| Literature DB >> 32902275 |
Ganesha Rai1, Daniel J Urban1, Bryan T Mott1, Xin Hu1, Shyh-Ming Yang1, Gloria A Benavides2, Michelle S Johnson2, Giuseppe L Squadrito2, Kyle R Brimacombe1, Tobie D Lee1, Dorian M Cheff1, Hu Zhu1, Mark J Henderson1, Katherine Pohida1, Gary A Sulikowski3, David M Dranow4, Md Kabir1, Pranav Shah1, Elias Padilha1, Dingyin Tao1, Yuhong Fang1, Plamen P Christov3, Kwangho Kim3, Somnath Jana3, Pavan Muttil5, Tamara Anderson5, Nitesh K Kunda5, Helen J Hathaway5, Donna F Kusewitt6, Nobu Oshima7, Murali Cherukuri7, Douglas R Davies4, Jeffrey P Norenberg5, Larry A Sklar6, William J Moore8, Chi V Dang9,10, Gordon M Stott8, Leonard Neckers7, Andrew J Flint8, Victor M Darley-Usmar2, Anton Simeonov1, Alex G Waterson3, Ajit Jadhav1, Matthew D Hall1, David J Maloney1.
Abstract
Lactate dehydrogenase (LDH) catalyzes the conversion of pyruvate to lactate, with concomitant oxidation of reduced nicotinamide adenine dinucleotide as the final step in the glycolytic pathway. Glycolysis plays an important role in the metabolic plasticity of cancer cells and has long been recognized as a potential therapeutic target. Thus, potent, selective inhibitors of LDH represent an attractive therapeutic approach. However, to date, pharmacological agents have failed to achieve significant target engagement in vivo, possibly because the protein is present in cells at very high concentrations. We report herein a lead optimization campaign focused on a pyrazole-based series of compounds, using structure-based design concepts, coupled with optimization of cellular potency, in vitro drug-target residence times, and in vivo PK properties, to identify first-in-class inhibitors that demonstrate LDH inhibition in vivo. The lead compounds, named NCATS-SM1440 (43) and NCATS-SM1441 (52), possess desirable attributes for further studying the effect of in vivo LDH inhibition.Entities:
Mesh:
Substances:
Year: 2020 PMID: 32902275 DOI: 10.1021/acs.jmedchem.0c00916
Source DB: PubMed Journal: J Med Chem ISSN: 0022-2623 Impact factor: 7.446