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D5314

Sigma-Aldrich

DPQ

≥98% (HPLC), solid

Sinonimo/i:

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

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About This Item

Formula empirica (notazione di Hill):
C18H26N2O2
Numero CAS:
129075-73-6
Peso molecolare:
302.41
Numero MDL:
MFCD01866274
Codice UNSPSC:
12352200
NACRES:
NA.77

Origine biologica

synthetic (organic)

Livello qualitativo

200

Saggio

≥98% (HPLC)

Forma fisica

solid

Punto di fusione

107-109  °C

Solubilità

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

Temperatura di conservazione

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)
RVOUDNBEIXGHJY-UHFFFAOYSA-N

Applicazioni

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.

Azioni biochim/fisiol

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.

Codice della classe di stoccaggio

11 - Combustible Solids

Classe di pericolosità dell'acqua (WGK)

WGK 3

Dispositivi di protezione individuale

dust mask type N95 (US), Eyeshields, Gloves

Certificati d'analisi (COA)

Cerca il Certificati d'analisi (COA) digitando il numero di lotto/batch corrispondente. I numeri di lotto o di batch sono stampati sull'etichetta dei prodotti dopo la parola ‘Lotto’ o ‘Batch’.

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Sigma-Aldrich

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Sigma-Aldrich

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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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