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Merck
CN

5.08194

Sigma-Aldrich

HDAC6 Inhibitor III

Synonym(s):

HDAC6 Inhibitor III

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About This Item

Empirical Formula (Hill Notation):
C20H19N3O3
CAS Number:
Molecular Weight:
349.38
UNSPSC Code:
12352200
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Assay

≥98% (HPLC)

Quality Level

form

powder

potency

29 nM IC50

manufacturer/tradename

Calbiochem®

storage condition

OK to freeze
protect from light

color

cream

solubility

DMSO: 10 mg/mL

storage temp.

−20°C

General description

A cell-permeable, quinazolin-4-one based hydroxamic acid containing compound that acts as a potent and selective inhibitor of histone deacetylase 6 (HDAC6; IC50 = 29 nM). Exhibits high selectivity over other HDACs (IC50 = 1.88, 6.45, 1.75, and 4.08 µM for HDAC1, 2, 8, and 11, respectively). Does not affect hERG activity (>10 µM) or p450 activity (IC50 >6.5 µM). Blocks b-amyloid (Ab) aggregation in the presence of zinc (IC50 = 9.5 µM) and improves learning-based performance in mice. Induces neurite outgrowth (EC50 = 7.3 and 9.2 µM in PC12 and SH-SY5Y cells, respectively) and enhances synaptic activity (EC50 = 6.5 and 6.8 µM in PC12 and SH-SY5Y cells, respectively). Shown to enhance acetylated a-tubulin levels in hippocampus region of mice with Ab lesions.

Please note that the molecular weight for this compound is batch-specific due to variable water content.

Biochem/physiol Actions

Cell permeable: yes
Reversible: yes

Packaging

Packaged under inert gas

Other Notes

Yu, C.W., et al. 2013. J. Med. Chem.56, 6775.

Legal Information

CALBIOCHEM is a registered trademark of Merck KGaA, Darmstadt, Germany

Disclaimer

Toxicity: Standard Handling (A)

Storage Class Code

11 - Combustible Solids

WGK

WGK 3

Flash Point(F)

Not applicable

Flash Point(C)

Not applicable

Regulatory Information

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Certificates of Analysis (COA)

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Cancer is a complex disease manifestation. At its core, it remains a disease of abnormal cellular proliferation and inappropriate gene expression. In the early days, carcinogenesis was viewed simply as resulting from a collection of genetic mutations that altered the gene expression of key oncogenic genes or tumor suppressor genes leading to uncontrolled growth and disease (Virani, S et al 2012). Today, however, research is showing that carcinogenesis results from the successive accumulation of heritable genetic and epigenetic changes. Moreover, the success in how we predict, treat and overcome cancer will likely involve not only understanding the consequences of direct genetic changes that can cause cancer, but also how the epigenetic and environmental changes cause cancer (Johnson C et al 2015; Waldmann T et al 2013). Epigenetics is the study of heritable gene expression as it relates to changes in DNA structure that are not tied to changes in DNA sequence but, instead, are tied to how the nucleic acid material is read or processed via the myriad of protein-protein, protein-nucleic acid, and nucleic acid-nucleic acid interactions that ultimately manifest themselves into a specific expression phenotype (Ngai SC et al 2012, Johnson C et al 2015). This review will discuss some of the principal aspects of epigenetic research and how they relate to our current understanding of carcinogenesis. Because epigenetics affects phenotype and changes in epigenetics are thought to be key to environmental adaptability and thus may in fact be reversed or manipulated, understanding the integration of experimental and epidemiologic science surrounding cancer and its many manifestations should lead to more effective cancer prognostics as well as treatments (Virani S et al 2012).

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