For research use only. Not for use in humans.
Molecular Weight(MW): 331.8
PJ34 HCl is the hydrochloride salt of PJ34, which is a PARP inhibitor with EC50 of 20 nM and is equally potent to PARP1/2.
Selleck's PJ34 HCl has been cited by 13 publications
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LN229 GBM cells were treated with PJ34 (20 µM), TRAIL (200 ng/ml) or the combination of both and analyzed for the expression of DR5, caspase-9 (CP9) and cleaved caspase-3 (cCP3). The vertical line on the immunoblot indicates that the first and second samples were noncontiguous, but run on the same gel simultaneously with the other samples.
PLoS One, 2014, doi:10.1371/journal.pone.0114583. PJ34 HCl purchased from Selleck.
Effect of PJ34 treatment on expression of IL-1ß, IL-6 and TNF-α at 24h after SAH.(A) Representative Western blots showing levels of IL-1ß, IL-6 and TNF-α. (B)-(D) The relative band densities of IL-1ß,IL-6 and TNF-α. The densities of the protein bands were analyzed and normalized to ß-actin. The bars represent the mean±SD. n=6. *p<0.05 vs sham, #p<0.05 vs SAH+Vehicle.
Brain Res, 2016, 1644:32-8. PJ34 HCl purchased from Selleck.
Effect of PJ34 treatment on expression of MMP-9, occludin and claudin-5 at 24 h after SAH. (A) Representative Western blots showing levels of MMP-9, occludin and claudin-5. (B)-(D) The relative band densities of MMP-9, occludin and claudin-5. The densities of the protein bands were analyzed and normalized to ß-actin. The bars represent the mean±SD. n=6. *p<0.05 vs sham, #p<0.05 vs SAH+Vehicle.
Brain Res, 2016, 1644:32-8.. PJ34 HCl purchased from Selleck.
Purity & Quality Control
Choose Selective PARP Inhibitors
|Description||PJ34 HCl is the hydrochloride salt of PJ34, which is a PARP inhibitor with EC50 of 20 nM and is equally potent to PARP1/2.|
|Features||Water-soluble PARP1/2 inhibitor with >10,000-fold potentcy vs. 3-aminobenzamide (prototypical PARP inhibitor). Potential uses in cardiovascular diseases (stroke, cerebral ischemia, & myocardial ischemia).|
PJ34 is a potent, phenanthridinone PARS inhibitor, which is approximately 10,000 times more potent than the prototypical PARS inhibitor 3-aminobenzamide. PJ34 inhibited peroxynitrite-induced cell necrosis with EC50 of 20 nM. PJ34 provides cardioprotection by decreasing myocardial infarct size and enhancing postischemic regional and global functional recovery. 
|In vivo||PJ34 suppresses the development of clinical signs of EAE in MBP-immunized PLSJL mice. PJ34 exerted therapeutic effects at the onset of EAE that are associated with reduced CNS inflammation and the maintenance of neurovascular integrity. PJ34 partially inhibits the expression of TNF-α and ICAM-1 in the Spinal Cord Tissues of MBP-Immunized Mice. PJ34 provides significant, dose-dependent, anti-inflammatory effects in a variety of local inflammation models. PJ34 dose-dependently suppresses neutrophil infiltration and nitric oxide (but not KC and IL-1β) production in peritonitis. In a model of systemic endotoxemia, PJ34 pretreatment significantly reduces plasma levels of TNF-α, IL-1β and nitrite/nitrate (breakdown products of nitric oxide) production. PJ34 treatment (oral gavage) induces a significant suppression of the inflammatory response in dextran sulfate colitis, multiple low dose streptozotocin diabetes and cyclophosphamide-accelerated autoimmune diabetes in the non-obese diabetic mice, and reduces the degree of mononuclear cell infiltration into the iris in an endotoxin-induced uveitis model. |
|In vitro||DMSO||66 mg/mL (198.91 mM)|
|Water||66 mg/mL (198.91 mM)|
|In vivo||Add solvents to the product individually and in order(Data is from Selleck tests instead of citations):
30% PEG400+0.5% Tween80+5% propylene glycol
For best results, use promptly after mixing.
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