| Identification | Back Directory | [Name]
BENZOTRIAZOL-1-YL-(2,4-DICHLORO-PHENYL)-METHANONE | [CAS]
200626-61-5 | [Synonyms]
CS-2249
ITSA-1(ITSA1)
IFLAB-BB F0451-3184
1-(2,4-Dichlorobenzoyl)-1H-benzotriazole
BENZOTRIAZOL-1-YL-(2,4-DICHLORO-PHENYL)-METHANONE
Methanone, 1H-benzotriazol-1-yl(2,4-dichlorophenyl)- | [Molecular Formula]
C13H7Cl2N3O | [MDL Number]
MFCD00195103 | [MOL File]
200626-61-5.mol | [Molecular Weight]
292.12 |
| Hazard Information | Back Directory | [Uses]
Histone deacetylase (HDAC) inhibitors?are able to interrupt cell cycle progression in transformed cell lines and may be explored as new clinical agents in cancer therapy. 1-(2,4-Dichlorobenzoyl)-1H-benzotriazole has been shown to suppress the biological effects induced by the HDAC inhibitor, Trichostatin A (T774710). | [Definition]
ChEBI: 1-(2,4-dichlorobenzoyl)-1H-1,2,3-benzotriazole is a member of the class of benzamides that is obtained by the formal condensation of 2,4-dichlorobenzoic acid and benzotriazole. It acts as an inhibitor for tubulin acetylation mediated by trichostatin A. It has a role as an inhibitor. It is a member of benzotriazoles, a member of benzamides and a dichlorobenzene. It is functionally related to a 2,4-dichlorobenzoic acid and a benzotriazole. | [Biological Activity]
itsa-1 (itsa1) is an hdac activator through trichostatin a (tsa) suppression.trichostatin a (tsa), a streptomyces metabolite, can specifically inhibit mammalian histone deacetylase at a nanomolar concentration causing accumulation of highly acetylated histone molecules in mammalian cells. | [in vitro]
previous study reported that in murine embryonic stem cells, tsa treatment for 23 hours inhibited brdu incorporation compared with the control. tsa-pretreated cells incubated with itsa1, however, could incorporate brdu at concentrations where it was inhibited by tsa alone. moreover, itsa1 treatment was able to revert the tsa-arrested population to a normal cell cycle distribution. tsa treatment at 300 nm to a549 cells for 2 hours noticeably increased the levels of acetyl-histone h3, whereas subsequent incubation with itsa1 at 50 μm for 2 hours reduced histone acetylation to the baseline level. in addition, cells pretreated with itsa1 before addition of tsa showed increased acetylation levels, which was a characteristic of tsa treatment alone. these results suggested that the target of itsa1 was not present until induced by tsa. furthermore, the itsa1 treatment alone at 50 or 100 μm was not effective on hdac activity, demonstrating that itsa1 could directly affect hdac function [1]. | [References]
[1] koeller km, haggarty sj, perkins bd, leykin i, wong jc, kao mc, schreiber sl. chemical genetic modifier screens: small molecule trichostatin suppressors as probes of intracellular histone and tubulin acetylation. chem biol. 2003 may;10(5):397-410. |
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