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Key Documents

D5314

Sigma-Aldrich

DPQ

≥98% (HPLC), solid

Synonyme(s) :

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

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About This Item

Formule empirique (notation de Hill):
C18H26N2O2
Numéro CAS:
129075-73-6
Poids moléculaire :
302.41
Numéro MDL:
MFCD01866274
Code UNSPSC :
12352200
Nomenclature NACRES :
NA.77

Source biologique

synthetic (organic)

Niveau de qualité

200

Pureté

≥98% (HPLC)

Forme

solid

Pf

107-109  °C

Solubilité

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

Température de stockage

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)

Clé InChI

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.

Actions biochimiques/physiologiques

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.

Code de la classe de stockage

11 - Combustible Solids

Classe de danger pour l'eau (WGK)

WGK 3

Équipement de protection individuelle

dust mask type N95 (US), Eyeshields, Gloves

Certificats d'analyse (COA)

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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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Nature medicine, 3(10), 1089-1095 (1997-10-23)
Nitric oxide (NO) and peroxynitrite, formed from NO and superoxide anion, have been implicated as mediators of neuronal damage following focal ischemia, but their molecular targets have not been defined. One candidate pathway is DNA damage leading to activation of
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