Discovery of PF-06928215 as a high affinity inhibitor of cGAS enabled by a novel fluorescence polarization assay

J. Perry Hall(Pfizer (United States)), Amy Brault(Pfizer (United States)), Fabien Vincent(Pfizer (United States)), Shawn Weng(Pfizer (United States)), Hong Wang(Pfizer (United States)), Darren S. Dumlao(Pfizer (United States)), Ann Aulabaugh(Pfizer (United States)), Dikran Aivazian(Pfizer (United States)), Dana Castro(Pfizer (United States)), Ming Chen(Pfizer (United States)), Jeffrey S. Culp(Pfizer (United States)), Ken Dower(Pfizer (United States)), Joseph P. Gardner(Pfizer (United States)), Steven J. Hawrylik(Pfizer (United States)), Douglas T. Golenbock(University of Massachusetts Chan Medical School), David Hepworth(Pfizer (United States)), Mark Horn(Pfizer (United States)), Lyn H. Jones(Pfizer (United States)), Peter Jones(Pfizer (United States)), Eicke Latz(University of Massachusetts Chan Medical School), Jing Li(Pfizer (United States)), Lih‐Ling Lin(Pfizer (United States)), Wen Lin(Pfizer (United States)), David W. Lin(Pfizer (United States)), Frank Lovering(Pfizer (United States)), Nootaree Niljanskul(Pfizer (United States)), Ryan Nistler(Pfizer (United States)), Betsy S. Pierce(Pfizer (United States)), Olga Plotnikova(Pfizer (United States)), Daniel C. Schmitt(Pfizer (United States)), Suman Shanker(Pfizer (United States)), James F. Smith(Pfizer (United States)), W.B. Snyder(Pfizer (United States)), Timothy A. Subashi(Pfizer (United States)), John I. Trujillo(Pfizer (United States)), Edyta Tyminski(Pfizer (United States)), Guoxing Wang(Pfizer (United States)), Jimson Wong(Pfizer (United States)), Bruce A. Lefker(Pfizer (United States)), Leslie Dakin(Pfizer (United States)), Karen L. Leach(Pfizer (United States))
PLoS ONE
September 21, 2017
Cited by 161Open Access
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Abstract

Cyclic GMP-AMP synthase (cGAS) initiates the innate immune system in response to cytosolic dsDNA. After binding and activation from dsDNA, cGAS uses ATP and GTP to synthesize 2', 3' -cGAMP (cGAMP), a cyclic dinucleotide second messenger with mixed 2'-5' and 3'-5' phosphodiester bonds. Inappropriate stimulation of cGAS has been implicated in autoimmune disease such as systemic lupus erythematosus, thus inhibition of cGAS may be of therapeutic benefit in some diseases; however, the size and polarity of the cGAS active site makes it a challenging target for the development of conventional substrate-competitive inhibitors. We report here the development of a high affinity (KD = 200 nM) inhibitor from a low affinity fragment hit with supporting biochemical and structural data showing these molecules bind to the cGAS active site. We also report a new high throughput cGAS fluorescence polarization (FP)-based assay to enable the rapid identification and optimization of cGAS inhibitors. This FP assay uses Cy5-labelled cGAMP in combination with a novel high affinity monoclonal antibody that specifically recognizes cGAMP with no cross reactivity to cAMP, cGMP, ATP, or GTP. Given its role in the innate immune response, cGAS is a promising therapeutic target for autoinflammatory disease. Our results demonstrate its druggability, provide a high affinity tool compound, and establish a high throughput assay for the identification of next generation cGAS inhibitors.


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