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The Tocriscreen compound libraries are composed of biologically active compounds that have proven pharmacological activity against GPCRs, ion channels, kinases, enzymes, nuclear receptors and transporters.
|Cat. No.||Product Name / Activity|
|7150||Tocriscreen 2.0 Max|
|A library of 1280 biologically active compounds (250 μL 10 mM DMSO solutions)|
|7152||Tocriscreen 2.0 Micro|
|A library of 1280 biologically active compounds (15 μL 10 mM DMSO solutions)|
|7151||Tocriscreen 2.0 Mini|
|A library of 1280 biologically active compounds (50 μL 10 mM DMSO solutions)|
|6801||Tocriscreen Epigenetics Library|
|A library of 101 epigenetic compounds (250 μL, 10 mM DMSO solutions)|
|7200||Tocriscreen FDA-Approved Drugs Library New|
|Drug repurposing library; a library of 190 compounds equivalent to active components of drug formulations approved by the FDA|
|6268||Tocriscreen Kinase Inhibitor Library|
|A library of 160 kinase inhibitor compounds (250 μL 10 mM DMSO solutions)|
Compound libraries can be used in a wide array of experiments, in all areas of research, for drug re-profiling, receptor de-orphaning, target validation, tool compound identification and assay development. Below you will find some examples of how other researchers have used Tocriscreen compound libraries.
The blood brain barrier (BBB) stops conventional chemotherapy agents from reaching brain tumors, which means that brain cancers such as gliomas are hard to treat. Traditional methods for testing the BBB permeability of a compound via high throughput screening is limited to radio- or fluorescently-labeled compounds passing through a monolayer cell culture. In their paper Sherman & Rossi outlined the development of a 3D BBB plus glioma model, which allows for investigation of a compounds BBB permeability alongside its tumor cytotoxicity. They validated this model by screening compounds from the Tocriscreen Kinase Inhibitor Library for their toxicity, and compared this to their activity in a standard tumor cell model to identify brain permeable hits.
Sherman & Rossi (2019) A novel three-dimensional glioma blood-brain barrier model for high-throughput testing of tumoricidal capability. Front.Oncol. 351, eCollection. PMID: 31131260
Fujita et al screened compounds from the Tocriscreen Mini Library for their activity against CCL17 activity in the HaCat human epidermal keratinocyte cell line. CCL17 production was induced by TNF-α and/or IFN-γ. Of the compounds that were identified to affect CCL17 activity, GW 9508 (Cat. No. 2649) showed the highest potency, indicating a new action for this compound, which has previously been shown to be a free fatty acid receptor 1 (FFA1/GPR40) agonist.
Fujita et al (2011) A GPR40 agonist GW9508 suppresses CCL5, CCL17, and CXCL10 induction in keratinocytes and attenuates cutaneous immune inflammation. J.Invest.Dermatol. 13, 1660. PMID: 21593768
CRISPR-Cas9 technology has emerged as a powerful tool for sequence-specific gene knockout through non-homologous end joining. However, the experimental process required is inefficient for the precise editing of genome sequences. In this paper, Yu et al screened compounds from the Tocriscreen Plus Library to identify small molecules that can enhance the efficacy of CRISPR-Cas9 mediated homology-directed repair, and identified a range of compounds in diverse cell types.
Yu et al (2015) Small molecules enhance CRISPR genome editing in pluripotent stem cells. Cell Stem Cell. 16, 142. PMID: 25658371
Satori et al showed that expression of BIN1, a commonly identified risk factor gene for Alzheimer's disease, modulates its interaction with Tau, possibly through signaling pathways that regulate Tau phosphorylation. To investigate these signaling pathways further, they developed a high throughput screening approach using primary hippocampal neuron cultures. They tested compound from the Tocriscreen Mini Library, with subsequent cellular assays for validation, and identified two compounds that modulated the BIN1-Tau interaction in neurons. Both compounds were known to target regulators as tau phosphorylation within calcineurin and MEK-dependent signaling pathways.
Sartori et al (2019) BIN1 recovers tauopathy-induced long-term memory deficits in mice and interacts with Tau through Thr348 phosphorylation. Acta.Neurophathol. 138, 631. PMID: 31065832