Discovery and Optimization of Potent, Cell-Active Pyrazole-Based Inhibitors of Lactate Dehydrogenase (LDH)

Ganesha Rai(National Institutes of Health), Kyle R. Brimacombe(National Institutes of Health), Bryan T. Mott(National Institutes of Health), Daniel J. Urban(National Institutes of Health), Xin Hu(National Institutes of Health), Shyh‐Ming Yang(National Institutes of Health), Tobie D. Lee(National Institutes of Health), Dorian M. Cheff(National Institutes of Health), Jennifer Kouznetsova(National Institutes of Health), Gloria A. Benavides(University of Alabama at Birmingham), Katie Pohida(National Institutes of Health), Eric J. Kuenstner(National Institutes of Health), Diane K. Luci(National Institutes of Health), Christine Lukacs(Beryllium (United States)), D.R. Davies(Beryllium (United States)), David M. Dranow(Beryllium (United States)), Hu Zhu(National Institutes of Health), Gary A. Sulikowski(Vanderbilt University), William Moore(Leidos (United States)), Gordon M. Stott(Leidos (United States)), Andrew Flint(Leidos (United States)), Matthew D. Hall(National Institutes of Health), Victor Darley‐Usmar(University of Alabama at Birmingham), Leonard Μ. Neckers(National Cancer Institute), Chi V. Dang(Cancer Research Institute), Alex G. Waterson(Vanderbilt University), Anton Simeonov(National Institutes of Health), Ajit Jadhav(National Institutes of Health), David J. Maloney(National Institutes of Health)
Journal of Medicinal Chemistry
November 9, 2017
Cited by 154Open Access
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Abstract

We report the discovery and medicinal chemistry optimization of a novel series of pyrazole-based inhibitors of human lactate dehydrogenase (LDH). Utilization of a quantitative high-throughput screening paradigm facilitated hit identification, while structure-based design and multiparameter optimization enabled the development of compounds with potent enzymatic and cell-based inhibition of LDH enzymatic activity. Lead compounds such as 63 exhibit low nM inhibition of both LDHA and LDHB, submicromolar inhibition of lactate production, and inhibition of glycolysis in MiaPaCa2 pancreatic cancer and A673 sarcoma cells. Moreover, robust target engagement of LDHA by lead compounds was demonstrated using the cellular thermal shift assay (CETSA), and drug-target residence time was determined via SPR. Analysis of these data suggests that drug-target residence time (off-rate) may be an important attribute to consider for obtaining potent cell-based inhibition of this cancer metabolism target.


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