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D5314

Sigma-Aldrich

DPQ

≥98% (HPLC), solid

Synonym(s):

3,4-Dihydro-5-[4-(1-piperidinyl)butoxyl]-1(2H)-isoquinolinone

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About This Item

Empirical Formula (Hill Notation):
C18H26N2O2
CAS Number:
129075-73-6
Molecular Weight:
302.41
MDL number:
MFCD01866274
UNSPSC Code:
12352200
NACRES:
NA.77

biological source

synthetic (organic)

Quality Level

200

Assay

≥98% (HPLC)

form

solid

mp

107-109  °C

solubility

DMSO: 1 mg/mL, clear, colorless to faintly yellow

storage temp.

2-8°C

InChI

1S/C18H26N2O2/c21-18-16-7-6-8-17(15(16)9-10-19-18)22-14-5-4-13-20-11-2-1-3-12-20/h6-8H,1-5,9-14H2,(H,19,21)

InChI key

RVOUDNBEIXGHJY-UHFFFAOYSA-N

Application

DPQ has been used as a PARP1 (poly(ADP-ribose) polymerase 1) inhibitor in in vivo studies to determine the loss of γ-H2AX (H2A histone family member X) upon irradiation.

Biochem/physiol Actions

3,4-Dihydro-5-[4-(1-piperidinyl)butoxyl]-1(2H)-isoquinolinone (DPQ) is known to decrease the PARP 1 (poly(ADP-ribose) polymerase 1) mediated apoptosis under the influence of ischemia. It is considered as more effective inhibitor than the traditionally used PARP1 inhibitor 3-aminobenzamide.
DPQ is a very potent poly(ADP-ribose) polymerase (PARP) inhibitor.

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

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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M J Suto et al.
Anti-cancer drug design, 6(2), 107-117 (1991-05-01)
A series of dihydroisoquinolinones, formally rigid analogs of 3-substituted benzamides, and a series of 2,3-disubstituted benzamides were synthesized and evaluated as inhibitors of poly(ADP-ribose) polymerase. The results indicated that the orientation of the amide with respect to the substituent on
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Cell death induced by excessive glutamate receptor overactivation, excitotoxicity, has been implicated in several acute and chronic neurological disorders. While numerous studies have demonstrated the contribution of biochemically and genetically activated cell death pathways in excitotoxic injury, the factors mediating
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The repair of DNA double strand breaks (DSBs) in male germ cells is slower and differently regulated compared to that in somatic cells. Round spermatids show DSB repair and are radioresistant to apoptosis induction. Mutation induction studies using ionizing irradiation
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