ScriptaidScriptaid
MedChemExpress (MCE)
HY-15489
287383-59-9
Scriptide
GCK1026
98.0%
Powder -20°C 3 years 4°C 2 years In solvent -80°C 2 years -20°C 1 year
Room temperature in continental US
may vary elsewhere.
Scriptaid is a potent histone deacetylase (HDAC) inhibitor, used in cancer research. Scriptaid is also a sensitizer to antivirals and has potential for epstein-barr virus (EBV)-associated lymphomas treatment.
Scriptaid (1 μg/mL) treatment inhibits cell growth in breast cancer cell lines, results in increased accumulation of both acetyl H3 and acetyl H4 proteins in MDA-MB-231, MDA-MB-435, and Hs578t cells. Scriptaid also inhibits cell growth of MDA-MB-231, MDA-MB-435, and Hs578t cell lines, with IC50s of 0.5-1.0 μg/mL. Scriptaid (0.1-1.0 μg/mL) induces ER and PR mRNA expression in a dose dependent manner
when it is combined with AZA, they enhance ER expression and induce a functional ER protein[1]. Scriptaid and SAHA preferentially inhibit the Class I histone deacetylases, hdac1, 2, and 3. Scriptaid is a potent anti-T. gondii compound with low cytotoxicity, and the IC50 is 39 nM. Scriptaid has atypical effects in T. gondiiinfected HS68 cells[2]. Scriptaid inhibits the growth of HeLa cells with IC50 of 2 μM at 48 h in a dose-dependent manner. Scriptaid also affects cell-cycle and apoptosis[3].
Scriptaid (3.5 μg/g mouse, i.p.) clearly inhibits tumor growth in a xenograft mouse model[1].
Four to six week old athymic female nude mice are housed under laminar flow hoods in an environmentally controlled pathogen free animal facility for the duration of experiments. Mice are injected with 2×106 MDA-MB-231 human breast cancer cells into each flank. Tumors are allowed to grow to approximately 0.1 cm3 in diameter before treatment. Mice are then treated with Scriptaid (3.5 µg/g mouse), TSA (0.5 µg/g mouse), or DMSO vehicle intraperitoneally for five consecutive days with 2 days rest each week for a total of 4 weeks. Individual tumor measurements are recorded from each flank weekly[1].
IC50 concentrations of Scriptaid are determined in MDA-MB-231, MDA-MB-435 and Hs578t cells by MTT assay. For cell growth assays, MDA-MB-231, MDA-MB-435, and Hs578t cells are plated at a cell density of 5000 cells/well in 12 well plates and treated with 1.0 µg/mL Scriptaid for up to 3 days. Cells are counted daily using a Coulter counter. Percent growth inhibition is determined by comparison of treated and untreated cells[1].
HDAC
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[1]. Keen JC, et al. A novel histone deacetylase inhibitor, scriptaid, enhances expression of functional estrogen receptor alpha (ER) in ER negative human breast cancer cells in combination with 5-aza 2'-deoxycytidine. Breast Cancer Res Treat. 2003 Oct
81(3):177-86. [Content Brief]
[2]. Strobl JS, et al. Scriptaid and suberoylanilide hydroxamic acid are histone deacetylase inhibitors with potent anti-Toxoplasma gondii activity in vitro. J Parasitol. 2007 Jun
93(3):694-700. [Content Brief]
[3]. Janaki Ramaiah M, et al. Scriptaid cause histone deacetylase inhibition and cell cycle arrest in HeLa cancer cells: A study on structural and functional aspects. Gene. 2017 Sep 5
627:379-386. [Content Brief]
[4]. Ghosh SK, et al. Histone deacetylase inhibitors are potent inducers of gene expression in latent EBV and sensitize lymphoma cells to nucleoside antiviral agents. Blood. 2012 Jan 26
119(4):1008-17. [Content Brief]
