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D5314

Sigma-Aldrich

DPQ

≥98% (HPLC), solid

Synonym(e):

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

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About This Item

Empirische Formel (Hill-System):
C18H26N2O2
CAS-Nummer:
129075-73-6
Molekulargewicht:
302.41
MDL-Nummer:
MFCD01866274
UNSPSC-Code:
12352200
NACRES:
NA.77

Biologische Quelle

synthetic (organic)

Qualitätsniveau

200

Assay

≥98% (HPLC)

Form

solid

mp (Schmelzpunkt)

107-109  °C

Löslichkeit

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

Lagertemp.

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)

InChIKey

RVOUDNBEIXGHJY-UHFFFAOYSA-N

Anwendung

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. Wirkung

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.

Lagerklassenschlüssel

11 - Combustible Solids

WGK

WGK 3

Persönliche Schutzausrüstung

dust mask type N95 (US), Eyeshields, Gloves

Analysenzertifikate (COA)

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Sigma-Aldrich

496383

1,10-Phenanthrolin-5,6-dion

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Sigma-Aldrich

131377

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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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