bpV(phen)bpV(phen)
MedChemExpress (MCE)
HY-136065
42494-73-5
98.0%
4°C, sealed storage, away from moisture *In solvent : -80°C, 6 months
-20°C, 1 month (sealed storage, away from moisture)
Room temperature in continental US
may vary elsewhere.
bpV(phen), a insulin-mimetic agent, is a potent protein tyrosine phosphatase (PTP) and PTEN inhibitor with IC50s of 38 nM, 343 nM and 920 nM for PTEN, PTP-β and PTP-1B, respectively. bpV(phen) inhibits proliferation of the protozoan parasite Leishmania in vitro. bpV(phen) strongly induces the secretion of a large number of chemokines and pro-inflammatory cytokines, and it activates a Th1-type pathway (IL-12, IFNγ). bpV(phen) can also induce cell apoptosis, and has anti-angiogenic and anti-tumor activity.
bpV(phen) (5 μM
24.5 hours
H9c2 cells) treatment causes a further decrease of cell viability in H/R-injured H9c2 cells[1]. bpV(phen) (5 μM
24.5 hours
H9c2 cells) treatment increases the apoptosis of H/R-injured H9c2 cells[1]. bpV(phen) (5 μM
24.5 hours
H9c2 cells) treatment significantly promotes the accumulation of cytoplasmic Cytochrome C in H/R-injured H9c2 cells[1]. After stimulation of bpV(phen), PTEN-induced putative kinase protein 1 (PINK1)/Parkin-mediated mitophagy is inhibited[1]. bpV(phen) is an insulin-mimetic agent following insulin-receptor tyrosine kinase hyperphosphorylation and activation[4].
bpV(phen) (5 mg/kg
intraperitoneal injection
daily
for 38 days
male BALB/c nude (nu/nu) athymic mice) treatment causes a significant reduction in average tumor volume[1].
IC50: 38 nM (PTEN), 343 nM (PTP-β) and 920 nM (PTP-1B)[3] Parasite Leishmania[2] Apoptosis[1] In Vitro bpV(phen) (5 μM
24.5 hours
H9c2 cells) treatment causes a further decrease of cell viability in H/R-injured H9c2 cells[1]. bpV(phen) (5 μM
24.5 hours
H9c2 cells) treatment increases the apoptosis of H/R-injured H9c2 cells[1]. bpV(phen) (5 μM
24.5 hours
H9c2 cells) treatment significantly promotes the accumulation of cytoplasmic Cytochrome C in H/R-injured H9c2 cells[1]. After stimulation of bpV(phen), PTEN-induced putative kinase protein 1 (PINK1)/Parkin-mediated mitophagy is inhibited[1]. bpV(phen) is an insulin-mimetic agent following insulin-receptor tyrosine kinase hyperphosphorylation and activation[4]. MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only. 0 --> bpV(phen) Related Antibodies Cell Viability Assay[1] Cell Line: Hypoxia/reoxygenation (H/R)-injured H9c2 cells
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[1]. Tang W, et al. PTEN-mediated mitophagy and APE1 overexpression protects against cardiac hypoxia/reoxygenation injury. In Vitro Cell Dev Biol Anim. 2019 Oct
55(9):741-748. [Content Brief]
[2]. Caron D, et al. Protein tyrosine phosphatase inhibition induces anti-tumor activity: evidence of Cdk2/p27 kip1 and Cdk2/SHP-1 complex formation in human ovarian cancer cells. Cancer Lett. 2008 Apr 18
262(2):265-75. [Content Brief]
[3]. Schmid AC, et al. Bisperoxovanadium compounds are potent PTEN inhibitors. FEBS Lett. 2004 May 21
566(1-3):35-8. [Content Brief]
[4]. Band CJ, et al. Early signaling events triggered by peroxovanadium [bpV(phen)] are insulin receptor kinase (IRK)-dependent: specificity of inhibition of IRK-associated protein tyrosine phosphatase(s) by bpV(phen). Mol Endocrinol. 1997 Dec
11(13):1899-910 [Content Brief]
[5]. Chen Q, et al. Potassium Bisperoxo(1,10-phenanthroline)oxovanadate (bpV(phen)) Induces Apoptosis and Pyroptosis and Disrupts the P62-HDAC6 Protein Interaction to Suppress the Acetylated Microtubule-dependent Degradation of Autophagosomes. J Biol Chem. 201 [Content Brief]
