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P4365

PJ-34 hydrochloride hydrate

Name: PJ-34 hydrochloride hydrate
Brand: SIGMA

≥98% (HPLC), powder

Synonym(s):

PARP Inhibitor VIII, PJ 34 HCl, N-(6-Oxo-5,6-dihydrophenanthridin-2-yl)-(N,N-dimethylamino)acetamide hydrochloride

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About This Item

Empirical Formula (Hill Notation):

C₁₇H₁₇N₃O₂ · HCl · xH₂O

CAS Number:

344458-15-7

Molecular Weight:

331.80 (anhydrous basis)

UNSPSC Code:

12352200

PubChem Substance ID:

24898531

NACRES:

NA.77

Quality Level

100

Assay

≥98% (HPLC)

form

powder

storage condition

desiccated

color

white to yellow

solubility

H₂O: 22 mg/mL

SMILES string

Cl[H].[H]O[H].CN(C)CC(=O)Nc1ccc2NC(=O)c3ccccc3-c2c1

InChI

1S/C17H17N3O2.ClH.H2O/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;1H2

InChI key

YCALIZUKAFUQCH-UHFFFAOYSA-N

Application

PJ-34 hydrochloride hydrate has been used:

as a poly(ADP-ribose) polymerase (PARP) inhibitor 1 in rats to test the effect of PAPR1 in neuropathic pain
as a component of protein extraction buffer to enable visualization of the high-molecular-weight smear of PARylated proteins in various cell samples
as PARP inhibitor in murine MLE-12 epithelial cell line

Biochem/physiol Actions

PJ-34 is a prototypic poly(ADP-ribose) polymerase 1 (PARP-1) inhibitor.

PJ-34 is a potent poly(ADP-ribose) polymerase (PARP) inhibitor.

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Personal Protective Equipment

dust mask type N95 (US), Eyeshields, Gloves

Certificates of Analysis (COA)

Search for Certificates of Analysis (COA) by entering the products Lot/Batch Number. Lot and Batch Numbers can be found on a product’s label following the words ‘Lot’ or ‘Batch’.

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Protective effects of PJ34, a novel, potent inhibitor of poly(ADP-ribose) polymerase (PARP) in in vitro and in vivo models of stroke.

G E Abdelkarim et al.

International journal of molecular medicine, 7(3), 255-260 (2001-02-17)

Focal cerebral ischemia activates the nuclear protein poly(ADP-ribose) polymerase (PARP) by single DNA strand breaks which leads to energy depletion and cell necrosis. Deletion or inhibition of PARP protects against ischemic brain injury. Here we examined the neuroprotective effect of

PARP-1-regulated TNF-α expression in the dorsal root ganglia and spinal dorsal horn contributes to the pathogenesis of neuropathic pain in rats.

Yan Gao et al.

Brain, behavior, and immunity, 88, 482-496 (2020-04-14)

Emerging evidence has implicated poly-(ADP-ribose) polymerase 1 (PARP-1), a transcriptional coregulator, in a variety of inflammatory diseases. In the current study, the role of PARP-1 in neuropathic pain and the underlying mechanisms were investigated. Neuropathic pain was determined by assessing

Diabetic endothelial dysfunction: the role of poly(ADP-ribose) polymerase activation.

Garcia Soriano F et al.

Nature medicine, 7(1), 108-113 (2001-01-03)

Diabetic patients frequently suffer from retinopathy, nephropathy, neuropathy and accelerated atherosclerosis. The loss of endothelial function precedes these vascular alterations. Here we report that activation of poly(ADP-ribose) polymerase (PARP) is an important factor in the pathogenesis of endothelial dysfunction in

Daidzein suppresses pro-inflammatory chemokine Cxcl2 transcription in TNF-α-stimulated murine lung epithelial cells via depressing PARP-1 activity.

Hai-yan Li et al.

Acta pharmacologica Sinica, 35(4), 496-503 (2014-03-19)

Daidzein (4',7-dihydroxyisoflavone) is an isoflavone exiting in many herbs that has shown anti-inflammation activity. The aim of this study was to investigate the mechanism underlying its anti-inflammatory action in murine lung epithelial cells. C57BL/6 mice were intranasally exposed to TNF-α

Improved Reperfusion and Vasculoprotection by the Poly(ADP-Ribose)Polymerase Inhibitor PJ34 After Stroke and Thrombolysis in Mice.

Mohamad El Amki et al.

Molecular neurobiology, 55(12), 9156-9168 (2018-04-14)

Benefits from thrombolysis with recombinant tissue plasminogen activator (rt-PA) after ischemic stroke remain limited due to a narrow therapeutic window, low reperfusion rates, and increased risk of hemorrhagic transformations (HT). Experimental data showed that rt-PA enhances the post-ischemic activation of

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