV further enhanced insulin sensitivity in SH rats (3.6 +/- 0.4, P < 0.002 vs. untreated SH rats).(ABSTRACT TRUNCATED AT 250 WORDS)

Vibrational spectra of Bis(maltolato)oxovanadium(IV): a potent insulin mimetic agent

Spectrochim Acta A Mol Biomol Spectrosc 2011 Jan;78(1):133-5.PMID:20934377DOI:10.1016/j.saa.2010.09.010.

The FTIR and FT-Raman spectra of the oxovanadium(IV) complex of 3-hydroxy-2-methyl-4-pyrone (maltol) Bis(maltolato)oxovanadium(IV) were recorded and briefly discussed by comparison with the spectra of uncoordinated maltol and with some related species.