New Tocriscreen Epigenetics Library

New Tocriscreen Epigenetics Compound Library

Tocris is pleased to announce the release of a new TocriscreenTM Epigenetics Library (Cat. No. 6801); a collection of 101 compounds with proven biological activity against over 40 epigenetic targets, including epigenetic writers, readers, erasers and transcriptional regulators (Figure 1). Compounds are supplied pre-dissolved in DMSO (10 mM, 250 μL) in Matrix storage tubes with SepraSeal caps arranged in 96-well racks. As with all Tocriscreen small molecule libraries, the compounds contained within this Epigenetics library are of the same exceptional purity and quality as the rest of the Tocris catalog, with proven stability and solubility in DMSO. Full chemical and biological data are available for all compounds, many of which are exclusive to Tocris.

Targets within the Tocriscreen Epigenetic Compound Library

Figure 1: The proportion of compounds within the Tocriscreen Epigenetics library targeting epigenetic writers (e.g. DNA methyltransferases (DMNTs); histone acetyltransferases (HATs); lysine methyltransferases (KMTs) and protein arginine methyltransferases (PRMTs)), epigenetic readers, epigenetic erasers (e.g. histone deacetylases (HDACs) and histone demethylases (KDMs)) and transcriptional regulators.

The Tocriscreen range includes the Tocriscreen Plus libraries of 1280 bioactive compounds covering over 300 pharmacological targets, as well as smaller collections of compounds targeted towards a single research area or compound type (e.g. FDA-approved compounds).

To request the detailed compound list for the Tocriscreen Epigenetics Library, or other libraries from the Tocriscreen range, please complete the compound library inquiry form.

Example of how to use a compound library

Compound libraries can be used for target validation, drug repurposing and phenotypic screening, in a range of different assays. Andricovich et al. (2018) used the Tocriscreen Epigenetics Toolbox, a predecessor of the new Epigenetics library, to identify compounds that affect cell viability in Kdm6a-deficient pancreatic cell lines.

KDM6A is an X-chromosome encoded histone demethylase, responsible for removing methyl groups from lysine and arginine residues on histone tails. Loss of function mutations in the KDM6A gene are commonly identified in metastatic pancreatic cancer and there is an inverse relationship between pancreatic tumor grade and KDM6A protein expression.

Seventeen human pancreatic cells lines were screened against 78 small molecules from the Tocriscreen Epigenetics Toolbox at two concentrations for 72 hours; the effect on cancer cell viability was determined. Statistical analysis across all reagents tested allowed the researchers to define two groups of compounds. The first group of compounds consisted of non-specific histone deacetylase inhibitors, which inhibit cell growth and viability in all cell lines tested. The second group contained BET bromodomain and G9a/GLP histone lysine methyltransferase inhibitors, which specifically inhibited cell viability in Kdm6a-deficient cell lines. Further investigation demonstrated that the BET bromodomain inhibitors could reverse squamous differentiation of pancreatic cancer cells, both in vitro and in vivo.


Andricovich et al. (2018) Loss of KDM6A activated super-enhancers to induce gender-specific squamous-like pancreatic cancer and confers sensitivity to BET inhibitors. Cancer Cell. 33, 512. PMID: 29533787