2. PI3K/Akt/mTOR Apoptosis Autophagy Immunology/Inflammation NF-κB Metabolic Enzyme/Protease
  3. PTEN Apoptosis Autophagy Ferroptosis Reactive Oxygen Species (ROS) Interleukin Related Akt Keap1-Nrf2
  4. VO-OHPic

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.

For research use only. We do not sell to patients.

CAS No. : 675848-25-6

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VO-OHPic Related Antibodies

Top Publications Citing Use of Products

36 Publications Citing Use of MCE VO-OHPic

WB

    VO-OHPic purchased from MedChemExpress. Usage Cited in: Redox Biol. 2019 Jan;20:390-401.  [Abstract]

    Western analysis of related genes expression in mice with the treatment of TAC, TAC+RES, and TAC+RES+VO-Ophic.

    VO-OHPic purchased from MedChemExpress. Usage Cited in: Redox Biol. 2019 Jan;20:390-401.  [Abstract]

    Immunoblotting analysis show that RES treatment markedly inhibited Ang II-induced degradation of PTEN, activation of AKT and mTOR and inactivation of AMPK, but this effect is reversed by VO-OHpic.

    VO-OHPic purchased from MedChemExpress. Usage Cited in: Redox Biol. 2019 Jan;20:390-401.  [Abstract]

    Immunoblotting analysis show that RES treatment markedly inhibited Ang II-induced degradation of PTEN, activation of AKT and mTOR and inactivation of AMPK, but this effect is reversed by VO-OHpic.

    VO-OHPic purchased from MedChemExpress. Usage Cited in: Stem Cell Res Ther. 2019 Jul 29;10(1):217.  [Abstract]

    Western blot showing the levels of phosphorylated and non-phosphorylated PTEN, AKT, and mTOR proteins before and after VO-OHpic trihydrate treatment.

    VO-OHPic purchased from MedChemExpress. Usage Cited in: Mol Vis. 2018 Jul 23:24:485-494.  [Abstract]

    The miR-21 inhibitor promotes the expression of the PTEN protein and inhibits the expression of p-AKT, and VO-Ohpic trihydrate reverses the effect.

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    IL-1 IL-2 IL-3 IL-4 IL-5 IL-6 IL-8 IL-10 IL-12 IL-13 IL-15 IL-17 IL-23 IL-7 IL-33 IL-22 IL-18

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    Akt Akt1 Akt2 Akt3

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    Description

    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[4][5]

    Akt

     

    IL-10

     

    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].

    MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

    VO-OHPic Related Antibodies

    Cell Proliferation Assay[2]

    Cell Line: TSC2-/- murine embryonic fibroblasts (MEFs)
    Concentration: 1 µM
    Incubation Time: 24 h; 48 h; 72 h
    Result: Reduced relative cell viability significantly at 48 h (P=0.005) and 72 h (P<0.001).
    Showed no significant difference in relative cell viability at 24 h (P=0.333).

    Western Blot Analysis[2]

    Cell Line: TSC2-/- murine embryonic fibroblasts (MEFs)
    Concentration: 1 µM
    Incubation Time: 24 h; 48 h; 72 h
    Result: Reduced relative expression of LC3-I significantly at 24 h (P<0.001), 48 h (P=0.015), and 72 h (P=0.001).
    Reduced relative expression of LC3-II significantly at 24 h (P=0.020), 48 h (P<0.001), and 72 h (P=0.007).\nReduced relative expression ratio of p-PTEN/PTEN significantly at 24 h (P=0.001), 48 h (P=0.005), and 72 h (P=0.011).
    Reduced relative expression ratio of p-PRAS40/PRAS40 significantly at 48 h (P<0.001) and 72 h (P<0.001).
    Showed no significant difference in relative expression ratio of p-PRAS40/PRAS40 at 24 h (P=0.137).

    Cell Viability Assay[4]

    Cell Line: human nucleus pulposus (NP) cells
    Concentration: 10 μM; 30 μM; 50 μM; 100 μM
    Incubation Time: 48 h
    Result: Achieves the highest cell viability at 30 μM compared to all other tested concentrations.

