| Identification | Back Directory | [Name]
5-(2-Oxo-2-phenylethoxy)-3,4-dihydroisoquinolin-1(2H)-one | [CAS]
1048371-03-4 | [Synonyms]
CS-874
UPF 1069
UPF 1069 10MG
UPF1069/UPF-1069
UPF 1069;UPF-1069; UPF1069
5-(2-Oxo-2-phenylethoxy)-1(2H)-isoquinolinone
1(2H)-Isoquinolinone, 5-(2-oxo-2-phenylethoxy)-
6H-Oxazolo[4,5-g][3]benzazepine, 7,8,9,10-tetrahydro-8-
5-(2-Oxo-2-phenylethoxy)-3,4-dihydroisoquinolin-1(2H)-one
5-(2-Oxo-2-phenylethoxy)-3,4-dihydroisoquinolin-1(2H)-one USP/EP/BP | [Molecular Formula]
C17H13NO3 | [MDL Number]
MFCD14051631 | [MOL File]
1048371-03-4.mol | [Molecular Weight]
281 |
| Chemical Properties | Back Directory | [storage temp. ]
Store at RT | [solubility ]
Soluble in DMSO (up to 40 mg/ml). | [form ]
solid | [color ]
Off-white | [Stability:]
Stable for 2 years from date of purchase as supplied. Solutions in DMSO may be stored at -20° for up to 3 months. |
| Hazard Information | Back Directory | [Description]
UPF-1069 (1048371-03-4) is a selective PARP-2 inhibitor (IC50=0.3 μM and ~ 27-fold selective against PARP-1).1,2?Increases apoptosis in hippocampal slices but protects cortical cells in models of post-ischemic brain damage.3?Blocks the interaction between PARP-2 and FOXA1, attenuating androgen receptor-mediated gene expression and inhibiting androgen receptor-positive prostate cancer growth.4 | [Uses]
UPF 1069, is a Selective PARP-2 inhibitor. | [References]
1) Pellicciari?et al.?(2008),?On the way to selective PARP-2 inhibitors. Design, synthesis, and preliminary evaluation of a series of isoquinolinone derivatives; Chem. Med. Chem.,?3?914
2) Thorsell?et al.?(2017),?Structural Basis for Potency and Promiscuity in Poly(ADP-ribose) Polymerase (PARP) and Tankyrase Inhibitors; J. Med. Chem.,?60?1262
3) Moroni?et al.?(2009),?Selective PARP-2 inhibitors increase apoptosis in hippocampal slices but protect cortical cells in models of post-ischaemic brain damage; Br. J. Pharmacol.,?157?854
4) Gui?et al.?(2019),?Selective targeting of PARP-2 inhibits androgen receptor signaling and prostate cancer growth through disruption of FOXA1 function; Proc. Natl. Acad. Sci. USA,?116?14573 |
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