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PRODUCTS SPECIFICATIONS [66611-37-8]
Store
Catalog
SLK-S8370
Brand
Selleck
CAS
66611-37-8
DESCRIPTION [66611-37-8]
Overview
MDL
MFCD21603901
Molecular Weight
351.27
Molecular Formula
C14H22N4O2.2HCl
SMILES
N=C(NOCC(O)CN1CCCCC1)C2=CN=CC=C2.[H]Cl.[H]Cl
For research use only.
Storage
3 years,-20°C,powder 1 years,-80°C,in solvent
Shipping
Room temperature shipping(Stability testing shows this product can be shipped without any cooling measures.)
Preparing Stock Solutions
1 mg
5 mg
10 mg
1 mM
2.8468 mL
14.2341 mL
28.4681 mL
5 mM
0.5694 mL
2.8468 mL
5.6936 mL
10 mM
0.2847 mL
1.4234 mL
2.8468 mL
50 mM
0.0569 mL
0.2847 mL
0.5694 mL
Description
BGP-15, is a nicotinic amidoxime derivative with inhibitory activity. It has been demonstrated that BGP-15 protects against ischemia-reperfusion injury.
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. 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.
In vivo
BGP-15 improves cardiac function and reduces arrhythmic episodes in two independent mouse models, which progressively develop HF and AF. 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.