Document Type

Article

Publication Date

11-2014

Publication Source

Bioorganic & Medicinal Chemistry

Abstract

Calpain mediated cleavage of CDK5 natural precursor p35 causes a stable complex formation of CDK5/p25, which leads to hyperphosphorylation of tau. Thus inhibition of this complex is a viable target for numerous acute and chronic neurodegenerative diseases involving tau protein, including Alzheimer’s disease. Since CDK5 has the highest sequence homology with its mitotic counterpart CDK2, our primary goal was to design selective CDK5/p25 inhibitors targeting neurodegeneration. A novel structure-based virtual screening protocol comprised of e-pharmacophore models and virtual screening workflow was used to identify nine compounds from a commercial database containing 2.84 million compounds. An ATP non-competitive and selective thieno[3,2-c]quinolin-4(5H)-one inhibitor (10) with ligand efficiency (LE) of 0.3 was identified as the lead molecule. Further SAR optimization led to the discovery of several low micromolar inhibitors with good selectivity. The research represents a new class of potent ATP non-competitive CDK5/p25 inhibitors with good CDK2/E selectivity.

Inclusive pages

6409–6421

ISBN/ISSN

0968-0896

Document Version

Postprint

Comments

The document available for download is the authors' accepted manuscript, provided in compliance with the publisher's policy on self-archiving. Differences may exist between this document and the published version, available using the link provided. Permission documentation is on file.

Publisher

Elsevier

Volume

22

Issue

22

Peer Reviewed

yes

Link to published version

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