    Western Blot Analysis[5]

    Cell Line: rat endothelial progenitor cells (EPCs)
    Concentration: 1 μM
    Incubation Time: 48 h
    Result: Reversed MPS-induced increases in cleaved caspase-3, cleaved caspase-9, cytochrome C, and Bax protein expression.
    Restored MPS-reduced Bcl-xL expression and the p-Bad/Bad ratio.
    Suppressed MPS-promoted formation of the Bad/Bcl-xL pro-apoptotic complex.
    Attenuated MPS-induced Bax translocation to mitochondria and cytochrome C release from mitochondria to cytoplasm.\nReversed MPS-induced reductions in SIRT1, Nrf2, HO-1, NQO-1, and Trx protein expression.
    Increased nuclear Nrf2 localization, which was suppressed by MPS.

    ELISA Assay[5]

    Cell Line: rat endothelial progenitor cells (EPCs)
    Concentration: 1 μM
    Incubation Time: 48 h
    Result: Significantly increased VEGF concentration in the culture medium relative to the MPS-only group, reversing MPS-suppressed EPC VEGF secretion.
    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].

    MedChemExpress (MCE) has not independently confirmed the accuracy of these methods. They are for reference only.

    Animal Model: C57BL/6 (8-week-old male; surgically induced intervertebral disc instability)[3]
    Dosage: 10 mg/kg
    Administration: i.p.; every other day; 12 weeks
    Result: Reduced intervertebral disc degeneration histological score significantly compared to the IDD-only group.
    Improved intervertebral disc height significantly compared to the IDD-only group.
    Reduced bone volume/tissue volume (BV/TV) of the cartilage endplate significantly compared to the IDD-only group.
    Increased COL2-positive cell levels in the cartilage endplate compared to the IDD-only group.
    Decreased MMP3-positive cell levels in the cartilage endplate compared to the IDD-only group.
    Increased Nrf-2-positive cell levels in the cartilage endplate compared to the IDD-only group.
    Reduced COL10 and OCN-positive cell levels in the cartilage endplate compared to the IDD-only group.
    Animal Model: Sprague-Dawley (male, 7 weeks old, body weight 250-300 g, osteonecrosis of the femoral head model induced by LPS + Methylprednisolone)[5]
    Dosage: 10 mg/kg
    Administration: i.p.; every 2 days
    Result: Significantly increased bone volume and bone volume/total volume compared to the methylprednisolone-only group.
    Decreased bone surface/trabecular bone volume compared to the methylprednisolone-only group.
    Reduced the number of empty bone lacunae in the femoral head compared to the methylprednisolone-only group.
    Increased the relative staining intensity of CD31, VEGF, and VEGFR2 in subchondral bone trabeculae compared to the methylprednisolone-only group.
    Increased the number of CD31-positive and VEGFR2-positive blood vessels per field compared to the methylprednisolone-only group.
    Molecular Weight

    361.16

    Formula

    C12H10N2O8V
    CAS No.
    SMILES

    [OH2][V+2]([N]1=CC=CC(O)=C1C2=O)([O-]2)([O-]C3=CC=CN=C3C4=O)([O-]4)=O.[H+]
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    Storage

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    Purity & Documentation
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    VO-OHPic Related Classifications

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    • Do most proteins show cross-species activity?

      Species cross-reactivity must be investigated individually for each product. Many human cytokines will produce a nice response in mouse cell lines, and many mouse proteins will show activity on human cells. Other proteins may have a lower specific activity when used in the opposite species.

    Keywords:

    VO-OHPic675848-25-6PTENApoptosisAutophagyFerroptosisReactive Oxygen Species (ROS)Interleukin RelatedAktKeap1-Nrf2Phosphatase and tensin homologMMAC1ILPKBProtein kinase BAkt-GSK3βNrf-2/HO-1primary mouse CEP chondrocyteshuman nucleus pulposus cellsrat endothelial progenitor cellsacute myocardial infarctionintervertebral disc degenerationadult rat cardiac myocytesTSC2-/- MEFsInhibitorinhibitorinhibit

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