VO-OHPic
CAS No. : 675848-25-6
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| Cat. No. : | HY-110067 |
| M.Wt: | 361.16 |
| Formula: | C12H10N2O8V |
| Purity: | >98 % |
| Solubility: | 10 mM in DMSO |
VO-OHPic is a reversible, noncompetitive PTEN inhibitor with an human IC50 value of 46 nM. VO-OHPic inhibits PTEN signaling, activates Akt-GSK3β and Nrf-2/HO-1 pathways, induces apoptosis resistance and elevates IL-10 levels. VO-OHPic inhibits autophagy, ferroptosis and oxidative stress. VO-OHPic can be used for the research of acute myocardial infarction, intervertebral disc degeneration, cardiomyopathy and cancer[1][2][3][4][5][6].
IC50 & Target:IC50: 46 nM (PTEN)[1]
In Vitro:VO-OHpic (0.05-2.0 μg/mL; 2 h) dose-dependently improves viability of H/R-stressed isolated adult rat cardiac myocytes[1].
VO-OHpic (1 µM; 24-72 h) suppresses the proliferation of TSC2-/- MEFs in a time-dependent manner[2].
VO-OHpic (1 µM; 24-72 h) excessively inhibits autophagy in TSC2-/- MEFs[2].
VO-OHpic (1 µM; 24-72 h) modulates the PTEN/PRAS40 pathway in TSC2-/- MEFs[2].
VO-OHPic (1 μM; 24 h) inhibits TBHP-induced ferroptosis by restoring GPX4 and SLC7A11 expression in primary mouse CEP chondrocytes[3].
VO-OHPic (1 μM; 24 h) inhibits TBHP-induced ROS production in primary mouse CEP chondrocytes[3].
VO-OHPic (30 μM) alleviates IL-1β-induced degeneration in human nucleus pulposus cells by inhibiting PTEN and activating the PI3K/Akt pathway, thereby restoring collagen II and aggrecan levels[4].
VO-OHPic (30 μM) promotes proliferation in IL-1β-induced degenerated human nucleus pulposus cells by mediating cell cycle progression through the G1 to S phase[4].
VO-OHPic (30 μM) reduces oxidative stress in H2O2-induced degenerated human nucleus pulposus cells by lowering ROS levels and upregulating antioxidant enzymes SOD1, SOD2, CAT, and GSH[4].
VO-OHPic (1 μM; 48 h) activates the Nrf2 signaling pathway in Methylprednisolone (HY-B0260) -treated rat endothelial progenitor cells by increasing expression of Nrf2 and its downstream antioxidant proteins, and promoting Nrf2 nuclear translocation[5].
VO-OHPic (1 μM; 48 h) restores normal mitochondrial morphology in Methylprednisolone-treated rat endothelial progenitor cells[5].
VO-OHPic (1 μM; 48 h) suppresses Methylprednisolone-induced excessive reactive oxygen species generation in rat endothelial progenitor cells[5].
VO-OHPic (1 μM; 48 h) requires activation of Nrf2 to exert anti-apoptotic, antioxidant, and pro-angiogenic effects in Methylprednisolone-treated rat endothelial progenitor cells[5].
VO-OHpic (15-300 nM; 10 min) reversibly inhibits purified recombinant PTEN in a noncompetitive manner with an IC50 of 46 nM[6].
In Vivo:VO-OHpic (10 mg/kg; i.p.; every other day; 12 weeks) attenuates IDD progression and cartilage endplate calcification in surgically induced IDD mice[3].
VO-OHpic (10 mg/kg; i.p.; every 2 days) attenuates LPS (HY-D1056)- and Methylprednisolone-induced osteonecrosis of the femoral head in rats, increases bone volume parameters, reduces empty bone lacunae, and promotes angiogenesis in the femoral head[5].
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