BGP-15 2HCl

For research use only.

Catalog No.S8370

BGP-15 2HCl Chemical Structure

CAS No. 66611-37-8

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.
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].


Cell Research:


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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:


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  • Animal Models: NMRI CV1 mice, BD2F1 mice and Wistar rats
  • 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


CAS No. 66611-37-8
Storage powder
in solvent
Synonyms N/A
Smiles C1CCN(CC1)CC(CON=C(C2=CN=CC=C2)N)O.Cl.Cl

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PARP Signaling Pathway Map

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Cell Lines Assay Type Concentration Incubation Time Formulation Activity Description PMID