| Identification | Back 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 Properties | Back 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 |
| Hazard Information | Back Directory | [Uses]
Nullscript is a negative control for Scriptaid. Nullscript is a known inactive analog of Scriptaid[1]. Scriptaid is a representative HDAC inhibitor[2]. Nullscript inhibits Cryptosporidium (C. parvum) growth with the IC50 value of 2.1 μM[3]. | [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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