Droxinostat Property

Density 

1.252

storage temp. 

Inert atmosphere,2-8°C

solubility 

DMSO: ≥20mg/mL

form 

powder

color 

white to off-white

Safety

Hazard Codes 

Xn

Risk Statements 

22-37/38-41

Safety Statements 

26-39

WGK Germany 

3

Hazard and Precautionary Statements (GHS)

Symbol(GHS)

Signal word

Danger

Hazard statements

H302Harmful if swallowed

H315Causes skin irritation

H318Causes serious eye damage

H335May cause respiratory irritation

Precautionary statements

P261Avoid breathing dust/fume/gas/mist/vapours/spray.

P280Wear protective gloves/protective clothing/eye protection/face protection.

P305+P351+P338IF IN EYES: Rinse cautiously with water for several minutes. Remove contact lenses, if present and easy to do. Continuerinsing.

Droxinostat Chemical Properties,Usage,Production

Uses

Droxinostat is a histone deacetylase selective inhibitor and is used in cancer therapy and cancer research. Droxinostat is a selective inhibitor of HDAC3, HDAC6, and HDAC8.

Definition

ChEBI: 4-(4-chloro-2-methylphenoxy)-N-hydroxybutanamide is an aromatic ether.

Biological Activity

droxinostat is a selective inhibitor of hdac3, hdac6, and hdac8 with ic50 value of 16.9 ± 5.0 μm, 2.47 ± 1.09 μm, and 1.46 ± 0.11 μm, respectively [1].hdacs (histone deacetylases) are enzymes responsible of the deacetylation of lysine that residues of core histones and play a pivotal role in controlling chromatin remodeling and transcriptional activation. it is also reported that hdacs control the acetylation and activation status of multiple non-histone proteins, including the heat shock protein 90 (hsp90) which is an essential molecular chaperone for fungal virulence and antifungal resistance. multiple hdacs have been identified and hdac1 to hdac10 are shown to express in malignant cells which reminds the hdac inhibitor as a target for cancer therapy [2] [3].droxinostat is a selective hdac inhibitor and is different from the known pan-hdaci tsa which inhibits all tested hdac. when tested with prostate cancer line ppc-1 cells, droxinostat treatment selectively inhibited hdac3, hdac6, and hdac8 activity at the concentration of 50 μm/l which sensitized cells to death ligands [1]. in androgen-dependent cap cells, administration of droxinostat selectively inhibited hdacs and downregulated c-flp expression which resulted in cells apoptosis [4].

target

HDAC8

References

[1]. wood, t.e., et al., selective inhibition of histone deacetylases sensitizes malignant cells to death receptor ligands. mol cancer ther, 2010. 9(1): p. 246-56.
[2]. lamoth, f., p.r. juvvadi, and w.j. steinbach, histone deacetylase inhibition as an alternative strategy against invasive aspergillosis. front microbiol, 2015. 6: p. 96.
[3]. mackmull, m.t., et al., histone deacetylase inhibitors cause the selective depletion of bromodomain containing proteins. mol cell proteomics, 2015.
[4]. mccourt, c., et al., elevation of c-flip in castrate-resistant prostate cancer antagonizes therapeutic response to androgen receptor-targeted therapy. clin cancer res, 2012. 18(14): p. 3822-33.