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    PJ34 HCl
    PJ34 HCl

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    This product is for research use only, not for human use. We do not sell to patients.
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    InvivoChem Cat #: V0311
    CAS #: 344458-15-7Purity ≥98%

    Description: PJ34 HCl, the hydrochloride of PJ34, is a novel, potent and selective inhibitor of poly(ADP-ribose) polymerase (PARP) with potential anticancer and neuro-protective activities. It inhibits PARP with an EC50 value of 20 nM in a cell-free assay. PJ34 has neuro-protective effects and can enhance the chemotherapeutic effects in several tumor types. 

    References: Nat Med. 2001 Jan;7(1):108-13; J Pharmacol Exp Ther. 2004 Sep;310(3):1053-61. 

    Related CAS #: 344458-19-1 (free base); 344458-15-7 (HCl);   

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    Molecular Weight (MW)331.8
    CAS No.344458-15-7
    Storage-20℃ for 3 years in powder form
    -80℃ for 2 years in solvent
    Solubility (In vitro)DMSO: 66 mg/mL (198.9 mM)
    Water: 66 mg/mL (198.9 mM)
    Ethanol: <1 mg/mL
    Solubility (In vivo)30% PEG400+0.5% Tween80+5% propylene glycol: 14 mg/mL 

    Synonym: PJ-34; PJ34; PJ 34; PJ-34 HCl; PJ-34 hydrochloride.

    Chemical Name: 2-(dimethylamino)-N-(6-oxo-5,6-dihydrophenanthridin-2-yl)acetamide hydrochloride


    InChi Code: InChI=1S/C17H17N3O2.ClH/c1-20(2)10-16(21)18-11-7-8-15-14(9-11)12-5-3-4-6-13(12)17(22)19-15;/h3-9H,10H2,1-2H3,(H,18,21)(H,19,22);1H

    SMILES Code: O=C(NC(C=C1C2=C3C=CC=C2)=CC=C1NC3=O)CN(C)C.[H]Cl

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    In Vitro

    In vitro activity: 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.

    Kinase Assay: To assess the PARP-1 or PARP-2 inhibitory activity of FR247304, 3-AB, and PJ34, PARP activity is evaluated with minor modifications. PARP enzyme assay is carried out in a final volume of 100 μL consisting of 50 mM Tris-HCl (pH 8.0), 25 mM MgCl2, 1 mM dithiothreitol, 10 μg activated salmon sperm DNA, 0.1 μCi of [adenylate-32P]NAD, 0.2 units of recombinant human PARP for PARP-1 assay or 0.1 units of recombinant mouse PARP-2 for PARP-2 assay, and various concentrations of FR261529 or 3-AB. The reaction mixture is incubated at room temperature (23°C) for 15 min, and the reaction is terminated by adding 200 μL of ice-cold 20% trichloroacetic acid (TCA) and incubated at 4°C for 10 min. The precipitate is transferred onto GF/B filter and washed three times with 10% TCA solution and 70% ethanol. After the filter is dried, the radioactivity is determined by liquid scintillation counting.

    Cell Assay: PC12 cell cultured are grown in Dulbecco's modified Eagle's medium supplemented with 5% (v/v) fetal calf serum, 5% (v/v) horse serum, and a 1% (v/v) penicillin-streptomycin antibiotics mixture. Cells are grown in an atmosphere of 95% air and 5% CO2 at 37°C. For all experiment, cells are seeded at a density of 4×104 cells/well in 96-well culture plates and allowed to attach overnight. For assessment of cell viability, hydrogen peroxide-induced cytotoxicity is quantified by a standard measurement of LDH release with the use of the LDH assay kit. Briefly, 6 h after hydrogen peroxide exposure, 20 μL of medium of each well is collected, and the solution prepared from LDH assay kit is added. After incubation at room temperature for 30 min, the reaction is stopped by addition of 1 N HCl, and absorbance is measured at 450 nm using a microplate reader.

    In VivoPJ34 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.
    Animal modelFemale PLSJL mice
    Formulation & DosageDissolved in saline; 10 mg/kg; Oral administration

    Inflamm Res. 2001 Nov;50(11):561-9; Nat Med. 2001 Jan;7(1):108-13; J Pharmacol Exp Ther. 2004 Sep;310(3):1053-61. 

    These protocols are for reference only. InvivoChem does not independently validate these methods.


    PJ34 HCl


    PJ34 HCl


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