bpV(phen) trihydrate

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bpV(phen) trihydrate  纯度: ≥98.0%

bpV(phen) trihydrate，一种胰岛素模拟物，是一种有效的蛋白酪氨酸磷酸酶 (PTP) 和 PTEN 抑制剂，对 PTEN，PTP-β 和 PTP-1B 的 IC50 为 38 nM，343 nM 和 920 nM。bpV(phen) trihydrate 在体外抑制原生动物寄生虫利什曼原虫的增殖。bpV(phen) trihydrate 强烈诱导大量趋化因子和促炎性细胞因子的分泌，并激活 Th1 型途径 (IL-12，IFNγ)。bpV(phen) trihydrate 还可以诱导细胞凋亡 (apoptosis)，并具有抗血管生成和抗肿瘤活性。

bpV(phen) trihydrate

bpV(phen) trihydrate Chemical Structure

CAS No. : 171202-16-7

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生物活性

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].

IC50 & Target

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

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.
储存方式

4°C, sealed storage, away from moisture

*In solvent : -80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)
溶解性数据
In Vitro: 

H2O : 18.18 mg/mL (44.97 mM; Need ultrasonic)

配制储备液
浓度 溶剂体积 质量 1 mg 5 mg 10 mg
1 mM 2.4735 mL 12.3674 mL 24.7347 mL
5 mM 0.4947 mL 2.4735 mL 4.9469 mL
10 mM 0.2473 mL 1.2367 mL 2.4735 mL

*

请根据产品在不同溶剂中的溶解度选择合适的溶剂配制储备液；一旦配成溶液，请分装保存，避免反复冻融造成的产品失效。
储备液的保存方式和期限：-80°C, 6 months; -20°C, 1 month (sealed storage, away from moisture)。-80°C 储存时，请在 6 个月内使用，-20°C 储存时，请在 1 个月内使用。
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.

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