PJ34 [344458-19-1]
Cat# A3729-10mg
Size : 10mg
Brand : APExBIO Technology
Contact local distributor :
Phone : +1 850 650 7790
PJ34
Tyramide Signal Amplification (TSA)
TSA (Tyramide Signal Amplification), used for signal amplification of ISH, IHC and IC etc.
Phos Binding Reagent Acrylamide
Separation of phosphorylated and non-phosphorylated proteins without phospho-specific antibody
| Storage | Store at -20°C |
| M.Wt | 295.34 |
| Cas No. | 344458-19-1 |
| Formula | C17H17N3O2 |
| Synonyms | PJ-34;PJ 34 |
| Solubility | ≥50.9 mg/mL in DMSO; ≥5.76 mg/mL in EtOH with ultrasonic; insoluble in H2O |
| Chemical Name | 2-(dimethylamino)-N-(6-oxo-5H-phenanthridin-2-yl)acetamide |
| SDF | Download SDF |
| Canonical SMILES | CN(C)CC(=O)NC1=CC2=C(C=C1)NC(=O)C3=CC=CC=C32 |
| Shipping Condition | Small Molecules with Blue Ice, Modified Nucleotides with Dry Ice. |
| General tips | We do not recommend long-term storage for the solution, please use it up soon. |
| Cell experiment [1]: | |
| Cell lines | Mouse endothelial cells and human umbilical vein endothelial cells |
| Preparation method | The solubility of this compound in DMSO is > 10 mM. General tips for obtaining a higher concentration: Please warm the tube at 37 °C for 10 minutes and/or shake it in the ultrasonic bath for a while. Stock solution can be stored below - 20 °C for several months. |
| Reacting condition | 0.1 ~ 3 μM |
| Applications | In mouse endothelial cells, PJ34 significantly inhibited high glucose-induced PARP activation at the doses of 0.5 and 3 μM, as well as the development of endothelial dysfunction at the dose of 3 μM. Meanwhile, PARP inhibition caused by PJ34 (3 μM) did not alter the degree of NF-κB activation. In human umbilical vein endothelial cells, PJ34 at 1 μM exhibited marked inhibitory effect on high glucose-induced PARP activation. |
| Animal experiment [2]: | |
| Animal models | MBP-immunized PLSJL mice |
| Dosage form | 10 mg/kg; p.o.; b.i.d. |
| Applications | In MBP-immunized PLSJL mice, PJ34 inhibited the development of clinical signs of experimental allergic encephalomyelitis (EAE). PJ34 also suppressed the onset of EAE by reducing CNS inflammation and maintaining neurovascular integrity. In addition, PJ34 down-regulated the expression levels of TNF-α and ICAM-1 in the spinal cord tissues. |
| Other notes | Please test the solubility of all compounds indoor, and the actual solubility may slightly differ with the theoretical value. This is caused by an experimental system error and it is normal. |
| References: [1]. Garcia Soriano F, Virág L, Jagtap P, Szabó E, Mabley JG, Liaudet L, Marton A, Hoyt DG, Murthy KG, Salzman AL, Southan GJ, Szabó C. Diabetic endothelial dysfunction: the role of poly(ADP-ribose) polymerase activation. Nat Med. 2001 Jan;7(1):108-13. [2]. Scott GS, Kean RB, Mikheeva T, Fabis MJ, Mabley JG, Szabó C, Hooper DC. The therapeutic effects of PJ34 [N-(6-oxo-5,6-dihydrophenanthridin-2-yl)-N,N-dimethylacetamide.HCl], a selective inhibitor of poly(ADP-ribose) polymerase, in experimental allergic encephalomyelitis are associated with immunomodulation. J Pharmacol Exp Ther. 2004 Sep;310(3):1053-61. | |
| PJ34 is a novel potent specific inhibitor of PARP-l/2 with EC50 of 20 nM. | ||||||
| Targets | PARP | |||||
| IC50 | 20 nM (EC50) | |||||
Related Biological Data
