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].

Clinical trial: So far, no clinical study has been conducted.

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.