ChemicalBook--->CAS DataBase List--->300816-11-9

300816-11-9

300816-11-9 Structure

300816-11-9 Structure
IdentificationBack Directory
[Name]

NULLSCRIPT
[CAS]

300816-11-9
[Synonyms]

1H-Benz[de]isoquinoline-2(3H)-butanamide, N-hydroxy-1,3-dioxo-
1H-Benz[de]isoquinoline-2(3H)-butanamide, N-hydroxy-1,3-dioxo- (9CI)
[Molecular Formula]

C16H14N2O4
[MDL Number]

MFCD00405081
[MOL File]

300816-11-9.mol
[Molecular Weight]

298.29
Chemical PropertiesBack Directory
[Melting point ]

171-172℃
[storage temp. ]

−20°C
[solubility ]

≤2mg/ml in DMSO;2mg/ml in dimethyl formamide
[form ]

Yellow to off-white solid.
[Sensitive ]

Light Sensitive
Safety DataBack Directory
[Safety Statements ]

22-24/25
Hazard InformationBack Directory
[Definition]

ChEBI: 4-(1,3-dioxo-2-benzo[de]isoquinolinyl)-N-hydroxybutanamide is a member of isoquinolines.
[Biological Activity]

nullscript is an hdac inhibitor.histone deacetylase inhibitors (hdis) have been used in psychiatry and neurology as mood stabilizers and anti-epileptics, such as valproic acid. recently, hdis are being studied as a mitigator or treatment for neurodegenerative diseases. moreover, there has been an effort to develop hdis for cancer therapy.
[in vitro]

nullscript, a close analog of scriptaid, was found to be inactive in transcriptional facilitation at corresponding concentrations, which confirmed a minimal requirement for the length of the linker chain expected for this class of hdac inhibitors. in addition, nullscript was not able to induce the p6sbe-luc reporter construct, which was identified from the library using chemfinder by its structural similarity to scriptaid [1].
[in vivo]

a standard in vivo model of cardiac i/rwe was utilized to examine the in vivo consequences of hdac inhibition in the intact heart. results showed that the treatment with scriptaid led to a nearly identical effect when compared to nullscript, with a 46.8% reduction in infarct size. such results strongly suggested that in murine models, hdacis could reverse the induction of ischemia-induced hdac activity and reduced myocardial infarct size by more than 50% [2].
[References]

[1] g. h. su, t. a. sohn, b. ryu, et al. a novel histone deacetylase inhibitor identified by high-throughput transcriptional screening of a compound library. cancer research 60, 3137-3142 (2000).
[2] anne granger et al. histone deacetylase inhibition reduces myocardial ischemia-reperfusion injury in mice. faseb j. 2008 oct; 22(10): 3549–3560.
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