BGP-15 2HCl

Catalog No.S8370 Batch:S837001

Print

Technical Data

Formula

C14H22N4O2.2HCl
Molecular Weight 351.27 CAS No. 66611-37-8
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)
* <1 mg/ml means slightly soluble or insoluble.
* 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.
* Room temperature shipping (Stability testing shows this product can be shipped without any cooling measures.)

Preparing Stock Solutions

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 (from reference)

Cell Assay:

[1]
  • 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.
Animal Study:

[1]
  • Animal Models

    NMRI CV1 mice, BD2F1 mice and Wistar rats

  • Dosages

    100, 200 mg/kg

  • Administration

    p.o.

Selleck's BGP-15 2HCl has been cited by 4 publications

Attenuation of PM2.5-induced alveolar epithelial cells and lung injury through regulation of mitochondrial fission and fusion [ Part Fibre Toxicol, 2023, 20(1):28] PubMed: 37464447
Attenuation of PM2.5-induced alveolar epithelial cells and lung injury through regulation of mitochondrial fission and fusion [ Part Fibre Toxicol, 2023, 20(1):28] PubMed: 37464447
Role of mitochondrial fusion proteins MFN2 and OPA1 on lung cellular senescence in chronic obstructive pulmonary disease [ Respir Res, 2023, 24(1):319] PubMed: 38110986
" Chemical chaperones and heat shock protein induction inhibit the pro-inflammatory action of oxidized phospholipids in human endothelial cells"/submitted by Klara … K Hellauer [ unipub, 2021, ] PubMed: none

RETURN POLICY
Selleck Chemical’s Unconditional Return Policy ensures a smooth online shopping experience for our customers. If you are in any way unsatisfied with your purchase, you may return any item(s) within 7 days of receiving it. In the event of product quality issues, either protocol related or product related problems, you may return any item(s) within 365 days from the original purchase date. Please follow the instructions below when returning products.

SHIPPING AND STORAGE
Selleck products are transported at room temperature. If you receive the product at room temperature, please rest assured, the Selleck Quality Inspection Department has conducted experiments to verify that the normal temperature placement of one month will not affect the biological activity of powder products. After collecting, please store the product according to the requirements described in the datasheet. Most Selleck products are stable under the recommended conditions.

NOT FOR HUMAN, VETERINARY DIAGNOSTIC OR THERAPEUTIC USE.