1. PI3K/Akt/mTOR
    Metabolic Enzyme/Protease
    Anti-infection
    Apoptosis
  2. PTEN
    Phosphatase
    HIV
    Parasite
    Apoptosis
  3. bpV(phen)

bpV(phen) 

Cat. No.: HY-136065
Handling Instructions

bpV(phen) 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. bpV(phen) is an insulin-mimetic agent following insulin-receptor tyrosine kinase hyperphosphorylation and activation. bpV(phen) activates HIV-1 transcription and replication via NF-κB-dependent and independent mechanisms. 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.

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

bpV(phen) Chemical Structure

bpV(phen) Chemical Structure

CAS No. : 42494-73-5

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Description

bpV(phen) 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. bpV(phen) is an insulin-mimetic agent following insulin-receptor tyrosine kinase hyperphosphorylation and activation. bpV(phen) activates HIV-1 transcription and replication via NF-κB-dependent and independent mechanisms. 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[1][2][3][4][5].

IC50 & Target

IC50: 38 nM (PTEN), 343 nM (PTP-β) and 920 nM (PTP-1B)[3]
Parasite Leishmania[2]
HIV-1[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].

Cell Viability Assay[1]

Cell Line: Hypoxia/reoxygenation (H/R)-injured H9c2 cells
Concentration: 5 μM
Incubation Time: 24.5 hours (hypoxia for 24 h; reoxygenation for 30 minutes)
Result: Caused a further decrease of cell viability.

Apoptosis Analysis[1]

Cell Line: Hypoxia/reoxygenation (H/R)-injured H9c2 cells
Concentration: 5 μM
Incubation Time: 24.5 hours (hypoxia for 24 h; reoxygenation for 30 minutes)
Result: Increased the apoptosis of H/R-injured H9c2 cells.

Western Blot Analysis[1]

Cell Line: Hypoxia/reoxygenation (H/R)-injured H9c2 cells
Concentration: 5 μM
Incubation Time: 24.5 hours (hypoxia for 24 h; reoxygenation for 30 minutes)
Result: Showed an increased release of Cytochrome C.
In Vivo

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].

Animal Model: Male BALB/c nude (nu/nu) athymic mice (6-7 weeks old) injected with PC-3 cells[2]
Dosage: 5 mg/kg
Administration: Intraperitoneal injection; daily; for 38 days
Result: Caused a significant reduction in average tumor volume.
Molecular Weight

350.24

Formula

C₁₂H₈KN₂O₅V

CAS No.

42494-73-5

SMILES

O=[V+3]12([N]3=CC=C4)([O-][O-]1)([O-][O-]2)[N]5=C6C3=C4C=CC6=CC=C5.[K+]

Shipping

Room temperature in continental US; may vary elsewhere.

Storage

Please store the product under the recommended conditions in the Certificate of Analysis.

References
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Keywords:

bpV(phen)PTENPhosphataseHIVParasiteApoptosisPhosphatase and tensin homologMMAC1Human immunodeficiency virusPTPCytochrome CmitochondriahypoxiareoxygenationPINK1Peroxovanadiumsanti-tumoranti-proliferativeInhibitorinhibitorinhibit

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