BGP-15 2HCl

Catalog No.S8370

BGP-15 2HCl Chemical Structure

Molecular Weight(MW): 351.27

BGP-15, is a nicotinic amidoxime derivative with PARP inhibitory activity. It has been demonstrated that BGP-15 protects against ischemia-reperfusion injury.

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Biological Activity

Description BGP-15, is a nicotinic amidoxime derivative with PARP inhibitory activity. It has been demonstrated that BGP-15 protects against ischemia-reperfusion injury.
Targets
PARP [1]
In vitro

The hydroxylamine derivative BGP-15 is a coinducer of HSP72 in vitro, but only in the presence of cotreatment with heat and had no effect on HSP90 levels[3]. BGP-15 (200 μM) prevented the imatinib mesylate-induced oxidative damages, attenuated the depletion of high-energy phosphates, altered the signaling effect of imatinib mesylate by preventing p38 MAP kinase and JNK activation, and induced the phosphorylation of Akt and GSK-3beta. The suppressive effect of BGP-15 on p38 and JNK activation could be significant because these kinases contribute to the cell death and inflammation in the isolated perfused heart[4].

In vivo BGP-15 improves cardiac function and reduces arrhythmic episodes in two independent mouse models, which progressively develop HF and AF[2]. BGP-15 administered in 100-200 mg/kg oral doses shortly before cisplatin treatment either prevented or significantly inhibited the development of cisplatin-induced acute renal failure. BGP-15 had a significant effect on the antioxidant status of kidney during cisplatin-induced nephrotoxicity. It elevated the decreased glutathione and catalase levels, but did not affect SOD activity. BGP-15 treatment decreased the cisplatin-caused ROS production and restored the level of high energy phosphate intermediates. While BGP-15 protected against cisplatin-induced nephrotoxicity, it did not reduce the antitumor efficacy of this cytostatic agent. BGP-15 increased the survival of cisplatin-treated P-388 leukemia bearing mice. BGP-15 inhibits the cisplatin-induced poly-ADP-ribosylation in the kidney. At the same time, BGP-15 restored the cisplatin-induced disturbance in energy metabolism and preserved the ATP level in the protected tissue[1].

Protocol

Cell Research:

[1]

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  • Cell lines: Human tumor cell lines A549, HCT-15, HCT-116, and Du-145
  • Concentrations: 10, 30, 100 μg/mL
  • Incubation Time: 3 days
  • Method:

    Human tumor cell lines A549, HCT-15, HCT-116, and Du-145 were maintained in RPMI 1640 medium supplemented with 10% FCS in humidified air containing 5% CO2. For in vitro cytotoxicity assays, 5×103 to 5×104 cells were plated into the wells of 96-well plates in 100 μL culture medium. On the following day, cells were exposed to BGP-15 (10, 30, 100 μg/mL) and to a series of concentrations of cisplatin either by itself or in combination. Cultures were incubated in a total volume of 200 μL for 3 more days at 37°. Samples were prepared in duplicates or triplicates. Cell growth was evaluated by MTT or SRB assays. Growth inhibition curves were calculated.


    (Only for Reference)
Animal Research:

[1]

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  • Animal Models: NMRI CV1 mice, BD2F1 mice and Wistar rats
  • Formulation: water or physiological saline
  • Dosages: 100, 200 mg/kg
  • Administration: p.o.
    (Only for Reference)

Solubility (25°C)

In vitro DMSO 70 mg/mL (199.27 mM)
Water 70 mg/mL (199.27 mM)
Ethanol 70 mg/mL (199.27 mM)

* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.

Chemical Information

Molecular Weight 351.27
Formula

C14H22N4O2.2HCl

CAS No. 66611-37-8
Storage powder
Synonyms N/A

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Answers to questions you may have can be found in the inhibitor handling instructions. Topics include how to prepare stock solutions, how to store inhibitors, and issues that need special attention for cell-based assays and animal experiments.

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PARP Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID