Delineation of the molecular mechanisms of nucleoside recognition by cytidine deaminase through virtual screening.

ChemMedChem

Laboratory of Biological Modeling, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, DHHS, 12A South Drive, Bethesda, MD 20892, USA.

Published: August 2011

Cytidine deaminase (EC 3.5.4.5, CDA), an enzyme of the pyrimidine salvage pathways, is responsible for the degradation and inactivation of several cytidine-based antitumor drugs such as cytarabine, gemcitabine, decitabine, and azacytidine. Thus, CDA inhibitors are highly sought after as compounds to be co-administered with said drugs to improve their effectiveness. Alternatively, the design of antitumor drugs not susceptible to the action of CDA is also regarded as an attractive solution. Herein we describe a virtual screen for CDA ligands based on chemical similarity and molecular docking. The campaign led to the identification of three novel inhibitors and one novel substrate, with a 19 % hit rate, and allowed a significant extension of the structure-activity relationships, also in light of the compounds that resulted inactive. The most active compound identified through the screen is the inhibitor pseudoisocytidine, which has the potential to serve as a lead for highly stable compounds. The study also delineated the detrimental effect of 5-aza and 6-aza substitutions, the incompatibility of the presence of an amino group at the 3'-position, as well as the presence of very strict steric requirements around the 2'-arabino position and, even more, the N4-position. Importantly, these features can be exploited for the design of novel anti-neoplastic agents resistant to the action of CDA.

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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3193038PMC
http://dx.doi.org/10.1002/cmdc.201100139DOI Listing

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Article Synopsis
  • Gemcitabine (GEM) is widely used to treat solid tumors, but its effectiveness is limited by rapid metabolism into an inactive form (dFdU) by the enzyme cytidine deaminase (CDA), which decreases its oral bioavailability.
  • Cedazuridine (CDZ) has been identified as a potent inhibitor of CDA, and when combined with GEM, it may enhance GEM's oral bioavailability.
  • A study using HPLC-MS/MS confirmed that CDZ significantly improved GEM's bioavailability in mice by inhibiting its metabolism, suggesting potential benefits for clinical applications of the GEM-CDZ combination.
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