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[1][2][3][4][5].
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].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
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.
体内研究 (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].
Shanghai Jinpan Biotech Co Ltd has not independently confirmed the accuracy of these methods. They are for reference only.
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.
分子量
350.24
Formula
C12H8KN2O5V
CAS 号
42494-73-5
运输条件
Room temperature in continental US; may vary elsewhere.
储存方式
Please store the product under the recommended conditions in the Certificate of Analysis.
参考文献
[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.
[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.
[3]. Schmid AC, et al. Bisperoxovanadium compounds are potent PTEN inhibitors. FEBS Lett. 2004 May 21;566(1-3):35-8.
[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.
[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. 2015 Oct 23;290(43):26051-8.
bpV(phen) trihydrate, 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) trihydrate inhibits proliferation of the protozoan parasite Leishmania in vitro. bpV(phen) trihydrate 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) trihydrate can also induce cell apoptosis, and has anti-angiogenic and anti-tumor activity[1][2][3][4][5].
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].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
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.
体内研究 (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].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
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.
分子量
404.29
Formula
C12H14KN2O8V
CAS 号
171202-16-7
运输条件
Room temperature in continental US; may vary elsewhere.
[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.
[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.
[3]. Schmid AC, et al. Bisperoxovanadium compounds are potent PTEN inhibitors. FEBS Lett. 2004 May 21;566(1-3):35-8.
[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.
[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. 2015 Oct 23;290(43):26051-8.
Phen-DC3 Trifluoromethanesulfonate Chemical Structure
CAS No. : 929895-45-4
规格
价格
是否有货
数量
1 mg
￥1500
In-stock
5 mg
￥4500
In-stock
10 mg
￥7500
In-stock
50 mg
￥22500
In-stock
100 mg
询价
200 mg
询价
* Please select Quantity before adding items.
Phen-DC3 Trifluoromethanesulfonate 相关产品
•相关化合物库:
Bioactive Compound Library Plus
生物活性
Phen-DC3 Trifluoromethanesulfonate is a G-quadruplex (G4) specific ligand which can inhibit FANCJ and DinG helicases with IC50s of 65±6 and 50±10 nM, respectively.
In WT cells, a CEB1-WT array is rather stable but undergoes frequent rearrangements upon addition of 10 μM Phen-DC3 Trifluoromethanesulfonate (Phen-DC3). It is found that the c-Myc allele exhibits significant destabilization upon Phen-DC3 Trifluoromethanesulfonate treatment and PIF1 deletion. The CEB25-L111(T) array is stable in WT cells, it becomes unstable upon addition of Phen-DC3 Trifluoromethanesulfonate or deletion of PIF1. It is also highly destabilized in the presence of Phen-DC3 Trifluoromethanesulfonate or in the absence of PIF1. The CEB1-loop CEB25 allele remaines fully stable in both PIF1-treated and WT cells[2].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
分子量
848.75
Formula
C36H26F6N6O8S2
CAS 号
929895-45-4
运输条件
Room temperature in continental US; may vary elsewhere.
[1]. Sanjay Kumar Bharti, et al. Specialization among Iron-Sulfur Cluster Helicases to Resolve G-quadruplex DNA Structures That Threaten Genomic Stability. J Biol Chem. 2013 Sep 27; 288(39): 28217–28229.
[2]. Aurèle Piazza, et al. Short loop length and high thermal stability determine genomic instability induced by G-quadruplex-forming minisatellites. EMBO J. 2015 Jun 12; 34(12): 1718–1734.
Cell Assay [2]
Briefly, untreated WT cells and pif1Δ cells from a fresh patch of cells get from a single colony bearing the parental allele size are diluted in 5 mL of YPD (2×105 cells/mL), grown for 8 generations at 30°C with shaking, and spreaded as single colony on YPD plates. To measure minisatellite instability upon Phen-DC3 Trifluoromethanesulfonate treatment, WT cells from a fresh patch on YPD are grown for 8 generations at 30°C in liquid SC containing Phen-DC3 Trifluoromethanesulfonate at 10 μM. Isolated colonies or pools of colonies are analyzed by Southern blot using the EcoRI digestion that cuts at each side of the minisatellite[2].
上海金畔生物科技有限公司 has not independently confirmed the accuracy of these methods. They are for reference only.
参考文献
[1]. Sanjay Kumar Bharti, et al. Specialization among Iron-Sulfur Cluster Helicases to Resolve G-quadruplex DNA Structures That Threaten Genomic Stability. J Biol Chem. 2013 Sep 27; 288(39): 28217–28229.
[2]. Aurèle Piazza, et al. Short loop length and high thermal stability determine genomic instability induced by G-quadruplex-forming minisatellites. EMBO J. 2015 Jun 12; 34(12): 1718–1734.
