Molecular Weight(MW): 314.34
HPOB is a potent, selective HDAC6 inhibitor with IC50 of 56 nM, >30-fold selectivity over other HDACs.
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Effects of HPOB on GCs-induced apoptosis in PC12 and SH-SY5Y cells. (A) Effect of 48 h treatment with HPOB alone and (B) anti-apoptotic effect of HPOB pre-treatment for 24 h on Cort-induced apoptosis in PC12 cells. The results are expressed as the means ± SD of three independent experiments. ## indicates a significant difference from the control (P < 0.01). * indicates a significant difference from treatment with Cort alone at P < 0.05. ** indicates a significant difference from treatment with Cort alone at P < 0.01.
Neurochem Int, 2016, 99:239-51.. HPOB purchased from Selleck.
(C) Western Blot analysis of the expression level of p21 and H3Ac in MM cells treated by HPOB. β-actin and H3 were used as internal controls, respectively; (D) Western Blot analysis of p21, Caspase9, PARP1 and corresponding cleaved forms in RPMI-8226 and U266 cells transfected with p21 plasmids.
Molecules, 2018, 23(5). HPOB purchased from Selleck.
Purity & Quality Control
Choose Selective HDAC Inhibitors
|Description||HPOB is a potent, selective HDAC6 inhibitor with IC50 of 56 nM, >30-fold selectivity over other HDACs.|
In normal (HFS) and transformed (LNCaP, A549, and U87) cells, HPOB induces acetylation of α-tubulin, however, not histones, and inhibits cell growth, however, not viability. In HFS cells, HPOB enhances transformed cell death induced by etoposide, doxorubicin, or SAHA. HPOB also enhancing etoposide-induced transformed cell death via the apoptotic pathway in transformed cells. 
|In vivo||In mice bearing CWR22 human prostate cancer xenografts, HPOB (300 mg/kg/d i.p.), when in combination with SAHA, causes suppression of the growth of established tumors, while produces no significant suppression when used alone. |
In Vitro Enzymatic Assay for Histone Deacetylases:In vitro activities of the 11 recombinant human zinc-dependent HDAC enzymes are detected by ﬂuorigenic release of 7-amino-4-methylcoumarin from substrate upon deacetylase enzymatic activity. A series of dilutions of the unique HDAC6 compound, tubacin, and SAHA are prepared with 10% DMSO in HDAC assay buffer, and 5 μL of the dilution was added to a 50-μL reaction so that the ﬁnal concentration of DMSO is 1% in all of the reactions. The enzymatic reactions are conducted in duplicate at 37 °C for 30 min in a 50-μL mixture containing HDAC assay buffer, 5 μg BSA, an HDAC substrate, an HDAC enzyme, and a test compound. After enzymatic reactions, 50 μL of 2× HDAC developer is added to each well, and the plate is incubated at room temperature for an additional 15 min. Fluorescence intensity is measured at an excitation of 360 nm and an emission of 460 nm using a Synergy microplate reader. Negative (no enzyme, no inhibitor, a drug with no HDAC inhibition activity) and positive controls (known HDAC inhibitor SAHA) are included in the assays. IC50 is determined at the drug concentration that results in 50% reduction of HDAC activity compared with the control.
|In vitro||DMSO||62 mg/mL (197.23 mM)|
|Ethanol||38 mg/mL warmed (120.88 mM)|
* Please note that Selleck tests the solubility of all compounds in-house, and the actual solubility may differ slightly from published values. This is normal and is due to slight batch-to-batch variations.
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* When preparing stock solutions always use the batch-specific molecular weight of the product found on the vial label and MSDS / COA (available online).
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Molar mass (molar weight) is the mass of one mole of a substance and is expressed in g/mol.
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