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PJ34

37 Cited Publications
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Based on 37 publication(s) in Google Scholar

PJ34 is a potent specific inhibitor of PARPl/2 with IC50 of 110 nM and 86 nM, respectively.

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  • 純度: 99.66%
  • CAS 番号: 344458-19-1
  • 分子式: C17H17N3O2
  • 分子量:295.34
  • 保管条件:
    Powder   -20°C, 3 years , 4°C, 2 years ; In solvent   -80°C, 1 year , -20°C, 6 months
  • PJ34 Chemical Structure
    PJ34 構造式
  • Experimental Validation Results for PJ34
  • Experimental Validation Results for PJ34
  • Experimental Validation Results for PJ34
  • Experimental Validation Results for PJ34
  • Experimental Validation Results for PJ34
  • Experimental Validation Results for PJ34
CAS 番号: 344458-19-1
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  • PJ34 Chemical Structure
    PJ34 Chemical Structure
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  • 1/16

    PJ34 purchased from MedChemExpress. Usage Cited in: Nat Aging. 2024 Jun;4(6):771-782. [Abstract]

    Customer Validation
     IMR-90 human fibroblasts were incubated with the indicated death inhibitor or vehicle for 2 h, followed by H2O2 treatment (1 mM). Cell survival was measured using an MTS assay 24 h after 1 h H2O2 treatment of cells. The results showed that PJ34 (10 µM; pretreated for 2 h before applying H2O2) protected cells from oxidative stress-induced death, while no rescue was observed for other death inhibitors such as QVD (apoptosis), necrosulfonamide (necroptosis), ferrostatin-1 (ferroptosis), VX-765 (pyroptosis), pepstatin A (cathepsin D and E-induced death) and E64d (cathepsin B and L-induced, and calpain-induced death).

  • 1/16

    PJ34 purchased from MedChemExpress. Usage Cited in: Nat Aging. 2024 Jun;4(6):771-782. [Abstract]

    Customer Validation
     IMR-90 human fibroblasts were incubated with the indicated death inhibitor or vehicle for 2 h, followed by H2O2 treatment (1 mM). Cells were stained for PAR polymers after 15 min H2O2 exposure; n = 152 from three independent experiments. Quantification was performed on single cells with images taken from multiple microscopic fields of view. The results showed that cells exposed toH2O2 showed a strong nuclear poly-ADP-ribose (PAR) signal that was significantly suppressed by PJ34 (10 µM; pretreated for 2 h before applying H2O2), indicating an on-target effect of the inhibitor. Scale bar, 150 µm.

  • 1/16

    PJ34 purchased from MedChemExpress. Usage Cited in: Nat Aging. 2024 Jun;4(6):771-782. [Abstract]

    Customer Validation
     IMR-90 human fibroblasts were incubated with the indicated death inhibitor (PJ34 (10 µM)) or vehicle for 2 h, followed by H2O2 treatment (1 mM). Fourteen days after treatment cells were analyzed using quantitative PCR with reverse transcription (RT–qPCR) for expression of the indicated mRNAs relative to the housekeeping gene (tubulin); n = 6.

  • 1/16

    PJ34 purchased from MedChemExpress. Usage Cited in: Nat Aging. 2024 Jun;4(6):771-782. [Abstract]

    Customer Validation
     Immunofluorescence staining with TOM20 and endogenous HK-II of IMR-90 cells pretreated with vehicle or PJ34 exposed to H2O2 (1 mM); control, n = 94, H2O2 and H2O2 +  PJ34 (10 µM; pretreated for 2 h before applying H2O2), n = 87 from three independent experiments, Scale bar, 10 µm. The results showed that incubation with PJ34 in cells exposed to H2O2 was sufficient to retain the mitochondrial pool of HK-II.

  • 1/16

    PJ34 purchased from MedChemExpress. Usage Cited in: Nat Aging. 2024 Jun;4(6):771-782. [Abstract]

    Customer Validation
     Mice underwent unilateral kidney IRI with the administration of the PARP inhibitor PJ34 (10 mg/kg) or vehicle. Three days after induction of IRI, kidney tissues were collected for histological and molecular analysis. Periodic acid–Schiff staining was used to detect the necrotic area (defined by a red line), n = 5 for vehicle-treated and n = 6 for PJ34-treated mice. Scale bar, 100 µm. The results showed that IRI was characterized by an increased necrotic area, which was considerably reduced by PJ34 treatment.

  • 1/16

    PJ34 purchased from MedChemExpress. Usage Cited in: Sci Rep. 2017 May 23;7(1):2268. [Abstract]

    Customer Validation
     The PARP inhibitor PJ34 prevents TCDD toxicities while increasing NAD+ levels. (a,b) Western blots on homogenates of liver and thymus glands from CE treated with TCDD or vehicle with or without PJ34.

  • PJ34